PHYSIOLOGY

EXAM 2

Lecture 9/11

Digestive System in two categories

1. Alimentary Canal (GI tract): tube where food and chyme passes; mouth  pharynx 
esophagus  stomach  small intestine  large intesting
2. Accessory Structures: aid in breakdown of food; liver, gallbladder, pancreas, salivary glands

Alimentary Canal

- Made of four layers

- Lumen: hole that food/chyme passes through
1. Mucosa
a. made of epithelium (direct contact)
b. lamina propria (made of blood vessels and lymphatic vessels), mucosa (associated with
lymphatic tissue or MALT)
i. MALT = immune response
c. Muscularis mucosae: smooth muscle
i. Causes folding and increases the surface area
2. Submucosa: contains blood vessels and lymphatic vessels; also composed of submucosal glands
a. Submucosal glands = release digestive (juices?)
3. Muscularis: necessary for movement of food and chyme and its mechanical digestion
a. Circular muscle
b. Longitudinal muscle
4. Serosa: holds organism in place
a. Areolar connective tissue
b. Epithelium

Digestive Processes

- Ingestion = entry of food into the alimentary canal

- Propulsion = movement of food/chyme
o Peristalsis = alternating waves of contraction and relaxation of the muscularis layer
of the alimentary canal
- Mechanical digestion = breaking down food into smaller pieces
o Mastication = chewing
o Segmentation = like peristalsis; contraction of muscularis layer with back and forth
movement.
- Chemical Digestion = enzymes breakdown food into smaller and smaller molecules into
small building blocks
- Absorption = primarily done in small intestine; movement of nutrients from alimentary canal
into the blood  once in blood nutrients go where the need to
- Defecation = elimination of undigested materials
Alimentary Canal

Mouth

- Other accessory organs

o Teeth: aid in mastication; mechanical digestion of food
o Tongue: moves the chewed food into a bolus and swallows the bolus; synthesizes
and secretes enzymes
o Salivary glands: secrete saliva which has ions, glycoproteins, enzymes, waste
products, water, and lysosomes  these maintain the pH of the saliva and
lubricates the bolus so its easier to swallow
- Enzymes are produced in the mouth = chemical digest
o Salivary amylase  breakdown starches
 Active in mouth, pharynx, and esophagus
 Becomes inactive in the stomach
o Lingual lipase = breakdown lipinds
 Inactive in the mouth
 Active in the stomach

Pharynx

- Bolus enters the pharynx and esophagus after the mouth

- Both air and food

Esophagus

- Bolus must pass through the upper esophageal sphincter FIRST

o Controls the movement of food from the pharynx into the esophagus
o Mainly composed of skeletal muscle (allows us to decide when to swallow)
- Upper 2/3 is composed of both skeletal and smooth muscle
o Skeletal = voluntary
o Smooth = involuntary
- Bolus undergoes peristalsis at the point
- Lower 1/3 of the esophagus is mainly smooth muscle
o Decrease in skeletal muscle moving down the esophagus
- Lower esophageal sphincter
o Only smooth muscle
o Functions to prevent stomach juices from entering the esophagus

Stomach

- Top end of the stomach is the fundus

- Most of the stomach is the body
o Contains rugae/folding  allows for stomach to stretch when it is full
- Way out of the stomach is the pylorus region
- Next to the pylorus region is the pyloric sphincter
o Exit out of the stomach and into the small intestine
 - Most of the stomach is made of surface mucus cells
o Secrete surface mucus that is alkaline
o Alkaline helps with the control of gastric acids so the acids don’t hurt the stomach
wall
- Gastric pits line the stomach wall
o Composed of parietal cells that secrete hydrochloric acid
 HCL kills the microorganisms that we cell
 Also secretes intrinsic factor = necessary for the absorption of B12
o Mucus neck cells = secretes different mucus than surface; unknown function
o Chiefs cells: synthesize and secrete pepsinogen, the inactive form of pepsin
o Enteroendocrine cells: secrete various hormones (ex. Gastrin from G-cells)
- What digestive processes occur in the stomach?
o Propulsion
o Mechanical (gastric mixing)
o Chemical (enzymes like pepsin and gastric lipase and lingual lipase)
- Stomach empties through gastric emptying
o Goes out the pyloric sphincter ~30 mL at a time
o 2-4 to completely empty

Small intestine

- Fenum
- Jejunum
- Ileum
- What occurs in the small intestine?
o Propulsion
o Chemical digestion
o Mechanical digestion (segmentation)
o Absorption – biggest primary function of small intestine
- Circular folds: inc surface to inc absorption
- Vili: inc surface area
o Microvilli/brush border: contains enzymes that break down and chemically digest
chyme
- Goblet Cell: secretes mucus
- Crypt of lieberkhan: secretes intestinal juices that help with buffering gastric acids from
stomach

Large intestine:

- Ileocecal valve/sphincter
- Cecum: blind alley gut
- Veriform appendix: vestigial organ; seed of microbiota of gut
- Ascending colon:
- Transverse colon:
 - Descending colon:
- Sigmoid colon:
- Rectum
- Anal canal
- Main function to finish absorption of nutrients and reabsorb as much water as possible
o Reabsorbing water allows feces to form
o Then feces are eliminated
o Make certain vitamins
- Digestive processes?
o Absorption
o Mechanical digestion
 mass movement – strong contraction that move chyme
 haustral contractions – sluggish segmentation
o propulsion (peristalsis)

lecture 9/14

Accessory Organs

- liver: heavy lifting; many functions and secretions

1. secretes bile
2. removes old RBC
3. processes metabolic nutrients after meals
a. excess glucose  stored as glycogen
b. turn some amino acids into fatty acids
c. synthesize triglycerides and cholesterol
4. processes metabolic nutrients between meals
a. turn glycogen  glucose
b. AA  glucose
c. Fatty acids  ketones  energy sources
5. Synthesizes hormones
6. Synthesizes plasma proteins
7. Helps with elimination of waste
8. Stores essential molecules
- gallbladder: storing and concentrating bile

Bile Salts

- synthesized in liver from cholesterol

- secreted in bile to duodenum
- amphipathic molecule (nonpolar and polar parts)
- main function: emulsify fat

Emulsification of fat globule

- turns a really big fat globule  many little fat droplets

o creates an increase of surface
 - nonpolar parts interact with the fat while the polar parts interact with water
o allows water to surround the little fat droplets

Pancreas: synthesizes the pancreatic juice

- components of pancreatic juice

o zymogens: inactive enzymes that breakdown proteins (proteases)
o bicarbonate buffer juice: buffer gastric juice
o colipase: helps load lipase onto fats
o pancreatic amylase: starch breakdown
o pancreatic lipase: breakdown fats

Zymogens

- inactive storage form of proteases produced via exocrine acinar cells of the pancreas
o trypsinogen
o chymotrypsinogen
o procarboxypeptidase
- Stored in zymogen granules (secretory vesicles)
- Secreted by exocytosis from acinar
- Activated in small intestine by proteolytic activation
- Pancreatic duct binds with bile duct
o When joined together = ampulla of vader
- Has to pass through the sphincter of oddi to enter the duodenum

How are zymogens produced?

- DNA  mRNA  peptide in RER  travels to the golgi apparatus  packaged into
secretory vesicles (zymogen vesicles)  exocytosed into pancreatic duct  ampulla of
vader  through sphincter of oddi  duodenum of small intestine  activated through
proteolytic activation  able to chemical digest more proteins

Proteases = hydrophilic

- Left through exocytosis (if hydrophobic they would’ve diffused through the membrane)

Lecture 9/14

Most absorption occurs in the small intestine

First digested in lumen  nutrients cross the apical membrane into the epithelial cell  leave epithelial
cell through the basolateral membrane  nutrients can enter the bloodstream and go throughout the
body

Amylase: generic term for the enzymes that breakdown polysaccharides

- Secreted and synthesized in the salivary glands

o Salivary glands = salivary amylase
o Pancreas = pancreatic amylase
- Starch/glycogen  maltose + limit (alpha) dextrins (brush border enzymes)
 o Starch = from plants
o Glycogen = skeletal and liver muscles
o Maltose broken by maltase into 2 glucose
o Limit (alpha) dextrins broken by dextrinase into glucose

Absorption of carbohydrates

- Only monosaccharides can be absorbed

o Glucose, galactose, fructose
- Absorption crosses two membranes
o Apical first (glucose = secondary active transport)
o Basolateral second (glucose = facilitated diffusion)
- Glucose movement
o Concentration gradient from sodium potassium pump
 Needs to hydrolyze ATP
 Primary active transport
 Need Na lower inside cell; allows Na to go down its gradient from the lumen
into the epithelial cell
 Allows glucose to go from low concentration to high concentration
 Glucose uses secondary active transport with Na (Cotransport w Na)
 High gluc inside cell and low glucose outside the basolateral membrane
transport (passive transport = facilitated diffusion to cross basolateral
membrane)
o Galactose uses same mechanism
- Fructose movement
o Uses facilitated diffusion for BOTH apical and basolateral

Proteins

- Typical diet: 125g/day protein

o Only require 40-50 g
- Proteins to be digested and absorbed include
o Consumed in diet
o Secreted into lumen of intestinal tract (e.g. enzymes)
o Sloughed off with cells lining intestinal tract (e.g. enterocytes)
- Proteases = breakdown proteins
- Protein digestion products
o Amino acids
o Dipeptides (two AA’s)
o Tripeptides (3 AA’s)

Types of Proteases

- Endopeptidases
o Endo = in
o Split polypeptide at interior peptide bond
 o Product = small peptide fragments (tripeptides and dipeptides
- Exopeptidases
o Exo = out
o Cleave off amino acids from one end of polypeptide
o Product = individual amino acids

Overview: Protein Digestion in GI tract

- Zymogens = inactive proteases

o Trypsinogen
o Chymotrypsinogen
o Procarboxypeptidase
o Elastase
- Pancreatic proteases (actives of the zymogens)
o Trypsin
o Chymotrypsin
o Carboxypeptidase
- Stomach protease (1)
o Pepsinogen (inactivated)
o Pepsin (activated)
- Brush border proteases
o Peptidases (e.g. aminopeptidase, dipeptidase)
o Enteropeptidase (enterokinase)

Protein Digestion in the stomach

- Gastric pits
o Parietal cells = HCl secretion to kill off microorganisms and intrinsic factor for B12
absorption
o Chief cells = create pepsinogen (inactive form of pepsin)
o HCl released by parietal cells  half activates pepsinogen  converts more
pepsinogen into pepsin  pepsin breaks down protein into smaller peptide
fragments (endopeptidase)

Protein digestion in small intestine

- Smaller peptide fragments go through the pyloric sphincter  into the small intestine
- Pancreatic proteases
o Trypsin
o Chymotrypsin
o Carboxypeptidase
- Brush border proteases
o Aminopeptidase
o Enterokinase

Activations of Zymogens
 - Zymogens from acinar cells are released into the duodenum of small intestine 
trypsinogen makes way to enterokinase (=enteropeptidase)  trypsinogen converted into
trypsin  trypsin converts chymotrypsinogen into chymotrypsin  Trypsin also converts
procarboxypeptidase into carboxypeptidase  gives three active proteases
- Give protein trypsin = smaller peptides (endopeptidase)
- Give protein chymotrypsin = smaller peptides (endopeptidase)
- Give protein carboxypeptidase = individual amino acids (exopeptidase)
- Give protein pepsin = smaller peptide

Absorption of Amino Acids

- Na/K pump = primary active transport

- AA’s across apical membrane = secondary active transport (cotransport)
- AA’s across basolateral membrane = facilitated diffusion
- Set up chemical gradient for Na w sodium-potassium pump  Na out of cell and K+ into cell
 AA’s allowed to go against their gradient  high AA inside cell and low in interstitial fluid
 leave cell using facilitated diffusion across basolateral membrane  brush border
enzyme (aminopeptidase/dipeptidase) converts tri/dipeptides into individual amino acids

Absorption of Dipeptides and Tripeptides

- Secondary cotransport of H ions to allow di/tripeptides to go from low to high

concentrations (cotransport) across apical into the epithetlial  cytoplasmic peptidases
break them into individual amino acids  AA’s can leave basolateral membrane via
facilitated diffusion

Lipids

- Typical diet: 25-160 g lipids

o 90% triglycerides
- Lipids face special problem in digestion
o Not water soluble
o Doesn’t mix with stomach/intestinal contents
o Forms fat droplets

Lipid digestion

- Lipases = lipid digestion enzymes

o Water soluble; can only act on molecules near edge of fat droplet
- Bile salts increase surface area of droplets by breaking large droplet into several small
droplets = emulsification
o Made in liver from cholesterol
- Colipase = needed to help load lipase onto the lipid
- Lingual lipase = isn’t activated until stomach
- Gastric lipase = s/s from stomach
- Pancreatic lipase = s/s pancreas
- Colipase = s/s pancreas **not enzyme = doesn’t digest lipids
- Bile = made in liver; stored and concentrated in gall bladder **not enzyme
 - Lipoprotein lipase = blood

Action of Bile salts and Colipase

- Bile salts = emulsify fats  gives higher surface area to allow H2O lipase to do job
- Colipase = moves bile salts out of way and help load on lipase

Lipid Digestion

- Start with triglyceride  pancreatic lipase breaks into monoglyceride and free fatty acids (1
glycerol and 3 fatty acids)
- Bile salts and colipase enter small intestine from gall bladder and pancreas  bile salts
emulsify fat droplets  allows lipase to digest into fatty acids and monoglycerides  form
micelles (=loose aggregations) because both are lipophilic and hydrophobic  can fit into
microvilli

Absorption of Lipids

- Micelles release monoglyceride and fatty acids when close to villi/microvilli 

monoglycerides and fatty acids simple diffusion across apical membrane  enter smooth ER
in the epithelial cells where they are reassembled into triglycerides  triglycerides go into
the golgi apparatus where other proteins/lipids are added  turn them into a chylomicron
(hydrophilic/lipophobic)  leave basolateral membrane in secretory vesicles via exocytosis
 too large to enter the capillary  enters the lacteal of lymphatic system  chylomicrons
are dumped into the blood  lipoprotein lipase breaks them down into monoglycerides and
fatty acids  can enter cells via simple diffusion

What happens to the bile salts?

- Expensive to make
- Enterohepatic circulation
- We will reabsorb them in the ileum of the small intestine  those bile salts will then make
their way back to liver/gallbladder to be stored

Absorption of Vitamins

- Fat-soluble vitamin (A,D,E, and K)

o Absorbed with lipids
o Dissolve in micelles; simple diffusion
- Water-soluble Vitamins (B and C)
o Require special carrier proteins
- Vitamin B12
o Absorbed only when bound to intrinsic factor
 s/s from parietal cells in stomach

Absorption of Minerals: Calcium

- actively absorbed in duodenum and jejunum

o binds to brush border protein = calcium binding protein
  transported into the epithelial cell
o transported out of cell across basolateral membrane by Ca2+ pumo
- Hormones play a role

Absorption of Water

- Water in GI tract
o 7 liters from GI secretions
o 2 liters intake
- Water absorption is positive
- Water follows absorption of solutes by osmosis
o Hypotonic lumen  hypertonic blood

Mostly occurs in the Large intestine

Lecture 9/16

Metabolism = sum of all metabolic processes in the body

Anabolic = small molecules to larger molecules

Catabolic = large molecules to small molecules

ATP = nucleotide consisting of adenine, ribose sugar, and 3 phosphate groups

Oxidation-reduction reactions

- Oxidation = losing electrons

- Reduction = gaining
- (oil rig)

Glucose = hexose sugar that humans use as an immediate source of energy

Glycogen = storage form of glucose in animals (liver or skeletal muscle)

Hormonal Regulation of Metabolism

- Catabolic hormones = hormones involved in the breakdown of large molecules

o Cortisol
o Glucagon = released from alpha cells of the pancreas promotes glycogen  glucose
via glycogenolysis which results in a raised blood sugar level
o Epinephrine
 Adrenaline
- Anabolic Hormones = building of large molecules from smaller molecules
o Growth Hormone
o Insulin-like growth factor
 o Insulin = released from the beta cells in the pancreas and promotes glucose 
glycogen via of glycogenesis which lowers the blood sugar level
o Testosterone
o Estrogen

Cells Need ATP

- Powers nearly every activity requires energy input

o Chemical reactions
o Development from a fertilized egg
o Breathing
o DNA synthesis
o Digestion
o Reproduction
o Cell division
o Movement
- Mitochondria produces ATP

What happens if a cell lacks ATP?

- The cell will die

Sources of ATP

- Food intake  Proteins, complex carbs, triglycerides

- Complex carbs most commonly used
- Starch  broken down into glucose  absorbed into the body  some will enter blood and
excess amounts will be turned into glycogen  if we lack carbs then the body will break
down stored fat (triglyceride)  if out of both the body will cannibalize itself and
breakdown proteins

Key Players: ATP

- When ATP undergoes hydrolysis it will break into ADP + Energy

Electron Carrier Molecules

- NADH, Nicotine Adenine dinucleotide

o NAD+  NADH is reduction
o NADH  NAD+ is oxidation
- FADH2, Flavin Adenine dinucleotide
o Produced from riboflavin (Vitamin B2)
o FAD+  FADH2 is reduction
o FADH  FAD+ is oxidation

Enzymes
 - Substrate-level phosphorylation (SLP): ATP production by direct enzymatic transfer of
phosphate from an intermediate substrate to ADP
- “typical enzyme catalyzed reaction” = substrate binding to enzyme and products are
released

Carbohydrate metabolism

- Ingest pasta  breakdown begins in mouth from salivary amylase  pasta makes way to
through stomach into pancreas  pancreas releases pancreatic amylase  amylase turns
starch into maltose and limit (alpha) dextrins  brush border enzymes maltase and
dextrinasse turn them into glucose  glucose will pass through the apical membrane using
secondary co-transport with sodium  uses facilitated diffusion to get across the
basolateral membrane  into cell to become ATP  if excess glucose and ATP it will go to
liver and skeletal muscle to be stored as glycogen via glycogenesis

Presence of O2

- Complete oxidation
- Aerobic respiration (4 different pathways)
o Glycolysis
o Pyruvate oxidation
o Krebs cycle/TCA cycle/citric acid cycle
o Oxidative phosphorylation
 Electron transport chain
 Chemiosmotic coupling

No O2

- Incomplete oxidation
- Anaerobic respiration (2 pathways)
o Glycolysis
o Fermentation

Overview of Carbohydrate Metabolism

**don’t need to know steps in each pathway

- Know what goes in and what comes out**

First Pathway: Glycolysis

- Enters:
o One glucose
o Two ATPs
 o Two NAD+
o 4 ADPs
- Exits:
o Two ADP
o Two pyruvates
o Two NADH
o Four ATP
- Net:
o Two pyruvates
o Two ATP
o Two NADH
- Occurs within the cytoplasm

Second Pathway: Linking step, Pyruvate Oxidation

- Pyruvate made in glycolysis will enter the mitochondrial matrix  reduce NAD+ to NADH 
turn pyruvate into Acetyl CoA by adding Coenzyme A
- Enter:
o Two pyruvate
o Two NAD+
o 2 CoA
- Exit:
o 2 Co2
o 2 NADH
o 2 Acetyl CoA

Third Pathway: Krebs cycle

- Acetyl CoA from pyruvate oxidation enters the krebs cycle  enzymatic reactions reduce 3
NAD+ into NADH and one FAD+ into FADH2 and produce one ATP
- Enter:
o 2 Acetyl CoA
o 6 NAD+
o 2 FAD+
o 2 ADP

- Exit:
o 2 CoA
o 6 NADH
o 2 FADH
o 2 ATP
o CO2 byproduct

Fourth pathway: Oxidative phosphorylation

 - Two different pathways
o Electron transport chain
o Chemiosmotic couples
 NADHs and FADH2s from other chains donate their electrons to oxygen
(final electron receptor)  move through ETC as donating  creates proton
gradient between mitochondrial matrix and intermembrane space 
protons in intermembrane will move down ATP synthase and release energy
as they move  energy used to phosphorylate ADP into ATP
- Enter:
o NADH
o FADH2
o O2
o ADP
- Exit:
o NAD+
o FAD
o H2O
o ATP

For every glucose molecule put into aerobic respiration = 36 ATP produced

Excess glucose, now what

- Make glycogen via glycogenesis

- Store in adipose tissue via lipogenesis

No glucose, now what?

- Liver undergoes glycogenolysis to turns glycogen into glucose

- gluconeogenesis = turns non carbs into glucose
o pyruvate
o lactate
o glycerol
o some amino acids

Gluconeogenesis = process of turning non carbs into glucose

Glycogen = long term energy of glucose

Glycogenesis = glucose turning into glycogen

Glycogenolysis = turning glycogen into glucose

Glycolysis = turning glucose into pyruvate

Glucagon = catabolic hormone that raises your blood sugar

9/18 Lecture

Anaerobic Respiration: incomplete glucose oxidation = occurs when O2 is lacking

 - starts with glycolysis
- enter:
o 2 ATP
o 2 NADH
o 1 glucose
- Exit:
o 4 ATP
o 2 NAD+
o 2 pyruvate
- Glycolysis continues = build up of pyruvate and NADHs
- Pyruvate under goes fermatation  pyruvate turns into lactate  NADH is oxidized back
into NAD+  NAD+ can go back to being used as reactant in glycolysis
- Lactate then moved to liver where it can be converted into glucose via gluconeogenesis

Anaerobic respiration only results in two ATP

- Reasons for anaerobic respiration

o Cell might lack O2
o Non-functional mitochondria
o Cell lacks mitochondria (ex: red blood cells)

Cells can also use amino acids, glycerol, and fatty acids for energy = last source

Lipid Metabolism

- Tongue = lingual lipase

- Stomach = gastric lipase
- Pancreas = pancreatic lipase
- Lipids are broken down into fatty acids and glycerol by lipase
o Lipase = hydrophilic (don’t interact well with lipids)
- Bile salts = emulsify fats (made in liver and stored in the gallbladder)
- Colipase = loads the lipase onto the fats (made in the pancreas)
- Monoglycerides and fatty acids will simply diffuse across the apical membrane
o Made into triglycerides in the epithelial cell  triglycerides are sent to the golgi
apparatus where we add proteins and other lipids  form chylomicrons  leave
basal lateral membrane via exocytosis  chylomicrons are too big to enter
bloodstream through capillaries  enter lymphatic system though lacteals  once
in lymphatic system it goes into the bloodstream  chylomicrons are broken down
with lipoprotein lipase into fatty acids and glycerol  can be transported to adipose
tissue to be stored as triglycerides or to the liver to undergo metabolic processes

Lipids

- Excess fatty acids and glycerol can be moved to adipose tissue and liver and be turned into
triglycerides via lipogenesis
- Fatty acids + glycerol = triglyceride via lipogenesis
 - Triglycerides undergo lipolysis (breakdown of triglycerides via hydrolysis reactions) when we
don’t have enough glucose
- Fatty acids converted into acetyl CoA through beta-oxidation  acyl-CoA enters krebs cycle
 results in 6 NADH, 2 FADH2, and 2 ATPs  NADH and FADH enter oxidative
phosphorylation and become ATP
- Glycerol from lipolysis is moved to liver  become glucose through gluconeogenesis 
glucose enters glycolysis and be converted into pyruvate  pyruvate can become acetyl-
CoA through pyruvate oxidation  NADH and FADH2 from krebs cycle go into oxidative
phosphorylation

Lipid metabolism produces more ATP, but also produces ketones which can result in ketoacidosis

Ketogenesis

- Excess acetyl CoA will enter ketogenesis and produce ketones and CO2 as a byproduct
o Ketones and CO2 cause blood to become more acidic
o Ketones can be used as energy source directly from the brain
o Ketones are good, but don’t want to much

Metabolic acidosis

- Headache
- Hyperkalemia = excess of potassium ions
- Low blood pressure
- Lower muscle tone and reflexes = confusion and increased drowsiness
- Kussmaul respirations (Compensatory hyperventilation)
- Muscle twitching
- Warm, flushed skin (vasodilation)
- Nausea, vomiting
- Causes: increase H+ production (DKA, hypermetabolism), decrease H+ elimination (renal
failure), decreased HCO3 production (dehydration, liver failure), increase HCO3 elimination
(diarrhea, fistulas)

Excess glucose

- Excess enters glycolysis  turned into pyruvate  pyruvate becomes acetyl-CoA via
pyruvate oxidation  acetyl-CoA can be converted into fatty acids  fatty acids form
triglycerides that will be stored in adipose tissue until needed  or acetyl CoA can be
converted into cholesterol  used to make steroid hormones or bile  steroid hormone
location is dependent on hormone  bile is made in the liver and stored in the gall bladder
- Excess glucose into lipids = lipogenesis

Protein Metabolism

- Last resort and only used in dire circumstances

- Proteases
o Pepsin = made in stomach = endopeptidase
 o Trypsin = pancreatic protease = endopeptidase
o chymotrypsin = pancreatic protease = endopeptidase
o carboxypeptidase = final pancreatic protease = exopeptidase
o enterokinase = converts trypsinogen into trypsin  trypsin then converts
chymotripsinogen into chymotrypsin and procarboxypeptidase into
carboxypeptidase
o cytoplasmic peptidase = convert di/tri peptides into amino acids inside epithelial
cells  aa’s cross the apical membrane via co-transport with sodium  di/tri
peptides cross apical membrane via co-transport with hydrogen  aa’s can cross
basolateral via facilitated diffusion  di/tri peptides converted into aa’s via
cytoplasmic peptidases which can leave via facilitated diffusion
- aa’s in blood stream can become new proteins, be converted into fats, into acetyl CoA, or
into pyruvate
o if pyruvate  go through linking step/pyruvate oxidation and become acetyl CoA 
enter krebs  produce NADH and FADH2  undergo oxidative phosphorylation and
become ATP
o if acetyl CoA  skip linking step and go directly into krebs  NADH and FADH2 go
into oxidative phosphorylation and produce ATP
o a couple can become glucose via gluconeogenesis
o Excess aa’s can be eliminated by deaminated them (removing NH2 amine group) 
produces ammonia (NH3)  ammonia is toxic so it travels to liver to be changed 
liver converts the ammonia into urea  urea travels to the kidneys  kidneys
eliminate urea via urine

Absorptive state = fed state = when body is absorbing nutrients

- Increase: glucose oxidation (more glucose into the cell), glycogen synthesis (glycogenesis),
fat synthesis (lipogenesis), protein synthesis (proteogenesis)
- Insulin released in response to high amino acids and high glucose
o Peptide hormone released by beta cells in pancreas
- How would this affect the function of plasma, conc of glucose, fatty acids, and amino acids
o Causes decrease because theyre being actively used

Postabsorptive state = fasted state = no food intake

- Decrease: blood glucose

- Glucagon released from alpha cells in the pancreas and also a peptide hormone
o Causes increase in glycogenolysis, gluconeogenesis, and ketogenesis
- Why is it important that these functions occur during a fasted state?
o Provide substrates to make energy (ATP) to prevent hypoglycemia (low blood sugar)
- Occurs when amino acids levels are low and blood glucose is low

Lecture 9/21

Intercellular communication = how cells communicate with one another

Chemical messengers
 - Functional classification = based on what they do
o Direct = this type of direct communication
o Paracrine (indirect)
o Neurotransmitters (indirect)
o Hormones (indirect)
o Neurohormones (indirect)
- Chemical classification = based on chemical property
o Lipophilic (hydrophobic) or lipophobic (hydrophilic)
o 4 classes of chemical messengers
 Amino acids
 Amines
 Peptides/proteins
 Steroids

Direct communication = Gap junctions

- Pass ions and small molecules from one cell to adjacent cell
- Bridge from cell to the other

Basics of indirect intercellular communication

- The secretory cell secretes the ligand (also known as the chemical messenger) which travels
through the interstitial fluid and/or blood to reach the target cell where the ligand must
bind to the receptor on/in the target cell which brings about a target cell response

Indirect communication: Paracrine

- Messenger = paracrine
- No specific target cell, but must be neighboring cell
- No specific secretory cell
- Message travels through interstitial fluid
- Secretory cells and target cells must be nearby
- Ex: Histamine, prostaglandins, cytokines, growth factors, clotting factors

Indirect communication: Neurotransmitters

- Messenger = neurotransmitters
- Released by neurons
- Target = close by cell = postsynaptic cell
- Secretory cell = presynaptic cells
- Only travels through interstitial cells
- Only targets nearby cells
- Ex: glutamate, acetylcholine, norepinephrine

Indirect Communication: Hormones

- Messenger = hormones
- Target cell = none specific
 - Released from endocrine cells
- Travel through interstitial fluid then diffuses into blood
- Target far away cells
- Ex: thyroid hormone, adrenocorticotropic hormone, gonadotropin releasing hormone,
insulin

Indirect communication: Neurohormones

- Messenger = neurohormones
- Released from neurosecretory cell
- No specific target cells
- Travel through interstitial fluid then blood
- Target far away cells
- Ex: vasopressin (ADH), epinephrine

Chemical classification of messengers

- Amino acids = neurotransmitters only

- Amine = paracrine, neurotransmitters, hormones
- Peptides/proteins = paracrines, neurotransmitters, hormones
- Steroids = hormones only

Chemical properties of messengers

- Amino acids = lipophobic

- Amines = lipophobic except thyroid hormone (lipophilic)
- Peptides/proteins = lipophobic
- Steroids = lipophilic

Synthesis and Release Characteristics

- Lipophilic ligands (steroid hormones and thyroid hormones)

o Synthesized on demand
o Immediate release from the secretory cell
 Not stored (fat loving = able to pass through bilayer easily)
 Will diffuse away from storage vesicle
- Lipophobic ligands (amino acids, peptides/proteins, and amines)
o Synthesis is independent of demand
o Stored in secretory vesicles of secretory cell until needed
o Released by exocytosis
o Release rate determined by exocytosis
 Cant easily pass through membrane so they can be stored

Example: Amine Synthesis

- All amines are derived from amino acids (tryptophan = melatonin)

- Amino acids  amines via enzyme-catalyzed reactions
- Other examples: histidine = from histamine and thyroid hormone = from tyrosine
Catecholamines synthesis (group of amines)

- All derived from tyrosine via series of enzyme catalyzed reactions

o Creates dopamine, norepinephrine (noradrenaline), epinephrine (adrenaline)
- Dopamine and norepinephrine = neurotransmitter
- Epinephrine = neurohormone

Peptide and Protein synthesis

- Formed by cleaving larger proteins

- Start as prepropeptide  propeptide  peptide  if peptide is hormone becomes
preprohormone  prohormone  hormone
- mRNA translated into prepropeptide  modified and cleaved into propeptide  propeptide
is sent to the golgi apparatus  golgi apparatus bundles it into secretory vesicles  more
amino acids are cleaved after secretory vesicles  becomes peptide and leaves cell via
exocytosis

Steroids (ex of how steroid hormones are synthesis)

- start with cholesterol  becomes steroid hormone via series of enzymatic catalyzed
reactions

Properties of chemical messengers using chemical classification

- amino acids = lipophobic = independent of demand = stored and released via exocytosis =
made from enzymatic catalyzed reactions = interstitial fluid = short half life
- amines = lipophobic* = independent of demand = stored and released via exocytosis = made
from enzymatic catalyzed reactions from amino acids = interstitial fluid only or IF and blood
= dissolved in plasma = short half life
- peptides/proteins = lipophobic = independent of demand = stored and released via
exocytosis = made from protein synthesis = IF only or IF and blood = dissolved in plasma =
short half life
- steroids = lipophilic = on demand = immediate release via simple diffusion = made from
enzymatic catalyzed reactions from cholesterol = IF and blood = bound to carrier protein =
long half life

Two types of transport

- diffusion through interstitial fluid

o secretory cell and target are nearby
o ligand is quickly degraded
o examples: paracrines, and NTs
- blood borne transport
o secretory cell and target are far away
o lipophobic (hydrophilic): dissolved in plasma
o lipophilic (hydrophobic): bound to carrier protein
o ex: hormones, neurohormones
Messenger Half-Life

- how long does it take for half of the messenger to disappear

- messengers dissolved in plasma have a short half-life compared to messengers bound to
carriers
- liver degrades the chemical messengers
- kidney secretes chemical messengers

Lecture 9/23

Properties of Receptors

- specificity
- binding is brief and reversible
- affinity = how strong the interaction between receptor and messenger is
- one messenger can bind many receptor types
- one target may have many types of receptors
- number of receptors per cell varies and is dynamic

Magnitude of Response

- Affinity for the messenger

o Increase the affinity = increase of likelihood receptor binds to the messenger =
increase response
- Number of receptors
o More receptors = larger response
o Plateau on graph represents receptor saturation
- Concentration of the messenger
o Increase of messengers = increase likelihood of receptor binding to response =
stronger response

Receptor Agonist and Antagonists

- Agonists = chemical which binds to the receptor

o Action mimics normal response
- Antagonist = competes with normal ligand or agonist for same binding site
o If the antagonist binds the ligand cannot bind = decrease cell response

Signal Transduction Pathways

Mechanisms: Signal Transduction

- Intracellular mediated response

o Receptor is located within the cell either in cytoplasm or nucleus
o Ligand is lipophilic
o Chemical classes = steroids (thyroid hormone)
o Target cell response = relatively slow
 Gene activation = some inactivation
- Membrane bound receptor mediated responses
 o Within the membrane
o Ligand is lipophobic
o Chemical classes = amino acids, amines (except thyroid hormone), and peptide
proteins
o Target cell response = relatively fast
 Enzyme activation
 Changes membrane permeability

Intracellular mediated response

- Occur when the ligand is lipophilic

- Steroid hormone simply diffuses through membrane  binds to receptors in cytoplasm or
nucleus  binding forms the hormone receptor complex  hormone receptor complex
binds to DNA at the hormone response element  when bind it will either turn on or turn
off genes  genes turned on will make more proteins and genes turned off will stop making
proteins

Membrane bound receptor mediated responses

- Occurs when ligand is lipophobic

- Types:
o Ligand (chemically) gated
 Channel-linked
 G-protein linked
o Enzyme-linked
- When ligands binds to the receptor on target cell
o Permeability of the target to ions may be alters
o Enzymes may be activated

Types of Channels

- Leak = always open

- Gated = open or close in response to stimulus
o Voltage gated = change in response to membrane potential
o Chemically (ligand) gated = open/close in response to ligand binding to a receptor
o Mechanically gated = something physically has to open/close it
o Thermally gated = changes in temperatures open/closes the gates

Ligand gated channels = ligand must bind to the ligand gated channel

- Two types: fast and slow channels

o Fast channels = when receptor and channel are the same protein (ionotropic
channels)
o Slow channels = when the receptor and channel are different proteins
(metabotropic)

Channel-linked receptors
 - Fast ligand gated
- Ligand binds to receptor and causes it to open  allows ions to move through  changes
electrical property of cell
- Can only open in response to ligand binding to it
- Ligand will just fall off to close it
- Ex: calcium channels

G protein-linked receptors

- Three subparts
o At rest a GDP is attached to the alpha subunit
o Ligand binds to the receptor  activates the G protein and GDP falls off  the GTP
comes on the alpha subunit  causes the alpha subunit (with GTP) to slide over 
will either bump an ion channel (may open or close it) or it will alter the enzyme
activity on the cytoplasmic side of the membrane
o Ligand falls off the receptor  GTP is hydrolyzed back into GDP  and the alpha
subunit slides back and re associates with the beta and gamma subunits  G
protein is inactivated
o All are SLOW ligand gated channels = open/close channels or alter enzyme activity
of the cell
o Receptor and channel are different proteins
o Two types of mechanisms:
 Direct coupling
 Second messenger

Direct coupling

- Activate G-protein  slides over  bumps into channel  causes channel to open or close
 change in electrical properties of the cell

Second Messenger System

- Triggered by first messenger (ligand) activates the G-protein which activates an amplifier
enzyme which activates the second messenger production which activates or inhibits
pathways
- Two types of G-proteins
o Gi = inhibitory amplifier enzyme = decrease cell response
o Gs = stimulatory amplifier enzyme = increase cell response

Amplifier enzymes = make second messenger

- Three types: adenylate cyclase, guanylate cyclase, and phospholipase C

Second messenger systems

- cAMP = adenylate cyclase

- cGMP = guanylate cyclase
o both cyclic nucleotides
 - DAG
- IP3
o Both lipid derived made by phospholipase C
- Calcium = ion

cAMP

- Turn on
o Ligand binds to the receptor  activates G protein  alpha subunit with GTP slides
over into adenylate cyclase  converts ATP into cAMP  cAMP activates protein
kinase  phosphorylates a protein by taking a phosphate from an ATP and putting
it on a protein phosphorylated protein causes cell response
- Turn off
o Ligand falls off the receptor  hydrolyze GTP back to GDP causing re-association of
the alpha subunit  break down second messenger (cAMP) with an enzyme
(phosphodiesterase: PDE)  remove phosphate from the phosphorylated protein
with phosphatase

IP3/DAG

- Turn on
o Messenger binds to receptor and activated the G protein  amplifier enzyme
phospholipase C is active by G protein  phospholipase C converts PIP2 into DAG
and IP3  DAG stays in the membrane and activates protein kinase C  protein
kinase takes phosphate from ATP and phosphorylates a protein that causes a cell
response  IP3 travels into the smooth ER inside the cell and bind to the receptor
on smooth ER  causes receptor channel to open  calcium leaves smooth ER and
can either bind to calmodulin to form calcium calmodulin complex  activates a
protein kinase which causes cell response  OR calcium can have its own cell
response
- Turn off f
o Same as cAMP but degrading designated second messenger enzyme
 Also requires calcium re-uptake to put it back into the smooth ER

Signal Amplification

- A little does a lot

- One messenger can cause phosphorylation of lots of proteins

Enzyme-linked receptors

- Ex: insulin = glut4 transported inserted in plasma membrane of skeletal muscle

- Ligand binds to receptor  causes a conformational change  phosphorylates a tyrosine on
a protein  phosphorylated protein causes cell response
- Insulin receptor = tyrosine kinase

Long distance communication

- Endocrine system
 o Uses hormones
o Travel through IF then blood
o Slower system than nervous system
 Can have longer effect because slower
- Nervous system
o Neurons and glial cells
o Neurons are used for short communication but long axons cause longer distance
o Uses neurotransmitter to communicate signals
 use voltage gated channels and ligand gated channels

Nervous Communication

- dendrites = coated with ligand gated channels

- soma = cell body
- axon = voltage gated channels
- axon terminal = released the neurotransmitter into the synapse or area between the pre
synaptic cell and post synaptic cell
- receptor found on post synaptic cell

**Table 5.6

- Nervous system
o Secretory cell = neuron
o Target cell = neuron, muscle or gland
o Messenger = neurotransmitter
o Pathway for communication = across synapse
o Basis of specificity = receptors on postsynaptic target cell
o Time to onset of effect = immediate
o Duration of effect = brief
- Endocrine system
o Secretory cell = endocrine cell
o Target cell = most cell types in the body
o Messenger = hormone
o Pathway of communication = via bloodstream
o Basis of specificity = receptors on target cells throughout body
o Time to onset of effect = delayed
o Duration of effect = long

Lecture 9/25

Classification of Hormones

- Steroid hormones
o Lipophilic
o Derived from cholesterol
o Ex: testosterone, progesterone, estrogen, hormones secreted by the adrenal cortex
 - Peptide/protein hormones
o Lipophobic
o Ex: ADH, insulin, GH, and PRH
- Amine Hormones
o Derived from amino acids
o Lipophobic except for the thyroid hormone (TH)
o Ex: melatonin, thyroid hormones, and catecholamines

Focus on regulation of the synthesis and secretion of hormones

Hormones to know

- Hypothalamus
o DA = dopamine
o TRH = thyrotropin releasing hormone
o CRH = corticotropin releasing hormone
o GHIH = somatostain (SS)
o GHRH = growth hormone releasing hormone
o GnRH = Gonadotropin releasing hormone
- Anterior pituitary
o TSH = thyroid stimulating hormone
o ACTH = adrenocorticotropic hormone
o GH = growth hormone
o LH = luteinizing hormone
o TH = thyroid hormone
- Endocrine glands
o IGFs = insulin-like growth factors = formerly known as somatomedins
o PTH = parathyroid hormone
o Calcitonin
o Aldosterone
o Melatonin
o Epinephrine
o Insulin
o Glucagon
Posterior Pituitary
o Oxytocin
o ADH = antidiuretic hormone (vasopressin)

Control of Endocrine system

- Humoral control = receptor in body detects concentration of ions of metabolites in blood to

keep the balance
o Low calcium level in blood triggers parathyroid gland to secrete parathyroid
hormone to bring calcium back up
- Neural = a nerve cell synthesis and secretes the hormone
 o
Ex: nerve cell in sympathetic nervous system stimulates the medulla of the adrenal
gland to secrete catecholamines
- Hormonal = another hormone causes the synthesis and secretion of the final hormone
o Ex: hypothalamus release hormone that triggers a cascade to finally release a final
hormone like TH, cortisol, or testosterone

Pituitary Gland

- Most of the hormonal control

- Size of lima bean
- Below the hypothalamus
o Connected to hypothalamus by the infundibulum stock
- Posterior Pituitary = Neurohypophysis = extension of the neural tissue
o Stores neural hormones
- Anterior Pituitary = Adenohypophysis = true endocrine gland of epithelial origin
o Synthesis and stores hormones

Pituitary Gland: Posterior

- Hormone is made and packaged in the cell body of neuron and stored in secretory vesicle
that is transported down the axon of the neuron  when the reach the axon terminal they
are stored in posterior pituitary until they’re needed The neural hormones are released
into the blood via exocytosis upon stimulation
o Lipophobic

Hypothalamus and Anterior Pituitary: Tropic Hormones

- Tropic hormone regulates hormone secretion by another endocrine gland

o Hypothalamus will release a releasing hormone  releasing hormone will travel to
the anterior pituitary and binds to excitatory receptor  excitatory receptor cause
release of a stimulating hormone from anterior pituitary  stimulating hormone
travels to final endocrine gland and binds to excitatory receptor on it  causes the
release of the final endocrine hormone  final endocrine hormone will travel to the
target tissue where it binds to excitatory receptors and causes a cell response
o RH = releasing hormone
o IH = inhibiting hormones
- Hypothalamus creates thyrotropin releasing hormone (TRH)  TRH travels via the
hypothalamic pituitary portal system to the anterior pituitary  binds to excitatory
receptors on anterior pituitary  release of thyroid stimulating hormone  thyroid
stimulating hormone travels to the thyroid gland  binds to excitatory receptors on the
thyroid gland  causes a release of thyroid hormone (final hormone)  travels to target
tissue and bind to excitatory receptors  cell response
- Neurohormones are released into capillary bed via exocytosis  travel through blood to the
anterior pituitary  bind to the receptors on the endocrine cells in the anterior pituitary 
if those hormones are releasing hormones they will cause the anterior pituitary to release
 stimulating hormones  if they are inhibiting hormones then the anterior pituitary to stop
production of the stimulating hormone
- Goal = allow tropic hormones synthesize and secretion by the hypothalamus to get to the
anterior pituitary
- Capillary bed = within the infundibulum

Feedback loops

- Hormones levels controlled by negative feedback loops

Atrophied = decrease in size = fewer cells = less binding to inhibitory cells = increase of hypothalamus
and anterior pituitary hormone

Adenoma

- An adenoma is a benign or non-cancerous tumor that forms on glands in the body

o Functioning adenoma = hypersecretion of hormone
o Non-functioning adenoma = hyposecretion of hormone
- Hyposecretion = increase in ACTH and CRH
- Hypersecretion = decrease in ACTH and CRH

Primary endocrine disorder = problem with the final endocrine gland

Secondary endocrine disorder = problem with the hypothalamus or anterior pituitary

Summary of Abnormal secretion of hormones

- Hyposecretion
o Causes: nonfunctioning adenoma, gland atrophy (most common cause)
- Hypersecretion:
o Causes: functioning adenoma and cancerous tumors
- Abnormal tissue responsiveness
o Down regulation of receptors
o Receptor and signal transduction abnormalities
 E.g hormone cannot bind to the receptor
- Primary endocrine disorders
o Can be primary hypo- or hypersecretion
o Abnormality in endocrine organ that secretes the hormone
- Secondary endocrine disorders
o Can be secondary hypo or hypersecretion
o Abnormality in tropic hormone
 Hypothalamic tropic hormone
Anterior pituitary tropic hormone

Lecture 9/28

The posterior pituitary

- Will only store hormones

 o ADH (vasopressin) and oxytocin
- ADH = regulates water and osmolarity balance
o Primarily produced by paraventricular nuclei of the hypothalamus
o Target the kidneys
- Oxytocin =
o Produced primarily by the supraoptic nuclei of the hypothalamus
o Targets the uterus during childbirth and allows for greater contraction and also
targets the breasts during breast feeding
 Increases milk let down (mother-childing bonding)
- ADH and oxytocin are functionally classified as neurohormones and chemically classified as
peptides

ADH = decrease urination

- Diuretics cause you to urinate therefore an antidiuretic will cause a decrease in urination
and so the function of ADH is a decrease in urination
- What stimulates ADH release?
o Pain, low BP, stress
o Nicotine, morphine
- What inhibits ADH?
o Alcohol
- If ADH is hyposecreted = increase urine production
o Diabetes
 Symptoms = increase urination, thirst, dehydration, and headaches
 Treatments = drinking water and synthetic ADH (Desmopressin)

Anterior Pituitary hormones

Growth hormone

- Hypothalamus releases a growth hormone releasing hormone (GHRH)  GHRH travels to

the anterior pituitary and releases the growth hormone (GH)  GH will travel to liver and
release somatomedin (IGF-1) and travel throughout the body
- Hypothalamus will also release Growth Hormone Inhibiting Hormone (GHIH) in order to
control how much hormone is actually released
o All hormones are classified as peptides = lipophobic and hydrophilic

GH feedback loop

- Once IGF-1 is released it will target the bone and muscle cells to grow
- After GH is released it will travel to the adipose tissue and cause the lipolysis in adipose cells
into fatty acids and glycerol  glycerol will travel to liver and undergo gluconeogenesis into
glucose  fatty acid and glucose will travel to growing tissues (bone and muscle cells) GH
also travels to nongrowing tissues to decrease glucose utilization  allows bone and muscle
cells to use more glucose
- To shut down system GHIH will travel to anterior pituitary  stop producing GH  IGF-1
will travel to hypothalamus to cause GHIH to be released
Hyposecretion of GH: Dwarfism

- Upregulation = increase in receptors = increase in binding = increase in hormone

- Other disorders
o Acromegaly = hypersecretion of GH after puberty that results in soft tissue
enlargement
o Gigantism = GH hypersecretion before puberty that causes bone growth

Thyroid Hormone **LIPOPHILIC AMINE

- Hypothalamus releases thyrotropin releasing hormone  TRH travels to the anterior

pituitary and binds to excitatory receptors  anterior pituitary releases thyroid stimulating
hormone  TSH travels to thyroid gland the final endocrine gland and binds to excitatory
receptors  secretion of thyroid hormone  TH will be released in circulation and taken to
target tissues

Thyroid gland

- Secretes 3 types of hormones

o T3 = triiodothyronine
o T4 = tetraiodothyronine (thyroxine)
 T3/T4 = thyroid hormone TH
o Calcitonin

Synthesis and secretion of TH

- Two cell types

o Follicular cells = make up the wall of the follicle and surround colloid
o C cells (parafollicular cells) secrete calcitonin
- The mechanism:
o Follicular cells produce and secrete thyroglobin TG (precursor to TH) and bring
iodide into the colloid (iodide is brought into the follicular cells via A.T. from the
blood)
o Once follicular cells produce and secrete thyroglobin into the colloid  iodide is
added to the thyroglobin  1 iodide = monoiodityrosine (MIT) and two iodides =
diiodotyrosine (DIT)  DIT + MIT = T3 and DIT + DIT = T4  thyroglobin-thyroid
hormone complex  TSH from anterior pituitary binds to TSH receptor on cell wall
of the follicular cells  activates G protein  GDP and GTP comes on  alpha
subunit with GTP on it slides and bumps adenylate cyclase  adenylate cyclase
converts ATP to cAMP  cAMP activates protein kinase A  protein kinase A
phosphorylates a protein  phosphorylated protein causes phagocytosis of
thyroglobin-thyroid hormone complex  creates a phagosome  phagosome is
fused with lysosome with digestive enzymes to form phagolysosome  digestive
enzymes inside lysosome degrade thyroglobin-thyroid into T3/T4 hormones 
thyroglobin is recycled and put into colloid  T3/T4 diffuse out of follicular cells
(lipophilic) and travels in blood to target tissue  bind to receptors inside the cell
- Targets most tissues except the brain and gonads
 - Functions of TH
o Increase basal metabolic rate (increased rate of O2 consumption)
 Increase heat production
 Increase O2 consumption = increase rate of cellular respiration
o Increase rate of Na/K pump
 Increase rate ATP is hydrolyzed
 Aids in cellular uptake in nutrients
o Promote increased numbers of mitochondria in cells
o Increase of enzymes involved in oxidative phosphorylation
o Development of NS
o Necessary for growth and development in children
o Glycogenolysis/gluconeogenesis
 Increase glucose
o Lipolysis
 Makes more fatty acids and glycerol
 Fatty acids will be turned into Acetyl-CoA via beta oxidation
o Proteolysis
 Higher amino acid level which undergo gluconeogenesis and increase the
glucose concentration
o No level increase of glucose or acetyl-CoA because its being used as quickly as it is
being made

Hypothyroidism

- Low TH
- Low BMR
- Low heartrate
- Higher weight
- Lower heat production
- Cannot tolerate cold
- Treatment: synthetic thyroid hormone
- Lack TH from birth = cretinism
o Results in dwarfs and mentally underdeveloped (reversible)

Hyperthyroidism

- High TH
- High BMR
- High heart rate
- Decrease weight
- Higher heat production
- Cannot tolerate heat
- No treatment

Lecture 9/30
Adrenal glands = on top of kidneys

- Adrenal cortex = outer most layer

o Zona glomerulose = outermost layer
o Zona fasciculata = middle layer
o Zona reticularis = inner most layer
- Adrenal medulla = innermost layer

Hormones of the adrenal cortex: Adrenocorticoids = steroid hormones

- Zona glomerulosa
o Secretes mineralcorticoids (class of adrenocorticoids)
 Aldosterone
 Targets kidneys
 Reabsorbs sodium and potassium excretions
- Zona fasciculata
o Secretes glucocorticoids (adrenocorticoids)
 Primarily cortisol = stress hormone
- Zona reticularis
o Sex hormones
 primarily androgens

steroid hormones = lipophilic = membrane carrier in blood and require an intracellular protein

Control of aldosterone

- not controlled by hypothalamus hypophysiotropic and pituitary gland hormones

- controlled by humoral control
o Na low and K high cause synthesis and secretion of aldosterone to restore normal
levels

Cortisol = chemically classified as a steroid

- Corticotropic releasing hormone (CRH) is released from the hypothalamus  travels to

anterior pituitary and binds to excitatory receptors  anterior pituitary releases
adrenocorticotropic hormone (ACTH)  travels to adrenal cortex and binds to excitatory
receptors  synthesis and secretion of cortisol  cortisol travels to tissue to cause a cell
response
- Function of cortisol = free fuel
o Maintain normal levels of enzymes to breakdown fats, proteins, and glycogen
o Required for GH secretion (in synergism with TH)
o Gluconeogenesis = higher blood glucose levels
o Proteolysis in muscle = free amino acids
 Amino acids will travel to liver and undergo gluconeogenesis
o Lipolysis in adipose tissue = fatty acids and glycerol
 Glycerol will travel to the liver to undergo gluconeogenesis
  Fatty acids undergo beta-oxidation to make acetyl-CoA = increase in
gluconeogenesis
o Suppresses immune response (IR) = targets thymus
 Easy to get sick when stressed
- Circadian rhythm = increase of cortisol in the day and decrease at night

Effects of abnormal glucocorticoid secretion: hypersecretion

- If increase CRH secretion  increase ACTH secretion  increase cortisol secretion (levels)
- If increase ACTH  increase cortisol
- Increase cortisol levels = cushings disease
o Results in increase in gluconeogenesis  increase glucose levels  results in
hyperglycemia  glucosuria (glucose in urine)  results in adrenal diabetes
o Increase glucose levels = increase of adipose tissue in belly, face, and back
 Cortisol is relocating adipose tissue to most needed areas
o Increase proteolysis = decrease muscle mass, weakness and fatigue, and poor
wound healing

Thymus = immune response

- Secretes thymosin
o Regulates T cell function
 T-lymphocytes = type of WBC
o Cortisol suppresses the thymus

Adrenal Medulla

- Secretory cells = chromaffin cells (modified neurons)

o Secretes: 80% epinephrine, 20% norepinephrine, <1% dopamine
 Amines = catecholamines
- Under neural control = released from neurons
- Epinephrine causes increase in gluconeogenesis, glycogenolysis, lipolysis, and ketogenesis
o Increase fuel levels to make ATP

Pineal gland

- Glandular tissue in brain

- Secretes melatonin
o May be involved in circadian rhythm

Functions of Calcium in the body = very important

- Extracellular matrix
o 99% of body calcium
o Calcified matrix of bone
- Extracellular fluid
o 0.1%
 o “Cement” for tight junctions; role in myocardial and smooth muscle contraction;
neurotransmitter release at synapses; role in excitability of neurons; cofactor in
coagulation cascade
- Intracellular
o 0.9%
o Signal in second messenger pathways; role in muscle contraction

Three hormones control Ca balance

- Calcitonin
o Secreted from C cells (parafollicular cells) in thyroid
o Peptide
- parathyroid hormone (PTH)
o secreted from parathyroid gland embedded in thyroid
o peptide
- calcitriol
o not relevant

osteoclasts

- break down bone = increase Ca levels in plasma

Functions of calcitonin = decrease plasma calcium levels

- Targets bone:
o Calcitonin inhibits osteoclasts which will then inhibits breakdown of bone and
decrease plasma calcium levels
- Targets kidneys:
o Increase calcium excretion which decreases plasma calcium levels
- Targets small intestines:
o Decrease calcium absorption by the small intestines = decrease plasma calcium
levels
- caLcitonin = Lowers calcium
o uses cAMP pathway

Functions of PTH = increase plasma calcium levels

- targets bone:
o activates osteoclasts = increase bone breakdown and increases plasma calcium
levels
- targets kidneys:
o reabsorb calcium = increases plasma calcium levels
- targets small intestines:
o increases calcium absorption by small intestines = increase plasma calcium levels
- paRathyRoid hormone = Raises calcium levels
o uses cAMP pathway

Gonads
 - male = testes
o testosterone
o androstenedione
- female = ovaries
o estradiol/estrogen
o progesterone
o placenta of pregnant female
 estrogens and progesterone

Testosterone

- steroid
- hypothalamus secretes GnRH  binds to excitatory receptors on anterior pituitary to
secrete luteinizing hormone (LH)  travels to testes to create the secretion of testosterone
from the Leydig cells
- functions
o development of secondary sex characteristics
o protein synthesis
o promotes spermatogenesis in sertoli cells
o increases sexual drive in brain
o development of accessory reproductive organ