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Nutrigenomics: concept, advances and applications

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Asian J. Dairy & Food Res, 34(3) 2015: 205 -212 AGRICULTURAL RESEARCH COMMUNICATION CENTRE
Print ISSN:0971-4456 / Online ISSN:0976-0563 www.arccjournals.com

Nutrigenomics: concept, advanes and applications

Jagish Kour Reen*, Alok Kumar Yadav and Jitendra Singh
Dairy Cattle Breeding Division,
ICAR-National Dairy Research Institute, Karnal-132001, India
Recieved: 14-02-2015 Accepted: 13-08-2015
ABSTRACT
The interface between the nutritional environment and cellular/ genetic processes is referred to as Nutritional genomics or
Nutrigenomics. It seeks to understand the effects of diet on an individual’s genes and health. Nutrigenomics seeks to
provide a genetic understanding for how common dietary chemicals (i.e., nutrition) affect the balance between health and
disease by altering the expression or structure of an individual’s genetic makeup. It is the science that examines the response
of individuals to food compounds using post-genomic and related technologies (e.g. genomics, transcriptomics, proteomics,
metabolomics etc.). Nutritional genetics is considered as the combination of nutrigenomics and nutrigenetics. Nutrigenomics
is establishing the effects of ingested nutrients and other food components on gene expression and gene regulation. It will
also determine the individual nutritional requirements based on the genetic makeup of the person (personalized diet) as
well as the association between diet and chronic diseases which will help to understand the etiologic aspects of chronic
diseases such as cancer, type-2 diabetes, obesity and cardiovascular disease (CVS). Nutrigenetics on the other hand identifies
how the genetic makeup of a particular individual co-ordinates his or her response to various dietary nutrients. It also
reveals why and how people respond differently to the same nutrient. The long-term aim of nutrigenomics is to understand
how the whole body responds to real foods using an integrated approach termed ‘systems biology’. The huge advantage in
this approach is that the studies can examine people (i.e. populations, sub-populations - based on genes or disease and
individuals), food, life-stage and life-style without preconceived ideas. Nutrigenomic approaches will enhance researcher
abilities to maintain animal health, optimize animal performance and improve milk and meat quality.
Key words: Nutigenomics, Nutrient-gene interaction, Proteomics, and Post-genomics.
INTRODUCTION: bioactive substances that can through the interaction with
Nutritional genomics is the study of the interactions receptors activate or modulate the transcription of target
between our genetic makeup and the foods we consume, and genes or directly cause the rearrangement of chromatin
the health outcomes that may occur. Nutritional genomics structure, is widely accepted, but not often recognized in
is a relatively new field of study that encompasses two distinct the design and interpretation of genetic and epidemiologic
fields: nutrigenetics and nutrigenomics. Nutrigenomics studies.
focuses on how nutrients or non-nutritive bioactive The studies that follow the effect of a certain diet
components, such as enzyme inhibitors, found in the diet often disregard the possible effect of genetic variability
affect gene expression, protein and metabolite concentration within the studied cohort, on the other hand, some studies
and therefore metabolism, health status and risk of disease. analyzing the effect of candidate gene polymorphism on the
Nutri gen omi cs i s a di sci pli ne wit hin nut rit ion al studied trait (for example blood pressure, obesity) do not
genomics that studies the effects of foods on gene include the diet interference, which can dramatically
expression. This sounds complicated, but this should likely influence the resulting association. Nutritional genomics aims
be understood with some of the familiar examples of to resolve this evident discrepancy (Miggiano et al., 2006).
nutrigenomics (De-Busk et al., 2005). For example, red wine In a certain parallel to pharmacogenomics, the nutritional
has become something of a modern-day health food thanks genomics focuses on the bioactive substances found in
to the fact that it contains resveratrol. Resveratrol is a nutrient regular food and how those substances affect the balance
that stimulates a gene that protects tissues from free radical between health and disease via the interaction with the
damage. Another nutrient that affects your genes is folate, individual’s genome. These are 5 basic principles of
found in foods like fruits and green vegetables. Folate is a nutrigenomics (German, 2005):
nutrient needed by the body to make DNA. When you do 1. Substances contained in the food (micro- and macro-nutrients)
not take in enough folate, you have a higher risk of can directly or indirectly affect the human genome through
developing cancer. The fact, that common diet contains many changes in its structure and gene expression.
*Corresponding author’ e-mail and address: [email protected]
206 ASIAN JOURNAL OF DAIRY AND FOOD RESEARCH
2. Under certain circumstances and in some individuals the Dietary chemicals can also affect gene expression
diet can be an important risk factor for the development directly or indirectly. At the cellular level, nutrients may:
of the number of diseases. Act as ligands for transcription factor receptors
3. Some genes regulated by active substances in the diet Be metabolized by primary or secondary metabolic
probably play a crucial role in the onset, incidence, pathways, thereby altering concentrations of substrates
progression and severity of the disease. or intermediates; or
4. The degree to which diet influences the balance between health
Positively or negatively affect signal pathways
and disease may depend on individual’s genetic makeup.
5. Nutritional intervention is based on the knowledge of
individual’s nutritional status and needs as well as genotype
(individualized nutrition) and can be used for prevention,
mitigation or healing the chronic diseases.
A nutrient is not merely a chemical component
required for a particular metabolic function, but also that it
plays an informational or signaling role in the cell. As with
any system that transmits information, the signal must have
a sensor or receiver that can accept, decode, and relay the
information that has been transmitted. Cellular proteins that
receive and transmit this information are termed “receptors.”
The receptors then must relay this information via a
transducing mechanism to the part of the cell that is capable
of reprogramming the cell to adapt to the new environmental
conditions. This reprogramming can occur in the cell nucleus
or cytoplasm. It can involve changes in the expression of
genes (transcription and translation), the stability of
messenger RNA and protein, or the activity of proteins.
The key principle behind nutrient control of gene expression
is specificity. Each receptor must have the capability of
binding a nutrient-signaling molecule with specificity and
should initiate an adaptive change. It is reported that until FIG. 1. Fate and activities of nutrients in the cell. Nutrients may
recently, the regulation of gene expression in response to act directly as ligands for transcription factor receptors (pathway
A); may be metabolized by primary or secondary metabolic
changes in nutritional environment was thought to be
pathways, thereby altering concentrations of substrates or
mediated primarily by hormones and/or the nervous system. intermediates (pathway B) involved in gene regulation or cell
However, the last decade has provided evidence that signaling; or alter signal transduction pathways and signaling
major (glucose, fatty acids, and amino acids) or minor (pathway C).
(e.g., iron, vitamin) nutrients, or th ei r respecti ve
metabolites, regulate gene expression in a hormone- Macronutrients A deficiency of essential nutrients can
independent manner (Allan Walker, 2004) Thus Common modify genetic expression.
dietary chemicals (nutrients) affect balance between health Carbohydrates: The role of dietary carbohydrates in weight
and disease by impacting the expression of genes. gain has become an important question in the public
Nutrient-gene interaction: There are 3 major conceptual consciousness. Carbohydrates have been traditionally
groupings for thinking about nutrient-gene interactions: classified as simple (monomeric and dimeric) or complex
(1) Direct interactions: nutrients, sometimes after interacting (polymeric) on the basis of their chemical structure. A critical
with a receptor, behave as transcription factors that can defect of this classification is its inability to predict the plasma
bind to DNA and acutely induce gene expression. glucose and insulin responses associated with different types
(2) Epigenetic interactions: nutrients can alter the structure of carbohydrates. The glycemic index, developed two
of DNA (or of histone proteins in chromatin) so that gene decades ago (Jenkins et al., 2002)s allows comparison of
expression is chronically altered. different foods based on their physiologic effects rather than
(3) Genetic variations: common genetic variations [single- on their chemical composition. A positive association
nucleotide polymorphisms (SNPs)] can alter the between glycemic index and body weight has been shown in
expression or functionality of genes. All of these several short-term experimental studies and limited
mechanisms can result in altered metabolism of and altered observational studies (Ludwig et al., 1999). The possible
dietary requirements for nutrients. biologic mechanisms of glycemic index on body weight are
 Volume 34, Issue 3, 2015 207
thought to be related to insulin levels, hunger and satiation, Dietary fats : Fatty acids, in addition to their important role
and basic metabolic processes (Roberts, 2000). This finding as energy-yielding nutrients, may exert a significant influence
is consistent with the hypothesis that with increased glycemic on the regulation of gene expression (Jump et al., 1999).
index, more insulin is produced and more fat is stored, Several rodent studies indicate that dietary lipids
suggesting that type of carbohydrate may be related to body modulate the expression of genes in skeletal muscle, with
weight. an increase in the messenger RNA (mRNA) expression of
Glucose, the most abundant monosaccharide in genes involved in fatty acid metabolism after isoenergetic
nature, provides a very good example of how organisms have high-fat diets compared with low fat, high-carbohydrate
developed regulatory mechanisms to cope with a fluctuating diets (Samec et al., 1999).
level of nutrient supply. In mammals the response to The effect of altered dietary fat intake on the
dietary glucose is complex because it combines effects expression of genes encoding proteins necessary for fatty
related to glucose metabolism itself and effects secondary acid transport and ß-oxidation in skeletal muscle has been
to glucose-dependent hormonal modifications, mainly reported. A rapid and marked capacity for changes in dietary
pancreatic stimulation of insulin secretion and inhibition of fatty acid availability to modulate the expression of
glucagon secretion. In the pancreatic - cells, glucose is the mRNA-encoding proteins is necessary for fatty acid transport
primary physiological stimulus for the regulation of insulin and oxidative metabolism. This finding is evidence of
synthesis and secretion. In the liver, glucose, in the presence nutrient-gene interactions in skeletal muscle. Expression of
of insulin, induces expression of genes encoding glucose hepatic gene expression related to lipid metabolism in broiler
transporters and glycolytic and lipogenic enzymes, e.g. breeders declined sterol regulatory element binding protein
L-type pyruvate kinase (L-PK), acetyl-CoA carboxylase 1 (SREBP-1), ATP-citrate lyase (ACL), fatty acid synthetase
(ACC), and fatty acid synthetase, and represses genes of the (FAS), malic enzyme (ME), acetyl-CoA carboxylase (ACC),
gluconeogenic pathway, such as the phosphoenolpyruvate and stearoyl-CoA (9) desaturase 1 (SCD1) genes in ad lib
birds declined from their highest levels just prior to
carboxykinase gene. Although insulin and glucagon were
photo-stimulation to reduced levels as the birds came into
long known as critical in regulating gene expression, it is
and maintained egg production.(Richard et al., 2003)
only recently that glucose also has been shown to play a key
role in transcriptional regulation. The effects of dietary fat on gene expression reflect
an adaptive response to changes in the quantity and type of
Feeding high-energy diet to rats leads to early
fat ingested. In mammals, fatty acid regulated transcription
development of obesity and metabolic syndrome, apparently
factors include peroxisome proliferator–activated receptors
through an inability to cope with energy density of the diet
(PPAR, -, and -), HNF4, NFB, and SREBP1c. These
(Selman et al., 2006). Obesity is associated with increase in factors are regulated by
mRNA levels for the oxygenic neuropeptides, NPY (a) Direct binding of fatty acids, fatty acyl coenzyme A, or
(neuropeptides Y), Ag RP (Agouti Related Peptide) etc. oxidized fatty acids
Hyperglycemia activated AGT gene expression in liver. (b) Oxidized fatty acid regulation of G-protein–linked cell
It increased approximately 3 fold. surface receptors and Activation of signaling cascades
It is shown that in both animals and human subjects, targeting the nucleus
reduced expression of CAPN3 was associated with elevations (c) Oxidized fatty acid regulation of intracellular calcium
in circulating glucose and insulin concentrations, decreased levels, which affect cell Signaling cascades targeting
carbohydrate oxidation and the accumulation of body fat, the nucleus.
particularly in the abdominal region. The altered expression At the cellular level, the physiological response to fatty acids
of CAPN3 contributes to the development of insulin will depend on:
resistance, obesity and type 2 diabetes. Lower levels of (a) The quantity, chemistry, and duration of the fat ingested;
expression of calpain 3 in skeletal muscle were associated (b) Cell-specific fatty acid metabolism (oxidative pathways,
with reduced carbohydrate oxidation and elevated circulating kinetics, and
glucose and insulin concentrations, and also with increased Competing reactions);
body fat and in particular abdominal fat. Therefore, reduced (c) Cellular abundance of specific nuclear and membrane receptors
expression of calpain 3 in both humans and animals was (d) Involvement of specific transcription factors in gene
associated with phenotypes related to obesity and insulin expression.
resistance (Walder et al., 2002). It is postulated that dietary An important receptor that mediates the effects of
carbohydrates and thyroid hormones are major regulators dietary lipids on gene expression is the peroxisome
for expression of the lactase/phlorizin hydrolase in starved proliferator-activated receptor alpha (PPAR), which is
rats when they have a sustainable thyroid hormone level abundantly expressed in enterocytes. Nutrients impact gene
(Kuranuki et al., 2006). expression mainly by activating or suppressing specific
208 ASIAN JOURNAL OF DAIRY AND FOOD RESEARCH
transcription factors (Desvergne et al., 2006).The most to insulin biosynthesis, secretion and cellular remodeling.
important group of transcription factors involved in Normal insulin secretion is influenced by level of Protein
mediating the effect of nutrients and their metabolites on Kinase C (PKC), K+ channel protein, calcium ion (Ca 2+)
gene transcription is the super family of nuclear receptors, and PKA. Increased ATP to ADP ratio achieved through
which is subdivided into six families of which the NR1 glucose metabolism, close the K+ ATP channel, which leads
family is most relevant to nutrition. One important group of to depolarization of b-cells. Depolarized -cells opens the
receptors that mediates the effects of dietary fatty acids voltage dependent Ca 2+ channels which results in influx of
and its derivatives on gene expression are the Peroxisome calcium leads to exocytosis of insulin granules. Feeding low
Proliferator Activated Receptors (PPARs, NR1C) (Sampath protein diet also increased expression of PFK in islets
et al.,2005).Transcriptional regulation by PPARs (tetramers M, P, L, and C) results in defective glucose
requires heterodimerization with the retinoid X receptor metabolism; it further leads to deceased glucose induced
(RXR; NR2B). When activated by an agonist, the insulin secretion. Feeding low protein diet decreases insulin
PPAR/RXR heterodimer stimulates transcription via binding level, it also acts through decreased movement of
to DNA response elements (PPREs) present in and around intracellular calcium.
the promoter of target genes. Besides up regulating gene Amino acids: The first step of protein translation is the
expression, PPARs are also able to repress transcription formation of the 43s pre-initiation complex containing
by directly interacting with other transcription factors methionyl tRNA, eIF2, GTP.This is followed by the
and interfere with their signaling pathways, a mechanism association of methionyl tRNA and eIF2 – GTP that bind
commonly referred to as transrepression. to the 40s ribosomal sub unit. The GTP is hydrolyzed late in
Role of PPAR in intestinal fatty acid oxidation: the initiation process, and eIF2 is released from the ribosome
It is well established that PPAR serves as a master regulator as an inactive eIF2 – GTP complex. Formation of eIF2 – GTP
of fatty acid catabolism and regulate the following functions is mediated by the guanine –nucleotide exchange factor
PPAR regulates intestinal cholesterol flux eIF2B. The mechanism to regulate eIF2B activity may be
PPAR regulates intestinal nutrient transport and metabolism at the level of the ribosomal protein S6 and eukaryotic
PPAR regulates intestinal motility elongation factor 2 (eEF-2) which is phosphorylated in
response to many agents, including growth factors and
PPAR diminishes effects of oxidative stress. Hence hormones initiation process. Amino acids regulate protein
PPAR might be therapeutically valuable for patients translation through modulation of eIF2B activity, 4 E –BP
with inflammatory bowel disease. phosphorylation and protein S6 phosphorylation. Protein and
These mechanisms are involved in the control of amino acids the response of IGFBP-2 gene expression to
carbohydrate and lipid metabolism, cell differentiation and variations in nutritional status was rapid and different in
growth several tissues of young chickens, which would help modulate
PUFA: Lipogenic enzymes in liver decreased as result of the growth-promoting effect of circulating IGF-I by making
feeding a diet containing 60 % linoleic acid (Flick et al., 1977). the IGF-IGFBP complex (Kazumi Kita, 2002).
Fatty acids stimulated the expression of adipocyte fatty acid Caloric restriction: Early epidemiological studies neglected
binding protein (ap2) mRNA. In the 3T3 –L1 adipocyte cell to account for the differences in energy content between
line, arachidonic acid (n-6) decreased SCD1 m RNA stability carbohydrates and proteins (each at4 kcal/g) and lipids
in a dose dependent manner (80% maximum repression), as (9 kcal/g). Virtually all association studies show an increased
did linoleic and eicosapentanoic acids. risk for common diseases with increased energy intake
Protein : Protein is very essential for growth, to develop (Kant, 2000). Laboratory animal studies have consistently
immunity, normal maintenance of body function and structure shown that reducing caloric intake is the most effective means
apart from reproduction and production. The function of to reduce the incidence and severity of chronic diseases,
protein in body is not only at macro level but it also functions retard the effects of aging, and increase genetic fidelity
at gene level. A variety or number of genes responds to (Uyeda et al., 2002). Energy balance may be monitored
dietary protein both protein quantity as well as quality through changes in reducing equivalents. NAD also is a
influences gene expression. Insulin secretion was reduced cofactor for Sir2, a histone deacetylase involved in chromatin
in rats, which are fed with low protein diet due to reduction silencing of nucleolar DNA, telomere, and mating type locus
in pancreatic b-cell mass lower response of remaining (Gasser et al., 2001). In mammals, other cellular targets,
-cells to nutrients and lowered protein kinase activity such as uncoupling proteins, and neuroendocrine
(PKA). PKA is involved in potentiation of glucose induced peptides (e.g., leptin) of the central nervous system (CNS),
insulin secretion by gastrointestinal hormones such as GIP are potential targets of regulation by caloric restriction.
and GLP-1. Low protein diet feeding to rats altered the many Micronutrients : Vitamins are a class of organic compounds
gene expression, which are responsible for proteins related that are components of an adequate diet. They or their
 Volume 34, Issue 3, 2015 209
derivatives function as coenzymes, cellular antioxidants, preparation of HT-29 cells. The other protein have Zn in it
and/or regulators of gene expression. Various vitamins are as constituents are ATP synathase, cytochrome c, a, NADP
recognized in human nutrition (Vitamins A, D, E, K, B1, B2, dehydrogenase I and II regulated by Zn
B6, B12, C, niacin, folacin, pantothenic acid, biotin, choline), In mammals, evidence is emerging that biotin
with deficiencies or excesses in intake leading to changes in participates in processes other than classical carboxylation
protein, nucleic acid, carbohydrates, fat and/or mineral reactions. Specifically, novel roles for biotin in cell signaling,
metabolism. Thus, the integrity of physiological systems, gene expression, and chromatin structure have been
including those associated with detoxification, cellular repair, identified in recent years. The activity of cell signals such as
immune processes, and neural and endocrine function, biotinyl-AMP, Sp1 and Sp3, nuclear factor (NF)-B, and
depends upon the nutritional and vitamin status of the host. receptor tyrosine kinases depends on biotin supply.
For these reasons, it may be anticipated that the adequacy of Consistent with a role for biotin and its catabolites in
the vitamin supply to cells and tissues would affect the modulating these cell signals, many biotin-dependent gene
development, progress and outcome of cancers. products play roles in signal transduction and localize to the
Suboptimal intakes of specific micronutrients have cell nucleus, consistent with a role for biotin in cell signaling.
been associated with CVD (B vitamins, vitamin E, Posttranscriptional events related to ribosomal activity and
carotenoids), cancer (folate, carotenoids), neural tube defects protein folding may further contribute to effects of biotin on
(folate), and bone mass (vitamin D) (Fairfield et al., 2002). gene expression. Finally, research has shown that biotinidase
B6, B12, serum homocysteine levels. Hyperhomocysteinemia and holocarboxylase synthetase mediate covalent binding
is a risk factor and marker for coronary artery disease, but of biotin to histones (DNA-binding proteins), affecting
the mechanism(s) is not understood at the molecular level chromatin structure; Biotinylation of histones appears to play
(Falk et al., 2001). Deficiency of vitamins B12, folic acid, a role in cell proliferation, gene silencing, and the cellular
B6, niacin, C, or E, or iron or zinc appears to mimic radiation response to DNA repair (Janos Zempleni, 2005).This
in damaging DNA by causing single- and double-strand observation suggests that biotin metabolites that have been
breaks, oxidative lesions, or both (Ames, 2001) and the considered “metabolic waste” in previous studies might
various effects of micronutrient deficiency are presented in have biotin-like activities. These new insights into
the Table below. Nutrient deficiencies are orders of biotin-dependent gene expression are likely to lead to a better
magnitude more important than radiation because of understanding of roles for biotin in cell biology and fetal
constancy of exposure to milieu promoting DNA damage development. (Rodriguez, 2003)
(Ames et al., 2001). Folate deficiency breaks chromosomes PEPCK is vitamin A dependent enzyme involved
due to substantial incorporation of uracil in human DNA in conversion of oxaloacetate to phospho enol pyruvate, one
(4 million uracil/cell) (Blount et al., 1997). Single-strand of the important steps in gluconeogenesis
breaks in DNA are subsequently formed during base excision Phosphoenolpyruvate carboxykinase (PEPCK) gene
repair, with two nearby single-strand breaks on opposite DNA expression is decreased in vitamin A–deficient (VAD) mice.
strands leading to chromosome fragmentation Vitamin A deficiency condition leads to changes in
Zinc is an essential trace element with cofactor chromosomal structure of RARE (Retinoic Acid Responsive
functions in a large number of proteins of intermediary Element), which further leads to change in co regulator
metabolism, hormone secretion pathways and immune binding and activity The reduction in RNA Pol II association
defense mechanism. Zn is involved in regulation of is indicative of an interruption in the direct interactions of
small intestinal, thymus and hepatocytes gene expression. RNA Pol II with the PEPCK promoter, with general
(Tako et al., 2003) MTF-I (Metal Responsive element Factor- I) transcription factors and/or with co regulator molecules that
is a Zn dependent transcriptional activator regulates contribute to the activation of the PEPCK gene. These results
mettalothionin I and II through MRE(Menard,1981). increase understanding of the molecular basis for decreased
Zn dependent KLF4 transcription factor is involved in protein PEPCK gene expression in VAD mice in vivo and offer

Micronutrient deficiency and DNA damage

Micronutrient DNA Damage Health Effects
Folic acid Chromosome breaks Colon cancer; heart disease; brain dysfunction
Vitamin B12 Uncharacterized Same as folic acid; neuronal damage
Vitamin B6 Uncharacterized Same as folic acid
Vitamin C Radiation mimic (DNA oxidation) Cataracts; cancer
Vitamin E Radiation mimic (DNA oxidation) Colon cancer; heart disease; Immune dysfunction
Iron DNA breaks; radiation mimic Brain and immune dysfunction; cancer
Zinc Chromosome breaks; radiation mimic Brain and immune dysfunction; cancer
Niacin Disables DNA repair (polyADP ribose) Neurological symptoms; memory loss
210 ASIAN JOURNAL OF DAIRY AND FOOD RESEARCH
additional insight into the regulation of other retinoid- to vary depending on breed, suggesting differences in
responsive genes (Kelly et al., 2003) metabolism due to genotype. Determination of nutrient
Applications in animal sciences requirements of dogs participating in different physical
1. To develop animal feed/food matching to its genotype to activities (e.g., dog sled racing, sprint racing or hunting/
benefit health and enhance normal physiological processes herding) also would be a worthy research venture.
2. To select nutrients fine tuned with the gene of the animal. However refinements in sample handling, statistical
3. To understand the role of nutritional management in the analysis, and hierarchical clustering of expressed transcripts
performance (Production/disease) of the animal. and development of bovine-specific metabolic maps is
4. To understand the ageing process in animals. necessary for greater understanding of the complex molecular
Implications on Animal Nutrition basis of nutrient metabolism in support of milk production,
The central dogma of molecular biology states that growth and reproduction.
DNA makes RNA and RNA makes protein. The application Limitations : As of yet, nutrigenomics is in its infancy.
of molecular biology to understanding nutrient metabolism The tools to study protein expression and metabolite
centers on identifying conditions that lead to the amplification production have not yet developed to the point as to enable
of genetic information and synthesis of several copies of RNA efficient and reliable measurements.Presently the accurate
and ultimately the initiation and progression of protein measurement of dietary exposure will be fundamental if we
synthesis. The ultimate end point of these processes in want to understand the interaction of nutrition with the
livestock is a coordinated change in cellular and tissue genome. Transcript profiling using DNA micro arrays or
metabolism to maintain homeostasis or to undergo candidate gene analysis is a static measure of the pool size
homeorhesis to support a new physiological state. On these of individual mRNA in a cell or tissue and does not provide
lines of action theoretically it is possible to control and any information on the dynamics of mRNA synthesis
prevent any disease or disorder having a genetic component (Transcription) or RNA degradation (RNA stability).
by nutrient management and manipulation. Practically Determining the rate of mRNA synthesis typically involves
speaking, animal nutritionists have always been using dietary use of nuclear run-on assays that measure the relative amount
manipulations to affect and control the phenotype/ of new transcripts made from the previously initiated RNA
performance. However the exact genetic cascade that was polymerases and provides a measure of the in vivo rate of
being targeted by such manipulations were not known. transcription of DNA to mRNA. Levels of some key proteins
The recognition that fatty acids are regulators of (e.g., the transferrin receptor) are regulated at the level of
metabolism and act in the cell nucleus to control expression RNA stability; however, measures of RNA degradation rate
of genes for fatty acid synthesis has been extended to are presently not easily attainable in vivo and therefore
investigations on the origins of milk fat depression in dairy nutritional impacts on gene expression usually are only
cows. It has been observed that the reduction in milk fat described for transcription rate and mRNA abundance.
when fish oil is fed is linked to decreased mRNA abundance All these technologies are still in the process of
of acetyl CoA carboxylase, fatty acid synthetase, and development.There is a need to develop guidelines and
stearoyl-CoA desaturase (also known as9-desaturase). And standards, which incorporate the state-of-the-art and enable
also the potent action of trans-10, cis-12 CLA to reduce and encourage researchers to apply the ‘omics’ technologies
milk fat synthesis in lactating dairy cows involves a reduction in ways that can be replicated, so that comparisons between
in mRNA for acetyl CoA carboxylase, fatty acid synthetase, laboratories can be made and which facilitate pooling of
stearoyl-CoA desaturase, lipoprotein lipase, fatty acid samples and data.Also once such research has been achieved,
binding protein, and glycerol phosphate acyltransferase. it will need to be integrated together in order to produce
These changes are directly linked to a substantial reduction results and dietary recommendations. the prudent
in lipogenic activity in explant cultures in vitro. These data application of nutrigenomics hold great promise in
provide understanding of the molecular basis for milk fat countering this challenge and making desired manipulation
depression, a practical milk production problem that has been of genome expression by nutritional intervention to boost
recognized for several decades. up nutrient –gene status, a reality in years to come.
In addition to knowing the minimal nutrient CONCLUSION
concentrations required to avoid deficiency, determination Nutrigenomics offers the potential of important health
of optimal and toxic concentrations will be important. benefits for some individuals. Primary care physicians have
Nutritional effects on gene expression in different life stages minimal training in nutrition and genetics, and medical
and genotypes also must be a focus in companion animals. geneticists are in high demand and short supply. Dietetic
The importance of maternal nutrition during pregnancy on practitioners are experts in nutrition science and interest in
the gene expression and development of offspring was nutrigenomics is growing among members of this
demonstrated in sheep. In pigs, nutrient excretion was shown professional group. However, as with physicians, dietetics
 Volume 34, Issue 3, 2015 211
practitioners would require considerable training to bring in combination with twin studies may provide opportunities
nutrigenomics into their practice capacity (Castle and Ries, 2007). to understand the basis of complex traits and the role
In recent years, a high-resolution recombination map of the of individual genotypes on the development of polygenic
human genome has provided and increased the information diet-related diseases such as cancer and CVS (Boomsma et
on the genetic order of polymorphic markers and the SNP al., 2002). Thus nutrigenomics treats food as a major
map of the human genome. It is hoped that the map of SNPs environmental factor in the gene–environment interaction, with
in the human genome will provide powerful molecular tools the final aim to personalize food and nutrition and ultimately
to decipher the role of nutrition in human health and disease individualize strategies to preserve health, by tailoring the food
and help defining optimal diets. Advanced genetic analysis to individual genotype (Iacoviello et al., 2008).

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