فهرست مطالب حمید زند

Fibroblast growth factor-21 (FGF-21) is a potent activator of glucose uptake associated with insulin resistance, metabolic syndrome and obesity. The aim of this study was to assess relationships between the anthropometric parameters, body composition, and FGF-21 gene expression in peripheral blood mononuclear cells in healthy young adults.

This cross-sectional analytical study included 30 healthy young adults from Shahid Beheshti University of Medical Sciences, 1401. The FGF-21 gene expression in peripheral blood mononuclear cells was assessed using real-time polymerase chain reaction technique. Body composition was assessed using bioelectrical impedance analysis. Linear regression was used to assess relationships of anthropometric and body composition parameters with the gene expression.

The median (interquartile range) age and body mass indices of the participants were 22 (21–26) years and 23.3 (21.25–3.6) kg/m2, respectively. Significant inverse relationships were detected between FGF-21 ΔCT in peripheral blood mononuclear cells and body mass index (β = -0.516), waist-to-hip ratio (β = -0.477), total fat mass (β = -0.412) and visceral fat (β = -0.514) (p < 0.05). This indicated that higher values of these variables were associated to the increased FGF-21 gene expression. No significant relationships were observed between the muscle mass and FGF-21 gene expression.

Results of this study demonstrated significant positive associations between the FGF-21 gene expression in peripheral blood mononuclear cells and the body composition, waist-to-hip ratio, fat mass and visceral fat in healthy young individuals. Further studies are warranted to verify alignment of FGF-21 gene expression in peripheral blood mononuclear cells, as easily accessible human cells, with serum levels.

Senescence is linked to increases in oxidative stress and free radicals, which can potentially damage DNA. Furthermore, obesity is known to exacerbate these factors. In contrast, antioxidants may postpone tissue aging, including adipose tissues, by fighting with free radicals. To investigate this link, this study was carried out to assess associations between dietary antioxidant intake and visceral adipose tissue aging in obese adults.

A case-control study was carried out at Shahada Tajrish Hospital, Tehran, Iran, with 20 candidates of bariatric surgery and 20 adults of normal weight. The study assessed activity of beta-galactosidase in visceral adipose tissues. Assessment of dietary antioxidants was carried out using food frequency questionnaires.

Study indicated significant adverse correlations of the daily consumption of vitamin C and selenium with beta-galactosidase activity in visceral fat tissues of case group (p = 0.039 and p = 0.028, respectively). In the control group, significant adverse relationships were observed between the daily intake of vitamin C (p = 0.001), lycopene (p = 0.027), selenium (p = 0.037) and magnesium (p = 0.002) and beta-galactosidase activity in visceral fat tissues. Moreover, individuals with high beta-galactosidase enzyme activity in visceral fat tissues had a significantly lower daily intake of vitamin E (p = 0.046), vitamin C (p < 0.001), lycopene (p = 0.030), selenium (p = 0.035) and magnesium (p = 0.01), compared to those with low beta-galactosidase enzyme activity in visceral fat tissues.

Consuming diets high in antioxidants has been linked to decreased cellular senescence in the visceral adipose tissues of obese adults. To further investigate this relationship, studies including a variety of senescence markers are recommended.

such as the process of cellular respiration, which is scavenged by enzymatic and non-enzymatic antioxidant systems. Intake of antioxidants from food sources has always been considered in nutrition research. Therefore, the aim of the present study was to investigate antioxidant effects of crocin on the expression profile of genes involved in the enzymatic antioxidant systems in muscle cells.

After culturing and several passages, C2C12 muscle cells were differentiated into myotube cells and treated with various concentrations of crocin (10, 25, 50 and 100 μM) for 24 h. Gene expression of antioxidant enzymes (SOD1, SOD2, Gpx1 and catalase) was assessed using real-time polymerase chain reaction.

Crocin significantly decreased expression of SOD2, Gpx1 and catalase genes (p <0.05) with no effects on expression of SOD1 gene.

Findings of this study showed that receiving exogenous antioxidants such as crocin could possibly decrease needs of expression of enzymatic antioxidant genes through strengthening non-enzymatic antioxidant defense systems. However, further studies are needed to verify the results.

Embryonic cancers are very rare. However, the exact components preventing cancer development or progression in embryonic microenvironment are largely unknown. On the other hand, cancer stem cells with characteristics similar to embryonic stem cells are involved in cancer progression and resistance to treatment. The aim of this study was to investigate effects of unfertilized egg white, as an embryonic microenvironment model, on proliferation, self-renewal, stemness and migration of SW480 colon cancer cells and 5-fluorouracil (5FU) resistant subgroup.

In brief, SW480 and 5FU-SW480 cells were exposed to 10% (v/v) egg white. To assess viability, self-renewal and stemness characteristics and migratory capacity of the colon cancer cells, MTT, flow PI staining and flow cytometry, colony formation, spheroid and wound healing assays were used, respectively. Furthermore, expression levels of c-Myc, Nanog, Ndrg1 and E-cadherin genes were quantified using real-time polymerase chain reaction.

Findings showed that 10% volume of unfertilized egg white significantly decreased cell survival, inhibited cell cycle in G0/G1, decreased colony formation and sphere formation and inhibited migration ability in the two cell groups, compared to the control. Moreover, expression of c-Myc and Nanog decreased while expression of Ndrg1 and E-cadherin increased in SW480 cells. However, c-Myc gene expression increased in 5FU-SW480 with decreases in expression of Nanog and Ndrg1.

It seems that unfertilized egg white includes various mechanisms to control cancer development and progression. Further studies are needed to identify actual components affecting stemness and invasiveness of tumor cells, specifically cancer stem cells.

Cellular senescence has been known as a tumor suppressor mechanism; however, some evidence shows that cellular senescence is an inducer factor for metabolic disorders, such as insulin resistance and diabetes. In this study, the effect of senescence was assayed in the peripheral tissues of diet-induced obese rats. 30 male 5-week old wistar rats were randomly assigned into high-calorie diet through 416 kcal/100 g (researcher made) or control diet for 12 weeks. Weight changes, lipid profile, glucose, insulin levels and QUICKI (Quantitative Insulin Sensitivity Check Index) index were measured at the end of the 12th week. Also the tissue samples were isolated, and immune-blotting was performed to identify proteins P16INK4a and P53 (cell senescence markers). P53 levels in the fat tissue and other peripheral tissues of obese rats were significantly higher compared to the control group. P16INK4a expression was increased only in fat tissue but protein was not expressed in other tissues. In the obese rats, the serum levels of glucose (183/60±34/90 vs. 152/40±15/48 P=0.019), cholesterol (60/70±6/88 vs.46/60±7/82 P<0.001) and triglyceride (124/60±46/43 vs. 57/20±24/02 P<0.001) were more than in the control group but The QUICKI index was significantly lower in the obese rats compared to the control group (p=0.01). Our results suggest that cell senescence in fat tissue can be predisposed to the development of insulin resistance and age-related diseases by generating some alternation in the fat tissue.

Resveratrol is a natural phytoalexin found in certain plants, such as red grapes. Several studies confirm the beneficial effects of resveratrol on the cardiovascular system. Similar to many other polyphenols, resveratrol initiates the intracellular pathways which are activated under energy constraints. This review aimed to investigate the effects of resveratrol on the cardiovascular health, focusing on the associated cellular and molecular mechanisms. In this study, we searched for English and Persian articles in PubMed and SID databases using keywords such as resveratrol, nitric oxide (NO), endothelial, cardiovascular diseases, oxidative stress, vascular inflammation, cardiac protection and polyphenol. Related articles were mostly published during 2002-2013. The initial survey of 72 collected articles indicated that resveratrol is able to neutralize oxidative species and activate Nrf2 while minimizing antioxidant damage. In addition, this compound enhances vascular function through increasing the production and bioavailability of NO in blood vessels via the stimulation of estrogen receptors. On the other hand, resveratrol, similar to calorie restriction, activates SIRT1 which is an NAD-dependent deacetylase. In addition, resveratrol exerts anti-inflammatory effects on blood vessels through NF-кB and inhibits platelet aggregation using NO. Resveratrol also provides cardiac protection against reperfusion injuries and is able to slow down the process of aortic and cardiac hypertrophy resulting in hypotension. Resveratrol affects endothelial function, oxidative stress, vascular inflammation, platelet aggregation, hypertension, atherosclerosis and cardiac hypertrophy through a variety of mechanisms.

Eating disorders are complex and multi- faceted and is very sensitive to the social and cultural pressures and their treatment challenges the doctors and the medical team. It is more than half a century that various branches of science theories about the disorder and discusses the factors that influence it. This is a common thing in all these theories that nutrition is associated with psychological problems. Today, issues such as nutrition and its relationship with the individual's attitude to the world, and future desired and may lead to problems in eating and nutrition. Patients with anorexia nervosa manifest weight loss, fear of becoming fat, and disturbances in how they experience their body weight and shape. Patients with bulimia nervosa present with recurrent episodes of binge eating and inappropriate methods of weight control such as self- induced vomiting, and abuse of diuretics and laxatives. Major complications of eating disorders include severe fluid and electrolyte disturbances and cardiac arrhythmias. Individual and family psychotherapy are effective in patients with anorexia nervosa and cognitive- behavioral therapy is effective in bulimia nervosa. Pharmacotherapy is not universally effective by itself. Nutritionist plays an important role in the management of medical and nutritional complications for patients and families, and therefore needs proper knowledge of the methods of treatment and management of complications.

The immunological processes involved in the collaborative defence of organisms are affected by nutritional status. Thus, a positive chronic imbalance between energy intake and expenditure leads to situations of obesity, which may influenceunspecific and specific immune responses. the incidence and severity of specific types of infectious illnesses are higher in obese persons as compared to lean individuals, as well as poor antibody responses to vaccinations in overweight subjects. leptin may act as a link between the nutritional status and T cell function. Moreover, there is evidence that hyperleptinaemia induced by cytokines is an integral part of the acute phase response. Leptin deficiency in animal studies associated with a lower phagocyte activity، lymphopenia, lower lymphocyte and NK cell numbers as well as decreased cytotoxic activity. In human studies have been showed delayed cutaneous hypersensitivity, abnormal lymphoproliferative responses to mitogens and a reduction in intracellular bacterial killing capacity. obesity diminishes the immune response, but the mechanisms implicated in this process remain unclear. Obesity are associated with impaired immunity. Several factors, including nutritional, metabolic and endocrine, seem to be involved. There is evidence that obesity alters several functions of the immune defense mechanisms and thus, increases susceptibility to infections, diabetes and cancer development among other chronic diseases. Further research in this interesting area would be of help in predicting obesity-prone populations and so, development of prevention strategies and new pharmacological therapies.

Adipose tissue macrophages (ATMs) infiltrate adipose tissue during obesity and contribute to insulin resistance. This adipose tissue inflammation is characterized by changes in immune cell populations giving rise to alteredadipo/cytokine profiles andis perpetuated through chemokine secretion,adipose retention of macrophages, and elaboration of pro- inflammatory adipocytokines.Activation of various kinases modulates adipocyte transcription factors, including peroxisome proliferator- activated receptor- PPAR-  and NFkB, attenuating insulin signaling and increasingadipocytokine and free fatty acid secretion. Adipose inflammatory events induce a local and systemic inflammatory response, that can result in development of the metabolic syndrome, type 2 diabetes mellitus, and atherosclerotic cardiovascular disease (CVD). The sources of cytokines in insulin resistant states are the insulin target tissue themselves, primarily fat and liver, but to a larger extent the activated tissue resident macrophages. Chronic inflammation in these tissues could cause localized insulin resistance via autocrine/paracrine cytokine signaling and systemic insulin resistance via endocrine cytokine signaling all of which contribute to the abnormal metabolic state.

An ergogenic aid is any training technique, mechanical device, nutritional practice, pharmacological method, or psychological technique that can improve exercise performance capacity and/or enhance training adaptations. This includes aids that may help prepare an individual to exercise, improve the efficiency of exercise, and/or enhance recovery from exercise. Ergogenic aids may also allow an individual to tolerate heavy training to a greater degree by helping them recover faster or help them stay healthy during intense training. Research has clearly shown that athletes that do not ingest enough calories and/or do not consume enough of the right type of macronutrients may impede training adaptations while athletes who consume a good diet can help the body adapt to training. Moreover, maintaining an energy deficient diet during training may lead to loss of muscle mass, increased susceptibility to illness, and increase prevalence of overreaching and/or overtraining. The purpose of this review is to examine the usefulness of the commercially available supplements used for weight loss and Performance Enhancement according to the International Society of Sport position categorized them to four distinct category: Apparently Effective, Possibly Effective, Too Early To Tell and Apparently Ineffective to separate myth from scientific documentation.

Risk for heart disease, diabetes, and stroke increases with the number of the metabolic risk factors. In general, a person who has the metabolic syndrome is twice as likely to develop heart disease and five times as likely to develop diabetes as someone who does not have the metabolic syndrome. High-calorie-diet rodent models have contributed significantly to the analysis of the pathophysiology of the metabolic syndrome, but their phenotype varies distinctly between different studies and maybe is not very similar to a model of the metabolic syndrome in humans. We sought to create a model in this study close to the disease in humans.

Twenty male, Wistar rats were randomly assigned to the high-calorie diet group with 416 calories per 100 grams (researcher made) or the control diet group for 12 weeks. Weight changes, lipid profile, glucose, insulin levels, and QUICKI index (an indicator of insulin sensitivity) were measured. Weight changes were compared using the repeated measures and the independent t-test, and serum factors were compared using the independent t-test.

There was a significant change in weight, glucose, insulin, and lipid profile except for HDL at the end of the study. The QUICKI index (0.34 ± 0.02 vs. 0.40 ± 0.01; p value <0.0001) suggested that insulin resistance had been created in the high-calorie diet group.

The present study demonstrates the ability to make diet-induced metabolic syndrome domestically.