Nutritional Biochemistry

The objective of this study was to determine the effect of creatine supplementation on performance and body composition of swimmers. Eighteen swimmers were evaluated in terms of post-performance lactate accumulation, body composition, creatine and creatinine excretion, and serum creatinine concentrations before and after creatine or placebo supplementation. No significant differences were observed in the marks obtained in swimming tests after supplementation, although lactate concentrations were higher in placebo group during this period. In the creatine-supplemented group, urinary creatine, creatinine, and body mass, lean mass and body water were significantly increased, but no significant difference in muscle or bone mass was observed. These results suggest that creatine supplementation cannot be considered to be an ergogenic supplement ensuring improved performance and muscle mass gain in swimmers.

Vasquez A. Review of JAMA Cardiology’s 2018 “Associations of Omega-3 Fatty Acid Supplement Use with Cardiovascular Disease Risks”. Video presentation (http://www.ichnfm.org/jama2018n3) and official transcript (https://www.academia.edu/35935996) 2018 February.

During normal cellular activities, various processes inside of cells produce reactive oxygen species (ROS). Some of the most common ROS are hydrogen peroxide (H 2 O 2 ), superoxide ion (O 2 À ), and hydroxide radical (OH À ). These compounds, when present in a high enough concentration, can damage cellular proteins and lipids or form DNA adducts that may promote carcinogenic activity. The purpose of antioxidants in a physiological setting is to prevent ROS concentrations from reaching a high-enough level within a cell that damage may occur. Cellular antioxidants may be enzymatic (catalase, glutathione peroxidase, superoxide dismutase) or nonenzymatic (glutathione, thiols, some vitamins and metals, or phytochemicals such as isoflavones, polyphenols, and flavanoids).

Sarcopenia, the age-related loss of muscle mass and strength, is a fundamental cause of frailty, functional decline and disability. In the year 2000, $18.5 billion in health care costs were directly attributable to sarcopenia. This economic burden will increase dramatically as the elderly population grows over the next decade. The primary causes of sarcopenia include a sedentary lifestyle and malnutrition.

Polyphenols are wide variety of compounds that occur in fruits and vegetables, wine, tea, extra virgin olive oil, chocolate and other cocoa products. Several polyphenols have been demonstrated to have clear antioxidant properties in vitro, and many of their biological actions have been attributed to their intrinsic reducing capabilities. However, this concept appears now to be a simplistic way to conceive their activity. Evidence is indeed accumulating that polyphenols might exert several other specific biological effects that are as yet poorly understood. In this article we review the most recent data on the subject and describe the additional functions that polyphenols can have in biological systems, focusing on their effects on glutathione and its related enzymes. Experimental data indicate that polyphenols may offer an indirect protection by activating endogenous defense systems. Several lines of evidence suggest a tight connection between exogenous and endogenous antioxidants that appear to act in a coordinated fashion. It is reasonable to hypothesize that this is achieved, at least in part, through antioxidant responsive elements (AREs) present in the promoter regions of many of the genes inducible by oxidative and chemical stress. The latest studies strongly suggest that dietary polyphenols can stimulate antioxidant transcription and detoxification defense systems through ARE. D

Dietary risk factors for cardiometabolic health are generally well recognised; for mental health they are not so well understood. However lifestyle risk factors for poor physical health are the same risk factors for mental illness, including poor diet. This is reflected by the high level of poor physical health in people with mental illness. Mediterranean, whole food diets have been associated with reduced risk for chronic disease but very little research has investigated their mental health benefits. We provide a model for the pathways by which food components provided by a Mediterranean-style diet can facilitate healthy brain function. We then review evidence for the role of selected nutrients/food components -antioxidants, omega-3 fatty acids and B vitamins -in the brain and hence modulation of cognitive function and mental health. Converging evidence indicates multiple pathways by which these nutrients can assist in brain function, drawing from studies investigating them in isolation. There is very little work done on synergistic actions of nutrients and whole diets, highlighting a need for human intervention studies investigating benefits of Mediterranean-style diets for mental, as well as cardiometabolic health.

Alzheimer's disease (AD) brains are characterized by extensive oxidative stress. Additionally, large depositions of amyloid beta-peptide (Abeta) are observed, and many researchers opine that Abeta is central to the pathogenesis of AD. Our laboratory combined these two observations in a comprehensive model for neurodegeneration in AD brains centered around Abeta-induced oxidative stress. Given the oxidative stress in AD and its potentially important role in neurodegeneration, considerable research has been conducted on the use of antioxidants to slow or reverse the pathology and course of AD. One source of antioxidants is the diet. This review examines the literature of the effects of endogenous and exogenous, nutritionally-derived antioxidants in relation to AD. In particular, studies of glutathione and other SH-containing antioxidants, vitamins, and polyphenolic compounds and their use in AD and modulation of Abeta-induced oxidative stress and neurotoxicity are reviewed.

Butyrate is a four-carbon short-chain fatty acid that improves colonic trophism. Although several studies have shown the benefits of butyrate enemas in ulcerative colitis (UC), studies using the oral route are rare in the literature. In the present study, we evaluated the effect of butyrate intake in the immune response associated to UC. For that, mice were fed control or butyrate (0.5% sodium butyrate) diets for 14 days. Acute UC was induced by dextran sulphate sodium (DSS, 2.5%), replacing drinking water. The results showed that, in UC animals, oral butyrate significantly improved trophism and reduced leukocyte (eosinophil and neutrophil) infiltration in the colon mucosa and improved the inflammatory profile (activated macrophage, B and T lymphocytes) in cecal lymph nodes. In the small intestine, although mucosa histology was similar among groups, DSS treatment reduced duodenal transforming growth factor-β, increased interleukin-10 concentrations and increased memory T lymphocytes and dendritic cells in Peyer's patches. Butyrate supplementation was able to revert these alterations. When cecal butyrate concentration was analyzed in cecal content, it was still higher in the healthy animals receiving butyrate than in the UC +butyrate and control groups. In conclusion, our results show that oral administration of sodium butyrate improves mucosa lesion and attenuates the inflammatory profile of intestinal mucosa, local draining lymph nodes and Peyer's patches of DSS-induced UC. Our results also highlight the potential use of butyrate supplements as adjuvant in UC treatment.

Whether the beneficial effects of pomegranate are due to the ellagitannins or to their microbiota-derived urolithins is not known. Our objectives were to evaluate the effects of pomegranate intake and its main microbiota-derived metabolite urolithin-A (UROA) on colon inflammation and to assess whether UROA is the main anti-inflammatory compound. In addition, the effect of the inflammation on the phenolic metabolism was also explored. Male Fisher rats were fed with 250 mg kg −1 day −1 pomegranate extract (PE) or 15 mg kg −1 day −1 UROA for 25 days. Dextran sodium sulfate (5%) (DSS) was administered for the five last days and then rats were euthanized. DSS is a well-known model of inflammatory bowel disease. Colon tissue damage, microbiota changes, antioxidant status, prostaglandin E 2 (PGE 2 ), nitric oxide production, inducible nitric oxide synthase (iNOS), prostaglandin E synthase (PTGES), gene expression (microarrays and RT-PCR) and polyphenol metabolism (LC-MS-MS) were evaluated. Both PE and UROA decreased inflammation markers (iNOS, cycloxygenase-2, PTGES and PGE 2 in colonic mucosa) and modulated favorably the gut microbiota. The G 1 to S cell cycle pathway was up-regulated in both groups. UROA group showed various downregulated pathways, including that of the inflammatory response. PE, but not UROA, decreased oxidative stress in plasma and colon mucosa. Only UROA preserved colonic architecture. The normal formation of urolithins in PE-fed rats was prevented during inflammation. Our results suggest that UROA could be the most active anti-inflammatory compound derived from pomegranate ingestion in healthy subjects, whereas in colon inflammation, the effects could be due to the nonmetabolized ellagitannin-related fraction.

Polyphenol-rich dietary foodstuffs have attracted attention due to their cancer chemopreventive and chemotherapeutic properties. Ellagitannins (ETs) belong to the so-called hydrolysable tannins found in strawberries, raspberries, walnuts, pomegranate, oak-aged red wine, etc. Both ETs and their hydrolysis product, ellagic acid (EA), have been reported to induce apoptosis in tumour cells. Ellagitannins are not absorbed in vivo but reach the colon and release EA that is metabolised by the human microflora. Our aim was to investigate the effect of a dietary ET [pomegranate punicalagin (PUNI)] and EA on human colon cancer Caco-2 and colon normal CCD-112CoN cells. Both PUNI and EA provoked the same effects on Caco-2 cells: down-regulation of cyclins A and B1 and upregulation of cyclin E, cell-cycle arrest in S phase, induction of apoptosis via intrinsic pathway (FAS-independent, caspase 8-independent) through bcl-XL down-regulation with mitochondrial release of cytochrome c into the cytosol, activation of initiator caspase 9 and effector caspase 3. Neither EA nor PUNI induced apoptosis in normal colon CCD-112CoN cells (no chromatin condensation and no activation of caspases 3 and 9 were detected). In the case of Caco-2 cells, no specific effect can be attributed to PUNI since it was hydrolysed in the medium to yield EA, which entered into the cells and was metabolised to produce dimethyl-EA derivatives. Our study suggests that the anticarcinogenic effect of dietary ETs could be mainly due to their hydrolysis product, EA, which induced apoptosis via mitochondrial pathway in colon cancer Caco-2 cells but not in normal colon cells.

Epidemiological studies have described the beneficial effects of dietary polyphenols (flavonoids) on the reduction of the risk of chronic diseases, including cancer. Moreover, it has been shown that flavonoids, such as quercetin in apples, epigallocatechin-3-gallate in green tea and genistein in soya, induce apoptosis. This programmed cell death plays a critical role in physiological functions, but there is underlying dysregulation of apoptosis in numerous pathological situations such as Parkinson's disease, Alzheimer's disease and cancer. At the molecular level, flavonoids have been reported to modulate a number of key elements in cellular signal transduction pathways linked to the apoptotic process (caspases and bcl-2 genes), but that regulation and induction of apoptosis are unclear.

Because of its growing prevalence in Western countries, the metabolic syndrome, a common metabolic disorder that clusters a constellation of abnormalities, including central obesity, hypertension, dyslipidemia and insulin resistance, is emerging as one of the most important public health problems in the world, taking into account that it is a major risk factor mainly for type 2 diabetes and cardiovascular diseases, and also for many types of cancer. Although the pathogenesis of this syndrome is complex and not fully understood, obesity and insulin resistance, accompanied by an altered profile of number of hormones and cytokines produced by the adipose tissue, seem to be the main causative agents. A prime therapeutic approach to the prevention and treatment of this syndrome involves lifestyle changes. Among dietary modifications, dietary fiber intake could play an interesting role in the management of metabolic syndrome through different mechanisms related to its dietary sources, specific chemical structure and physical properties, or fermentability in the gut. According to all of these variables, the different types of dietary fibers have been reported to take part in the control of body weight, glucose and lipid homeostasis, insulin sensitivity and in the regulation of many inflammation markers involved in the pathogenesis of metabolic syndrome, and which are also considered to be among its features.

"The proximate, functional properties, In-vitro multi enzyme
protein digestibility and amino acid composition of velvet
tamarind (Dalium guineense) pulps were evaluated. The ash,
moisture, crude fat, crude fibre, crude protein and carbohydrate of
the velvet tamarind (Dalium guineense) pulp were: 4.63%, 8.22%,
5.80%, 7.15%, 24.3% and 49.9% respectively. The water and oil
absorption capacities were: 238% and 162% which makes the pulp
exhibit a high water retention capacity. The least gelation
concentration was 17.0% while the foaming capacity and stability
were: 43.5% and 62.2% respectively. The in-vitro protein
digestibility was 66%. Glutamic acid was the most concentrated
amino acid with the value of 14.8 mg/g crude protein while
histidine (2.12 mg/g crude protein) was the least concentrated
amino acid. The % total essential amino acid with histidine was
34.2% while the % total essential amino acid with histidine was
60.8%. The calculated isoelectric point was 0.54 while the
predicted protein efficiency ratio (P-PER*) was 2.62."

Several epidemiologic observations show that moderate wine drinking reduces cardiovascular morbidity and mortality. Wine contains several polyphenols, and among them, resveratrol in particular has been shown to exert a number of important biologic activities on the cardiovascular system that may contribute to the protective effects of wine. The mechanisms through which resveratrol and other wine polyphenols protect from ischemic cardiovascular events are many, but protection from oxidative stress and radical oxygen species production, a facilitating activity on nitric oxide production and activity and the ability to modulate the expression of adhesive molecules by blood cells and the vascular wall seem to be the most important. In this overview, the in vitro and in vivo evidence on the activity of resveratrol on vascular function and circulating blood cells, with a special emphasis on blood platelets, is thoroughly presented.

Iron deficiency is a micronutrient deficiency which is common in the developing regions of the world. Mangifera indica is one of the plants
used traditionally in the treatment of iron deficiency anaemia especially in the South Western region of Nigeria. This study was carried out to
determine the bioactive agent found in Mangifera indica responsible for its anti-anaemic action.
40 (forty) albino rats were used for the experiment, the iron deficient group were fed with an iron deficient feed for 8weeks, this induced
iron deficiency anaemia. The stem bark of Mangifera indica was pulverized, extracted with ethanol and subsequently with n-hexane and ethyl acetate solvents, these fractions were then concentrated using a rotary evaporator, the fractions were screened for the phytochemicals present.
The iron deficient animals were administered with 1ml of the ethyl acetate, n-hexane and ethanolic solvent fractions dissolved in distilled water for 2 weeks.
The results showed significant (P<0.05) increase in the PCV, RBC and the serum ferritin level of the groups administered with the extracts
when compared with the iron sufficient and iron deficient control groups and saponins were found to be present in the three extract fractions.
It was concluded that saponins might be the bioactive agent responsible for the heamotopoietic action of Mangifera indica by acting either as
a facilitator in diffusion of iron for absorption or making iron readily available for absorption as an antioxidant.

Whether the beneficial effects of pomegranate are due to the ellagitannins or to their microbiota-derived urolithins is not known. Our objectives were to evaluate the effects of pomegranate intake and its main microbiota-derived metabolite urolithin-A (UROA) on colon inflammation and to assess whether UROA is the main anti-inflammatory compound. In addition, the effect of the inflammation on the phenolic metabolism was also explored. Male Fisher rats were fed with 250 mg kg −1 day −1 pomegranate extract (PE) or 15 mg kg −1 day −1 UROA for 25 days. Dextran sodium sulfate (5%) (DSS) was administered for the five last days and then rats were euthanized. DSS is a well-known model of inflammatory bowel disease. Colon tissue damage, microbiota changes, antioxidant status, prostaglandin E 2 (PGE 2 ), nitric oxide production, inducible nitric oxide synthase (iNOS), prostaglandin E synthase (PTGES), gene expression (microarrays and RT-PCR) and polyphenol metabolism (LC-MS-MS) were evaluated. Both PE and UROA decreased inflammation markers (iNOS, cycloxygenase-2, PTGES and PGE 2 in colonic mucosa) and modulated favorably the gut microbiota. The G 1 to S cell cycle pathway was up-regulated in both groups. UROA group showed various downregulated pathways, including that of the inflammatory response. PE, but not UROA, decreased oxidative stress in plasma and colon mucosa. Only UROA preserved colonic architecture. The normal formation of urolithins in PE-fed rats was prevented during inflammation. Our results suggest that UROA could be the most active anti-inflammatory compound derived from pomegranate ingestion in healthy subjects, whereas in colon inflammation, the effects could be due to the nonmetabolized ellagitannin-related fraction.

In the present study the effect of quercetin and its major metabolites quercetin-3-glucuronide (Q3G) and isorhamnetin on inflammatory gene expression was determined in murine RAW264.7 macrophages stimulated with lipopolysaccharide. Quercetin and isorhamnetin but not Q3G significantly decreased mRNA and protein levels of tumor necrosis factor alpha. Furthermore a significant decrease in mRNA levels of interleukin 1β, interleukin 6, macrophage inflammatory protein 1α and inducible nitric oxide synthase was evident in response to the quercetin treatment. However Q3G did not affect inflammatory gene expression. Anti-inflammatory properties of quercetin and isorhamnetin were accompanied by an increase in heme oxygenase 1 protein levels, a downstream target of the transcription factor Nrf2, known to antagonize chronic inflammation. Furthermore, proinflammatory microRNA-155 was down-regulated by quercetin and isorhamnetin but not by Q3G. Finally, anti-inflammatory properties of quercetin were confirmed in vivo in mice fed quercetin-enriched diets (0.1 mg quercetin/g diet) over 6 weeks.

The antioxidant activity of green tea (GT) has been extensively studied; however, the results obtained from dietary intervention studies are controversial. In the present study we investigated the effect of the addition of two cups of GT (containing approximately 250 mg of total catechins) to a controlled diet in a group of healthy volunteers with respect to a group following the same controlled diet but not consuming GT. Antioxidant status and lipid profile in plasma, the resistance from oxidative damage to lipid and DNA, and the activity of glutathione peroxidase (GPX) in isolated lymphocytes were measured at the beginning and the end of the trial. After 42 days, consumption of GT caused a significant increase in plasma total antioxidant activity [from 1.79 to 1.98 Amol Trolox equivalent (TE)/ml, P b.001], significant decreases in plasma peroxides level (from 412 to 288 Carr U, P b.05) and induced DNA oxidative damage in lymphocytes (from 14.2% to 10.1% of DNA in tail, P b.05), a moderate although significant decrease in LDL cholesterol (from 119.9 to 106.6 mg/dL, P b.05) with respect to control. The present study suggests the ability of GT, consumed within a balanced controlled diet, to improve overall the antioxidative status and to protect against oxidative damage in humans.

Catechins, compounds derived from green tea, have been shown to reduce plasma cholesterol levels and the rate of cholesterol absorption. We investigated the dose response and the mechanism of action of epigallocatechin gallate (EGCG) on these parameters in rats. Wistar rats were fed a diet high in cholesterol and fat containing either none, 0.25% (0.2 g/day/kg BW), 0.5% (0.4 g/day/kg/BW) or 1.0% (0.7 g/day/kg BW) of EGCG. After 4 weeks of treatment, total cholesterol and low density lipoprotein plasma levels were significantly reduced in the group fed 1% EGCG when compared to the no treatment group. Plasma triglycerides and high-density lipoprotein levels did not change significantly. Following a single oral application of a liquid test-meal, intestinal cholesterol absorption in Wistar rats was 79.3% in the control group. In the group treated with 0.1 g/kg BW EGCG intestinal cholesterol absorption decreased to 73.7% and in the group treated with 0.5 g/kg BW of EGCG intestinal cholesterol absorption fell significantly to 62.7% (P ϭ 0.005). Total fat absorption was very efficient in the control group (99.5% of the applied dose) and decreased significantly but moderately in the group treated with the highest doses of EGCG (0.75, 1 g/kg BW). In an in-vitro biliary micelle model, the addition of 55 M to 1300 M EGCG not only decreased cholesterol solubility dose-dependently in these micelles but also altered the size of the mixed lecithin/taurocholate/cholesterol micelles as demonstrated by light scattering. This study provides evidence suggesting that the cholesterol-lowering effect of green tea is mainly elicited by EGCG, one of the most abundant catechins contained in green tea. It is suggested that one of the underlying mechanisms by which EGCG affects lipid metabolism is by interfering with the micellar solubilization of cholesterol in the digestive tract, which then in turn decreased cholesterol absorption.

Chronic low-grade inflammation in obesity is characterized by macrophage accumulation in white adipose tissue (WAT) and abnormal cytokine production. We tested the hypothesis that grape-seed procyanidin extract (PE), with known anti-inflammatory and antioxidant effects, would improve local and systemic inflammation in diet-induced obesity rats. First, we analyzed the preventive effects of procyanidins (30 mg/kg per day) on rats fed a 60% kcal fat diet for 19 weeks. Second, we induced cafeteria diet obesity for 13 weeks to investigate the corrective effects of two PE doses (25 and 50 mg/kg per day) for 10 and 30 days.

Natural products have potential for inducing apoptosis, inhibiting adipogenesis and stimulating lipolysis in adipocytes. The objective of this review is to discuss the adipocyte life cycle and various dietary bioactives that target different stages of adipocyte life cycle. Different stages of adipocyte development include preadipocytes, maturing preadipocytes and mature adipocytes. Various dietary bioactives like genistein, conjugated linoleic acid (CLA), docosahexaenoic acid, epigallocatechin gallate, quercetin, resveratrol and ajoene affect adipocytes during specific stages of development, resulting in either inhibition of adipogenesis or induction of apoptosis. Although numerous molecular targets that can be used for both treatment and prevention of obesity have been identified, targeted monotherapy has resulted in lack of success. Thus, targeting several signal transduction pathways simultaneously with multiple natural products to achieve additive or synergistic effects might be an appropriate approach to address obesity. We have previously reported two such combinations, namely, ajoene+CLA and vitamin D+genistein. CLA enhanced ajoene-induced apoptosis in mature 3T3-L1 adipocytes by synergistically increasing the expression of several proapoptotic factors. Similarly, genistein potentiated vitamin D&amp;amp;amp;amp;amp;amp;amp;#39;s inhibition of adipogenesis and induction of apoptosis in maturing preadipocytes by an enhanced expression of VDR (vitamin D receptor) protein. These two examples indicate that combination therapy employing compounds that target different stages of the adipocyte life cycle might prove beneficial for decreasing adipose tissue volume by inducing apoptosis or by inhibiting adipogenesis or both.

, which hinder the development of atherosclerosis. The goal of this study was to measure the total polyphenol and dietary fiber contents of some tropical fruits (i.e., pineapple, wax apple, rambutan, lichi, guava, and mango) and compare the results to the content of these substances in the better characterized persimmon. It was found that lichi, guava, and ripe mango (cv. Keaw) have 3. 35, 4.95, and 6.25 mg of total polyphenols in 100 g fresh fruit, respectively. This is significantly higher than in persimmon, pineapple, wax apple, mature green mango, and rambutan [P Ͻ 0.0005 for pineapple (Smooth Cayene variant), wax apple, persimmon, rambutan, mature green mango (cv. Keaw); the value of P Ͻ 0.001 is found only for pineapple (Phuket, Queen variant)]. The same relationship was observed for the contents of gallic acid and of dietary fiber. It can be supposed that among the studied fruit, lichi, guava, and ripe mango may be preferable for dietary prevention of atherosclerosis. (J. Nutr. Biochem. 10:367-371, 1999)

Honey in in great triumph on the trmendous using since the ancient times of the world history. The intent of this study was to hit upon the nutrition facts of mustard honey available in Bangladesh. Results divulged that there were found 14.36 ± 0.04% moisture, 0.19 ± 0.001% ash, 84.346% total carbohydrate and 71% TSS in mustard honey. It is a matter of great boost that none can jeer at the including this honey in diet planning in nutrition counseling as its (E d) n was found 307.63 Kcal / 100 g contributing 34.181Kcal / 100 g DIT level in human physiology.

Nonenzymatic glycation, the reaction of glucose and other reducing sugars with protein, reversibly produces Amadori products and over a fang period irreversible advanced glycation end products. In diabetes, these reactions are greatly accelerated and are important in the pathogenesis of diabetic complications.

Consumption of tea (Camellia sinensis) improves vascular function and is linked to lowering the risk of cardiovascular disease. Endothelial nitric oxide is the key regulator of vascular functions in endothelium. In this study, we establish that L-theanine, a non-protein amino-acid found in tea, promotes nitric oxide (NO) production in endothelial cells. L-theanine potentiated NO production in endothelial cells was evaluated using Griess reaction, NO sensitive electrode and a NO specific fluorescent probe (4-amino-5-methylamino-2',7'-difluororescein diacetate). L-Theanine induced NO production was partially attenuated in presence of L-NAME or L-NIO and completely abolished using eNOS siRNA. eNOS activation was Ca 2 + and Akt independent, as assessed by fluo-4AM and immunoblotting experiments, respectively and was associated with phosphorylation of eNOS Ser 1177. eNOS phosphorylation was inhibited in the presence of ERK1/2 inhibitor, PD-98059 and partially inhibited by PI3K inhibitor, LY-294002 and Wortmanin suggesting PI3K-ERK1/2 dependent pathway. Increased NO production was associated with vasodilation in ex ovo (chorioallantoic membrane) model. These results demonstrated that L-theanine administration in vitro activated ERK/ eNOS resulting in enhanced NO production and thereby vasodilation in the artery. The results of our experiments are suggestive of L-theanine mediated vascular health benefits of tea.

Dietary fish oil rich in (n-3) fatty acids plays an important role in reducing abnormalities associated with the metabolic syndrome and mortality from coronary heart disease. We investigated the effects of dietary fish oil on the metabolic syndrome in a high-sucrose-fed rat model. The model was achieved by the administration of 30% sucrose in drinking water in male Wistar rats during 21 weeks. After the metabolic syndrome rat model was established, fish oil was administered during 6 weeks. The metabolic syndrome rats showed significant increases in body weight, systolic blood pressure, serum insulin, total lipids, triacylglycerols, cholesterol, free fatty acids, LDL, total proteins, albumin, and serum tumor necrosis factor-␣ (TNF-␣). They also presented abdominal and epididymal fat accumulation and fatty liver. After fish oil diet administration, metabolic syndrome rats had a significant reduction in blood pressure, serum insulin, triacylglycerols, cholesterol, free fatty acids, and total lipids, but no change was observed in TNF-␣ concentration or fat accumulation. In conclusion, fish oil reversed the alterations on metabolic parameters and blood pressure exerted by sucrose administration, although it had no effect on TNF-␣ production and adiposity. This confirms the theory that the molecular etiology of the metabolic syndrome is multifactorial, as is the effect of n-3 polyunsaturated fatty acids (PUFAs) upon it, having complex and multifaceted actions.

For many years, clinical and animal studies on polyunsaturated n-3 fatty acids (PUFAs), especially those from marine oil, eicosapentaenoic acid (20:5,n-3) and docosahexaenoic acid (22:6,n-3), have reported the impact of their beneficial effects on both health and diseases. Among other things, they regulate lipid levels, cardiovascular and immune functions as well as insulin action. Polyunsaturated fatty acids are vital components of the phospholipids of membrane cells and serve as important mediators of the nuclear events governing the specific gene expression involved in lipid and glucose metabolism and adipogenesis. Besides, dietary n-3 PUFAs seem to play an important protecting role against the adverse symptoms of the Plurimetabolic syndrome. This review highlights some recent advances in the understanding of metabolic and molecular mechanisms concerning the effect of dietary PUFAs (fish oil) and focuses on the prevention and/or improvement of dyslipidemia, insulin resistance, impaired glucose homeostasis, diabetes and obesity in experimental animal models, with some extension to humans. D

Muscle growth mechanisms are controlled by different cellular and molecular pathways, and dietary supplemen-tation of nucleotides (NTs) may play an important role to influence such pathways in fish. In this study, we hypothesized that dietary supplementation of inosine monophosphate (IMP) would enhance cellular muscle growth, and upregulate growth-related gene expression in juvenile Nile tilapia Oreochromis niloticus. Five isonitrogenous (40% crude protein) and isocaloric (20.3 KJ/g diet) test diets were formulated by supplementing 0, 0.1, 0.2, 0.4 and 0.8% IMP in casein and fishmeal based semi-purified diet. Triplicate groups of juvenile Nile ti-lapia (0.59 ± 0.1 g) were stocked in 15 fiberglass tanks (150 L capacity), arranged in a simple biological filters-based closed system, with stocking density of 25 individuals per tank. The feed was applied at a daily feeding rate of 10% body weight (BW) initially and reduced to 5% BW finally for 60 days. Treatments results were compared using ANOVA (α = 0.05). At 60th day (60 D), final body weight of fish fed with 0.2–0.8% IMP were significantly higher than that of fish fed without IMP supplemented diet. At 60 D, both the hyperplastic (diameter class 10 = ≤10 μm) and hypertrophic (diameter class 60 = 50 N d ≤ 60 μm and class 70 = d N 60 μm) muscle fiber frequency were significantly higher in 0.2–0.8% IMP supplemented diets compared to 0–0.1% IMP supplemented diet. Two-way ANOVA result demonstrated that the pituitary GH, hepatic IGF-1 and GHR-1, and muscle-specific MyoD, myogenin and Pax7 gene expression were upregulated in fish fed with 0.2–0.8% IMP compared to the fish fed without IMP supplemented diet. However, hepatic IGF-2 and myostatin gene expression were not significantly affected by the dietary treatments. Real-time PCR data also demonstrated that myostatin gene expression was downregulated and all other gene expression were upregulated at the end of feeding trial (60 D) compared to the initial period (1 D). The results of the present study indicated that IMP supplementation enhanced the muscle growth by promoting hyperplasia and hypertrophy, and upregulating the growth-related gene expression in Nile tilapia. In conclusion, IMP is a potential feed additive and supplementation of ≥0.2% IMP is the most effective for enhancing growth of Nile Tilapia. Statement of relevance:-In most cases, fish growth was analyzed by calculating the increase in size or weight of fish. However, fish/mus-cle growth are controlled by different cellular and molecular pathways, which are poorly studied areas in aquaculture and nutritional studies. A research was conducted to investigate the effects of dietary supplementation of inosine monophosphate on: (1) cellular muscle growth characteristics, and (2) expression of major growth-related genes (GH, GHR-1, IGFs, MRFs, Pax7 and myostatin) in juvenile Nile tilapia. This research will help to understand the reason behind the improved growth or production of fish with a specific nutrient or diet.

Shea butter is the fat extracted from the nut of Africa Shea tree (Vitellaria paradoxa). It is used in cosmetic formulations and as a substitute for Cocoa butter in chocolate industries. It is edible and used cooking fat in Africa. The saponifiable fraction of Shea butter is composed primarily of stearic and oleic acids with lesser amounts of palmitic, linoleic and arachidic acids while the unsaponifiable fraction of Shea butter is composed of bioactive substances that are responsible for Shea butter’s medicinal properties. Shea butter is a solid at room temperature and melts at body temperature. It is therefore useful for skin care as it has sun screening properties and acts as an emollient and skin moisturizer. Topical use of Shea butter has also demonstrated anti-aging and anti-inflammatory properties. Dietary intake of Shea butter has hypocholesterolemic effect and reduces serum and organ protein concentrations.

Cereals are an important part of diets for hypercholesterolemic patients. However, some of these patients are allergic to these natural products. The purpose of the current study was to compare oatmeal with equal in nutritional values two allergy-free amaranth meals to determine whether this pseudocereal can be a substitute for allergic to cereals individuals. The total phenols of the samples were determined with the Folin-Chocalteu reagent, anthocyanins, and flavonoids spectrophotometrically. The antioxidant activities were estimated with nitric oxide scavenging radical (NO) and by ␤-carotene bleaching (␤-carotene). It was found that the contents of different protein fractions, antioxidant compounds, and the antioxidant activities of oatmeal were significantly higher than those of the two amaranth samples. The results of kinetic reactions showed that samples differed in their capacities to quench these radicals, and oats have shown more antioxidant activity than amaranth. High correlation was observed between antioxidant activities and phenols (R 2 ϭ 0.99). In the in vivo part of the investigation, 60 male Wistar rats were divided into five diet groups of 12 animals each; these groups were designated as Control, Chol, Chol/Oat, Chol/AmarI, and Chol/AmarII. The rats of the Control group were fed basal diet (BD) only. To the BD of the four other groups were added the following: 1% of cholesterol (Chol), 10% of oat meal and 1% of cholesterol (Chol/Oat), 10% of amaranth I meal, and 1% of cholesterol (Chol/AmarI) and 10% of amaranth II meal and 1% of cholesterol (Chol/AmarII). After 32 days of different feeding, diets supplemented with oat meal and, to lesser degree, with amaranth I and amaranth II hindered the rise in the plasma lipids: a) TC: 3.14 vs. 4.57 mmol/L, Ϫ 31.3%; 3.31 vs. 4.57 mmol/L Ϫ 27.6%; and 3.40 vs. 4.57, Ϫ 25.6%, respectively b) LDL-C: 1.69 vs. 3.31 mmol/L, Ϫ 49.9%; 2.05 vs. 3.31 mmol/L, Ϫ 38.1%; and 2.16 vs. 3.31 mmol/L, Ϫ 34.8%, respectively; c) TG: 0.73 vs. 0.88 mmol/L, Ϫ 17.1%; 0.75 vs. 0.88 mmol/L, Ϫ 14.8%; and 0.79 vs. 0.88 mmol/L, Ϫ10.2%, respectively. The HDL-PH was increased as follows: 0.79 vs. 0.63 mmol/L, Ϫ25.3%; 0.75 vs. 0.63 mmol/L, Ϫ23.0%; and 0.71 vs. 0.63 mmol/L, Ϫ12

Cereals are an important part of diets for hypercholesterolemic patients. However, some of these patients are allergic to these natural products. The purpose of the current study was to compare oatmeal with equal in nutritional values two allergy-free amaranth meals to determine whether this pseudocereal can be a substitute for allergic to cereals individuals. The total phenols of the samples were determined with the Folin-Chocalteu reagent, anthocyanins, and flavonoids spectrophotometrically. The antioxidant activities were estimated with nitric oxide scavenging radical (NO) and by ␤-carotene bleaching (␤-carotene). It was found that the contents of different protein fractions, antioxidant compounds, and the antioxidant activities of oatmeal were significantly higher than those of the two amaranth samples. The results of kinetic reactions showed that samples differed in their capacities to quench these radicals, and oats have shown more antioxidant activity than amaranth. High correlation was observed between antioxidant activities and phenols (R 2 ϭ 0.99). In the in vivo part of the investigation, 60 male Wistar rats were divided into five diet groups of 12 animals each; these groups were designated as Control, Chol, Chol/Oat, Chol/AmarI, and Chol/AmarII. The rats of the Control group were fed basal diet (BD) only. To the BD of the four other groups were added the following: 1% of cholesterol (Chol), 10% of oat meal and 1% of cholesterol (Chol/Oat), 10% of amaranth I meal, and 1% of cholesterol (Chol/AmarI) and 10% of amaranth II meal and 1% of cholesterol (Chol/AmarII). After 32 days of different feeding, diets supplemented with oat meal and, to lesser degree, with amaranth I and amaranth II hindered the rise in the plasma lipids: a) TC: 3.14 vs. 4.57 mmol/L, Ϫ 31.3%; 3.31 vs. 4.57 mmol/L Ϫ 27.6%; and 3.40 vs. 4.57, Ϫ 25.6%, respectively b) LDL-C: 1.69 vs. 3.31 mmol/L, Ϫ 49.9%; 2.05 vs. 3.31 mmol/L, Ϫ 38.1%; and 2.16 vs. 3.31 mmol/L, Ϫ 34.8%, respectively; c) TG: 0.73 vs. 0.88 mmol/L, Ϫ 17.1%; 0.75 vs. 0.88 mmol/L, Ϫ 14.8%; and 0.79 vs. 0.88 mmol/L, Ϫ10.2%, respectively. The HDL-PH was increased as follows: 0.79 vs. 0.63 mmol/L, Ϫ25.3%; 0.75 vs. 0.63 mmol/L, Ϫ23.0%; and 0.71 vs. 0.63 mmol/L, Ϫ12

The endothelium is involved in many of the processes related to the development of atherosclerosis, which is considered an inflammatory disease. Actually, traditional risk factors for atherosclerosis predispose to endothelial dysfunction, which is manifested as increase in the expression of specific cytokines and adhesion molecules. There is firm evidence supporting the beneficial effects of olive oil, as the most genuine component of the Mediterranean diet. Although the effects of olive oil and other oleic acid-rich dietary oils on atherosclerosis and plasma lipids are well-known, the roles of minor components have been less investigated. Minor components constitute only 1-2% of virgin olive oil and are comprised of hydrocarbons, polypohenols, tocopherols, sterols, triterpenoids, as well as other components usually found in traces. Despite their low concentration, non-fatty acid constituents may be of importance, since studies comparing monounsaturated dietary oils have reported different effects on cardiovascular disease. Most of these compounds have demonstrated antioxidant, anti-inflammatory and hypolipidemic properties. In the present review we summarize the current knowledge on the effects of these compounds contained in virgin olive oil on vascular dysfunction and the mechanisms by which they modulate endothelial activity. Such mechanisms involve the release of nitric oxide (NO), eicosanoids (protaglandins and leukotrienes) and adhesion molecules, in most cases by activation of nuclear factor κB (NFκB) by reactive oxygen species (ROS).

Human immunode~cien~y virus {HZV) infection and the deveIopment of AIDS facquired ~mmu~deficien~y syndrome) is beginning to be appreciated as a chronic, progressive disease. The impact of this disease on nutritional status is manifested most blatantly in the "wasting syndrome," but is seen in the vast majority of patients to a lesser extent. What is perhaps not as well recognized is the impact of malnutrition on the underlying immune competence of the individual and on the course of the HIV infection. The causes of malnutrition in this population are related to decreased nutrient intake, malabsorption, and altered metabolism in the setting of chronic HIV infection as well as intercurrent secondary infection. Management strategies for the treatment of malnutrition in patients with HIV infection should include, at a baseline, a high index of suspicion and early recognition of malnutrition. Processes underlying the development of ma&nutrition must be sought out and treated impossible. The goals of nutritional inte~ent~on should be to preserve lean body mass and provide adequate nutrients as well as to minimize symptoms of malabsorption and improve quali~ of life. options for specific nutritional therapy range from oral supplements to home TPN (total parenteral nutritt'on) and this must be individualized for each patient. (J. Nutr. Biochem. 6:2-l 1, 1995.)

Biomedical studies with animal models have demonstrated that cis-9, trans-11 conjugated linoleic acid (CLA), the predominant isomer found in milk fat from dairy cows, has anticarcinogenic effects. We recently demonstrated endogenous synthesis of cis-9, trans-11 CLA from ruminally derived trans-11 C18:1 by ⌬ 9 -desaturase in lactating dairy cows. The present study further examined endogenous synthesis of cis-9, trans-11 CLA and quantified its importance by increasing substrate supply using partially hydrogenated vegetable oil (PHVO) as a source of trans-11 C18:1 and blocking endogenous synthesis using sterculic oil (SO) as a source of cyclopropene fatty acids which specifically inhibit ⌬ 9 -desaturase. Four cows were abomasally infused with 1) control, 2) PHVO, 3) SO, and 4) PHVOϩSO in a 4 x 4 Latin square design. With infusion of PHVO, cis-9, trans-11 CLA was increased by 17% in milk fat. Consistent with inhibition of desaturase, SO treatments increased milk fat ratios for the fatty acid pairs effected by ⌬ 9 -desaturase, C14:0/cis-9 C14:1, C16:0/cis-9 C16:1, and C18:0/cis-9 C18:1. The role of endogenous synthesis of CLA was evident from the 60 -65% reduction in cis-9, trans-11 CLA which occurred in milk fat with SO treatments. cis-9 C14:1 originates from desaturation of C14:0 by ⌬ 9 -desaturase and can be used to estimate the extent of SO inhibition of ⌬ 9 -desaturase. When this correction factor was applied, endogenous synthesis was estimated to account for 78% of the total cis-9, trans-11 CLA in milk fat. Thus, endogenous synthesis was the major source of cis-9, trans-11 CLA in milk fat of lactating cows. The role of ⌬ 9 -desaturase in the production of cis-9, trans-11 CLA and other ⌬ 9 -desaturated fatty acids in milk fat.

The interrelationship between physical exercise, antioxidant supplementation, oxidative stress and plasma levels of homocysteine (Hcy) has not been adequately examined. The purpose of this study was to examine the effect of 2 months of vitamin E supplementation (800 IU/day alpha-tocopherol) (E) or placebo (P) in 38 triathletes on plasma Hcy concentrations, antioxidant potential and oxidative stress. It was hypothesized that vitamin E supplementation would reduce plasma Hcy and oxidative stress markers compared to placebo. Blood samples were collected 1 day prior to the race, immediately postrace and 1.5 h postrace. Plasma alpha-tocopherol was 75% higher ( P b.001) in E versus P prerace (24.1F1.1 and 13.8F1.1 Amol/L, respectively), and this group difference was maintained throughout the race. Cortisol was significantly increased in both E and P ( P b.001), but there was no difference in the pattern of change. There were no significant time, group or interaction effects on plasma Hcy concentrations between E and P. Plasma F 2 -isoprostanes increased 181% versus 97% during the race in E versus P, and lipid hydroperoxides were significantly elevated ( P = .009) 1.5 h postrace in E versus P. Plasma antioxidant potential was significantly higher 1.5 h postrace in E versus P ( P = .039). This study indicates that prolonged large doses of alpha-tocopherol supplementation did not affect plasma Hcy concentrations and exhibited pro-oxidant characteristics in highly trained athletes during exhaustive exercise. D

Strawberries are an important fruit in the Mediterranean diet because of their high content of essential nutrients and beneficial phytochemicals, which seem to exert beneficial effects in human health. Healthy volunteers were supplemented daily with 500 g of strawberries for 1 month. Plasma lipid profile, circulating and cellular markers of antioxidant status, oxidative stress and platelet function were evaluated at baseline, after 30 days of strawberry consumption and 15 days after the end of the study. A high concentration of vitamin C and anthocyanins was found in the fruits. Strawberry consumption beneficially influenced the lipid profile by significantly reducing total cholesterol, low-density lipoprotein cholesterol and triglycerides levels (−8.78%, −13.72% and −20.80%, respectively; Pb.05) compared with baseline period, while high-density lipoprotein cholesterol remained unchanged. Strawberry supplementation also significant decreased serum malondialdehyde, urinary 8-OHdG and isoprostanes levels (−31.40%, −29.67%, −27.90%, respectively; Pb.05). All the parameters returned to baseline values after the washout period. A significant increase in plasma total antioxidant capacity measured by both ferric reducing ability of plasma and oxygen radical absorbance capacity assays and vitamin C levels (+24.97%, +41.18%, +41.36%, respectively; Pb.05) was observed after strawberry consumption. Moreover, the spontaneous and oxidative hemolysis were significant reduced (−31.7% and −39.03%, respectively; Pb.05), compared to the baseline point, which remained stable after the washout period. Finally, strawberry intake significant decrease (Pb.05) the number of activated platelets, compared to both baseline and washout values. Strawberries consumption improves plasma lipids profile, biomarkers of antioxidant status, antihemolytic defenses and platelet function in healthy subjects, encouraging further evaluation on a population with higher cardiovascular disease risk.

Polyphenol Oxidase (PPO), a major enzyme responsible for manufacture of black tea from tea leaves (Camellia sinensis (L) O. Kuntze). Objective: To isolated and characterize the Polyphenol oxidase (PPO) enzyme from UPASI selected clone of Camellia sinensis (L.). PPO was purified via ammonium sulfate precipitation and gel filtration chromatography resulted in a recovery of 28.89% of total enzyme activity. Purified PPO was a monomeric protein of molecular weight 32 kDa. The most preferred substrate for PPO was catechin (10 mM) followed by catechol, caffeicacid, L-Dopa and pyrogallol. The K m and V max for PPO was1.22 mM ± 1.45 mM and 249.71 ± 1.86 U/ml/min using catechin as a substrate. Thermal stability of PPO was at 62°C. The enzyme activated monovalent cations namely, K + , and Na + . The most effective inhibitor was β -mercaptoethanol followed by EDTA and SDS. Activation energies were E (a) of PPO∆H* ( 1.3517 kJ mol -1 ), ∆G* ( 55402.96 kJ mol -1 ) and ∆S*(-185.82 J mol -1 K -1 ). Based on the results, this study can be concluded that the purified PPO showed greatest substrate specificity towards catechin (10 mM), high activity in the presence of K 2+ , Na 2+ and greatest inhibition with β-mercaptoethanol. Thus, isolated PPO enzyme from the selected clone of Camellia sinensis (L.) may be a potential source for pharmacology and functional food.

Polyphenols are wide variety of compounds that occur in fruits and vegetables, wine, tea, extra virgin olive oil, chocolate and other cocoa products. Several polyphenols have been demonstrated to have clear antioxidant properties in vitro, and many of their biological actions have been attributed to their intrinsic reducing capabilities. However, this concept appears now to be a simplistic way to conceive their activity. Evidence is indeed accumulating that polyphenols might exert several other specific biological effects that are as yet poorly understood. In this article we review the most recent data on the subject and describe the additional functions that polyphenols can have in biological systems, focusing on their effects on glutathione and its related enzymes. Experimental data indicate that polyphenols may offer an indirect protection by activating endogenous defense systems. Several lines of evidence suggest a tight connection between exogenous and endogenous antioxidants that appear to act in a coordinated fashion. It is reasonable to hypothesize that this is achieved, at least in part, through antioxidant responsive elements (AREs) present in the promoter regions of many of the genes inducible by oxidative and chemical stress. The latest studies strongly suggest that dietary polyphenols can stimulate antioxidant transcription and detoxification defense systems through ARE. D

We investigated the changes in adiposity, cardiovascular and liver structure and function, and tissue fatty acid compositions in response to oleic acid-rich macadamia oil, linoleic acid-rich safflower oil and α-linolenic acid-rich flaxseed oil (C18 unsaturated fatty acids) in rats fed either a diet high in simple sugars and mainly saturated fats or a diet high in polysaccharides (cornstarch) and low in fat. The fatty acids induced lipid redistribution away from the abdomen, more pronounced with increasing unsaturation; only oleic acid increased whole-body adiposity. Oleic acid decreased plasma total cholesterol without changing triglycerides and nonesterified fatty acids, whereas linoleic and α-linolenic acids decreased plasma triglycerides and nonesterified fatty acids but not cholesterol. α-Linolenic acid improved left ventricular structure and function, diastolic stiffness and systolic blood pressure. Neither oleic nor linoleic acid changed the left ventricular remodeling induced by high-carbohydrate, high-fat diet, but both induced dilation of the left ventricle and functional deterioration in low fat-diet-fed rats. α-Linolenic acid improved glucose tolerance, while oleic and linoleic acids increased basal plasma glucose concentrations. Oleic and α-linolenic acids, but not linoleic acid, normalized systolic blood pressure. Only oleic acid reduced plasma markers of liver damage. The C18 unsaturated fatty acids reduced trans fatty acids in the heart, liver and skeletal muscle with lowered stearoyl-CoA desaturase-1 activity index; linoleic and α-linolenic acids increased accumulation of their C22 elongated products. These results demonstrate different physiological and biochemical responses to primary C18 unsaturated fatty acids in a rat model of human metabolic syndrome.

Mercury is a heavy metal that exists naturally in the environment. Major sources include the burning of fossil fuels (especially coal) and municipal waste incineration. Mercury can exist in several forms, with the most hazardous being organic methylmercury. In waterways (lakes, rivers, reservoirs, etc.), mercury is converted to methylmercury, which then accumulates in fish, especially in large predatory fish. Fish and fish products are the major-if not the only-source of methylmercury in humans. Mercury has long been recognized as a neurotoxin for humans, but in the last 10 years, its potentially harmful effects on cardiovascular diseases (CVD) have raised a cause for concern, mostly due to the proposed role of mercury in oxidative stress propagation. Some epidemiological studies have indeed found an association between increased levels of mercury in the body and risk of CVD. There are several plausible mechanisms to explain the association; these are discussed in this review. We also review the epidemiological studies that have investigated the association between mercury and CVD. D

The correlation between decreased morbidity and mortality of cancer and exposure to sunlight is known. The many biological functions of vitamin D that contribute to cancer prevention have only recently begun to be appreciated. Once activated 1,25-dihydroxyvitamin D [1,25(OH) 2 D 3 ] functions as a potent inhibitor of normal and cancer cellular proliferation. Vitamin D deficiency in mice led to a 60% increase in colon tumor growth, compared to vitamin D-sufficient mice. The ligand binding domain of the Vitamin D receptor was shown to accommodate a class of 1,25(OH) 2 D 3 -analogs that possess an additional side-arm. These novel Gemini analogs were evaluated in vitro and in vivo. Select Gemini analogs were 100 times or more effective in inhibiting colon tumor growth in mice, compared to their parent compound. Correcting vitamin D deficiency may decrease the risk of developing colon cancer, while the novel Gemini 1,25(OH) 2 D 3 -analogs have the potential for therapeutic application in human colon cancer.

In spite of the wide literature describing the biological effects of phenolic compounds, scarce data are available on their absorption from diet. In the present work, we studied the absorption in humans of phenolic acids from beer, a common beverage rich in different phenolic acids with related chemical structures. Beer was analyzed for free and total (free+bound) phenolic acids. Ferulic, caffeic and sinapic acids were present in beer mainly as bound forms, while 4-hydroxyphenylacetic acid and p-coumaric acid were present mainly as free forms. Vanillic acid was present equally in the free and bound forms. Plasma samples were collected before and 30 and 60 min after beer administration and analyzed for free and conjugated phenolic acid content. A significant two-to fourfold increase in plasma levels of phenolic acids was detected with peak concentrations at 30 min after beer ingestion. 4-Hydroxyphenylacetic acid was present in plasma mainly as nonconjugated forms while p-coumaric acid was present equally as nonconjugated and conjugated forms. Ferulic, vanillic and caffeic acids were present in plasma predominantly as conjugated forms, with a slight prevalence of sulfates with respect to glucuronates. Our results indicate that phenolic acids from beer are absorbed from the gastrointestinal tract and are present in blood after being largely metabolized to the form of glucuronide and sulfate conjugates. The extent of conjugation is related to the chemical structure of phenolic acids: the monohydroxy derivatives showing the lowest conjugation degree and the dihydroxy derivatives showing the highest one.