Development Of Visceral Obesity Research Articles

Mitochondrial dysfunction of the inner membrane of hepatocytes in the development of glutamate-induced steatohepatosis and its correction

Elucidation of the mechanisms of the development of liver steatosis, which are at the heart of the pathogenesis of nonalcoholic fatty liver disease (NAFLD), will allow the introduction of new effective treatment methods into medical practice, as well as the development of new measures for the correction of this disease and accompanying pathologies. The purpose of the research is to establish the enzymatic activity of the complexes of the electron transport chain of the mitochondrial membrane of rat hepatocytes and to evaluate the corrective effect of the multiprobiotic “Symbiter acidophilic” concentrated or nanocrystalline cerium dioxide on the formation of steatohepatosis induced by neonatal sodium glutamate administration. The experiments were carried out on 50 white non-linear male rats; the direction included the study of the mechanisms of the development of steatohepatosis in 4-month-old rats, which were administered monosodium glutamate in the neonatal period, and the study of the functional state of the liver in rats after the neonatal administration of monosodium glutamate against the background of periodic administration of a multiprobiotic or nanocrystalline dioxide cerium. It was established that neonatal administration of monosodium glutamate causes metabolic changes in 4-month-old rats, manifested in the disproportionate accumulation of fat with the development of visceral obesity without hyperphagia, dyslipidemia, and steatohepatosis. In 4-month-old rats, after neonatal administration of sodium glutamate, the development of steatohepatosis was accompanied by mitochondrial dysfunction, which was manifested by changes in the lipid composition of the inner membrane of hepatocyte mitochondria with an increase in oxidized products and a change in the enzymatic activity of all complexes of the respiratory chain. In rats injected with monosodium glutamate in the neonatal period, periodic use of the multiprobiotic “Symbiter acidophilic” concentrated or nanocrystalline cerium dioxide significantly restored the functional state of the liver, reduced the manifestations of oxidative stress and prevented the development of steatohepatosis, which indicates the antioxidant effect of these drugs and the possibility of their use for prevention of steatohepatosis.

Development of Metabolic Disorders, Structural–Functional Changes of the Liver and Pancreas Against the Background of a High Calorie Carbohydrate and Fat Diets

Obesity becoms one of the most common pathologies, which is accompanied by a violation of energy metabolism in the body, increased accumulation of fat in tissues. The development of visceral obesity can develop against the background of a high calorie diet that is unbalanced in terms of carbohydrates and fats.
 The aim of the research: study of the hormonal-metabolic profile, structural-functional peculiarities of the liver and pancreas under the conditions of animals’ receiving high-carbohydrate or high-fat diets in dynamics.
 Research methods. The study was performed using sexually mature male rats receiving a standard food diet (control group) and received the high-carbohydrate or high-fat diets. Animals were removed out of the experiment during the 21st, 35th, 46th and 56th days of the study. Metabolic indices and functional markers of the hepatopancreatobiliary system were determined in the blood serum of experimental rats. Structural peculiarities of the liver and pancreas were studied using optical microscopy.
 Results and discussion. As a result of the study, in animals that were on high calorie diet, a significant increase in the content of leptin and insulin was observed against the background of a decrease in the level of ghrelin in the blood serum of experimental rats during the 35th day of the experiment with the progression of the identified dyshormonal disorders until the 56th day. Such changes in the hormonal profile occurred against the background of an increase in the concentration of glucose in the blood serum, an increase in the content of glycosylated hemoglobin (HbA1c), an increase in the HOMA-IR insulin resistance index and body mass index (BMI). During the 21st day of the research, the activation of cytolytic processes (increased activity of alanine aminotransferase – ALT, aspartate aminotransferase – AST, gamma-glutamyl transpeptidase – GGT, α-amylase, alkaline phosphatase – AF) was revealed; they progressed until the end of the experiment. During the morphological examination of the liver and pancreas in animals under the conditions of a high-fat diet, pronounced fatty infiltration was observed. In the pancreas of animals receiving the high calorie diet, morphological changes are manifested by edematous processes and disruption of the vascular component, with greater dominance in the case of a high-fat diet.
 Conclusions. The animals’ being on high-carbohydrate and high-fat diets leads to the development of metabolic disorders, functional and structural changes in the liver and pancreas, which characterize the development of insulin resistance, obesity, and metabolic syndrome.

Angiotensin II type 1 receptor-associated protein in immune cells: a possible key factor in the pathogenesis of visceral obesity

Background and aimDysregulation of angiotensin II type 1 receptor-associated protein (ATRAP) expression in cardiovascular, kidney, and adipose tissues is involved in the pathology of hypertension, cardiac hypertrophy, atherosclerosis, kidney injury, and metabolic disorders. Furthermore, ATRAP is highly expressed in bone marrow-derived immune cells; however, the functional role of immune cell ATRAP in obesity-related pathology remains unclear. Thus, we sought to identify the pathophysiological significance of immune cell ATRAP in the development of visceral obesity and obesity-related metabolic disorders using a mouse model of diet-induced obesity. MethodsInitially, we examined the effect of high-fat diet (HFD)-induced obesity on the expression of immune cell ATRAP in wild-type mice. Subsequently, we conducted bone marrow transplantation to generate two types of chimeric mice: bone marrow wild-type chimeric (BM-WT) and bone marrow ATRAP knockout chimeric (BM-KO) mice. These chimeric mice were provided an HFD to induce visceral obesity, and then the effects of immune cell ATRAP deficiency on physiological parameters and adipose tissue in the chimeric mice were investigated. ResultsIn wild-type mice, body weight increase by HFD was associated with increased expression of immune cell ATRAP. In the bone marrow transplantation experiments, BM-KO mice exhibited amelioration of HFD-induced weight gain and visceral fat expansion with small adipocytes compared BM-WT mice. In addition, BM-KO mice on the HFD showed significant improvements in white adipose tissue metabolism, inflammation, glucose tolerance, and insulin resistance, compared with BM-WT mice on the HFD. Detailed analysis of white adipose tissue revealed significant suppression of HFD-induced activation of transforming growth factor-beta signaling, a key contributor to visceral obesity, via amelioration of CD206+ macrophage accumulation in the adipose tissue of BM-KO mice. This finding suggests a relevant mechanism for the anti-obesity phenotype in BM-KO mice on the HFD. Finally, transcriptome analysis of monocytes indicated the possibility of genetic changes, such as the enhancement of interferon-γ response at the monocyte level, affecting macrophage differentiation in BM-KO mice. ConclusionCollectively, our results indicate that ATRAP in bone marrow-derived immune cells plays a role in the pathogenesis of visceral obesity. The regulation of ATRAP expression in immune cells may be a key factor against visceral adipose obesity with metabolic disorders.

Using amplitude-phase parameters of circadian rhythms as diagnostic markers of carbohydrate metabolism disorders

BACKGROUND: With the development of visceral obesity, against the background of insulin resistance (IR), lipo- and glucose toxicity in tissues progresses, which disrupts the metabolic balance of the body, and is the main factor in the development of type 2 diabetes mellitus (DM2). To date, a growing number of publications highlighting the role of circadian rhythms in the control of gluconeogenesis and lipogenesis. In the context of the development of DM2, the process of rhythm mismatch (desynchronosis) is increasingly mentioned, for the diagnosis of which the calculation of amplitude-phase parameters is used. Thus, the study of circadian rhythm disturbances using amplitude-phase parameters and factors influencing them is of particular interest in individuals with visceral obesity and prediabetes, since the data obtained can be used as markers for preclinical diagnosis of DM2.AIM: To identify significant differences in the parameters (amplitude, acrophase) of circadian rhythms (fasting glycemia, basal body temperature, heart rate) as markers of desynchronosis in groups without carbohydrate metabolism disorders, but with the presence of visceral obesity, prediabetes (impaired fasting glycemia, impaired glucose tolerance test) and DM2 and obesity.MATERIALS AND METHODS: The study was conducted in individuals with visceral obesity, as well as the presence of prediabetes or DM2, with a disease experience of not more than 5 years.In accordance with the study design, every 3 hours during the day, the participants made self-measurements of blood glucose at home (using individual glucometers), basal body temperature (BTT) in the armpit (using a mercury thermometer) and heart rate (HR) ( with the help of an electronic tonometer), with the fixation of the results in self-control diaries. To assess the reliability of the circadian rhythms of the studied indicators, the interpretation of chronobiological parameters (MESORa-Midline Estimating Statistic of Rhytm; amplitude; acrophase) was carried out using a single сosinor analysis.RESULTS: Of the 120 study participants, 73% were women and 27% were men. Mean age of participants was 58.6[52.2;56.7] years, BMI 31.3[29.7;33.9] and presence of visceral obesity WC 100 [93.8;104.7]. When conducting cosinor analysis, the daily rhythms of physiological indicators of fasting glycemia, BTT and heart rate differ from normal already in the group with visceral obesity without carbohydrate metabolism disorders and prediabetes, in the form of a decrease in the amplitude of daily rhythms (p<0.001), with a shift in their acrophases (p <0.001), no dynamics of night BBT decrease (р<0.001).CONCLUSION: Integral amplitude-phase parameters of circadian rhythms of physiological parameters (fasting glycemia, basal body temperature, heart rate), as markers of desynchronosis, can be used in the presence of visceral obesity for preclinical diagnosis of prediabetes and DM2, which will have a preventive focus. This method of chronodiagnostics can be useful in health and prevention centers for people at risk of developing DM2.

Beta-3-adrenergic Receptor rs4994 Polymorphism Is a Potential Biomarker for the Development of Nonalcoholic Fatty Liver Disease in Overweight/Obese Individuals.

Nonalcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic liver diseases. Obesity is the most common and well-established risk factor for NAFLD, but there are large interindividual differences in the relationship between weight status and the development of NAFLD. Beta-3-adrenergic receptor (ADRB3) plays a key role in the development of visceral obesity and insulin resistance; however, the effect of ADRB3 polymorphisms on the risk of NAFLD remains unclear. We investigated whether or not a common rs4994 polymorphism (T190C) in the ADRB3 gene is associated with the risk of NAFLD through an increase in the body mass index (BMI) among the general population. We performed cross-sectional and longitudinal analyses in a total of 591 Japanese health screening program participants. Among the overweight or obese subjects, but not normal-weight subjects, individuals with the C/C genotype had a higher risk of developing NAFLD in comparison to those with other genotypes in the cross-sectional analysis (odds ratio: 4.40, 95% confidence interval (CI): 1.08–17.93). Meanwhile, the receiver operating characteristic curve indicated that the association between an increase in the BMI and the presence of NAFLD in subjects with the C/C genotype (area under the curve: 0.91, 95% CI: 0.78–1.00) was more pronounced in comparison to subjects with other genotypes. These above-described findings were verified by the analyses using a replicated data set consisting of 5,000 random samples from original data sets. Furthermore, among the 291 subjects for whom longitudinal medical information could be collected and who did not have NAFLD at baseline, the Cox proportional hazard model also confirmed that overweight or obese status and the C/C genotype were concertedly related to the increased risk of NAFLD development. These results suggest that genotyping the ADRB3 rs4994 polymorphism may provide useful information supporting the development of personalized BMI-based preventive measures against NAFLD.

2031-P: Adipose-Specific Lack of Hexose-6-Phosphate Dehydrogenase Causes Inactivation of Adipose Glucocorticoids and Improves Metabolic Phenotype in Male Mice

Excessive glucocorticoids (GCs) production in adipose tissue promotes the development of visceral obesity and the metabolic syndrome. 11β-Hydroxysteroid dehydrogenase type 1 (11 β-HSD1) is critical for controlling intracellular GC production in adipose tissue, and this process is also regulated by hexose-6-phosphate dehydrogenase (H6PDH) that provides cofactor NADPH for 11β-HSD1 amplifying local GC production. To better understand the integrated molecular and physiological role of adipose H6PDH, we created a tissue specific knockout of H6PDH gene mouse model in adipocytes (H6PDHAcKO mice) and characterized the metabolic related phenotypes. H6PDHAcKO mice had decreased levels of intra-adipose corticosterone with reduction of 11β-HSD1 activity in response to H6PDH deletion in adipose tissue. Moreover, H6PDHAcKO mice also exhibited reduced fasting blood glucose levels and increased glucose tolerance with increased insulin sensitivity. In addition, plasma FFA levels were decreased with a concomitant decrease in the expression of lipase ATGL and HSL in the abdominal adipose tissue. These results indicate that inactivation of H6PDH expression in adipose tissue is sufficient to cause intra-adipose GC inactivation leading to the favorable pattern of metabolic phenotype. These data suggest that H6PDHAcKO mice may provide a good model for study the potential contributions of fat-specific H6PDH inhibition in the metabolic phenotype and other pathological disorders in vivo. Disclosure J. Wang: None. X. Wang: None. K. Lutfy: None. T. Friedman: None. M. Jiang: None. Y. Liu: None. Funding National Institute of Diabetes and Digestive and Kidney Diseases (SC1DK104821)

Endocannabinoid Signalling in Atherosclerosis and Related Metabolic Complications.

Endocannabinoids are a group of arachidonic acid-derived lipid mediators binding to cannabinoid receptors CB1 and CB2. An overactivity of the endocannabinoid system plays a pathophysiological role in the development of visceral obesity and insulin resistance. Moreover, elevated circulating endocannabinoid levels are also prevalent in atherosclerosis. The pathophysiological increase of endocannabinoid levels is due to an altered expression of endocannabinoid synthesizing and degrading enzymes induced by inflammatory mediators such as cytokines or lipids. Emerging experimental evidence suggests that enhanced endocannabinoid signalling affects atherosclerosis via multiple effects, including a modulation of vascular inflammation, leukocyte recruitment, macrophage cholesterol metabolism and consequently atherosclerotic plaque stability. In addition, recent findings in various metabolic disease models highlight the relevance of peripheral CB1 cannabinoid receptors in adipose tissue, liver and pancreas, which crucially regulate lipid and glucose metabolism as well as macrophage properties in these organs. This suggests that targeting the endocannabinoid system in the vasculature and peripheral organs might have a therapeutic potential for atherosclerosis by inhibiting vascular inflammation and improving metabolic risk factors. This review will provide a brief update on the effects of endocannabinoid signalling in atherosclerosis and related metabolic complications.

Morphophenotypic predictor of the development of visceral obesity in patients with schizophrenia receiving antipsychotic therapy

Objective:revealing the role of morphophenotypic indices in the development of visceral obesity in patients with schizophrenia receiving quetiapine and risperidone therapy.Materials and methods.56 indoor patients with schizophrenia who received quetiapine (n= 23) or risperidone (n= 33) at medium doses were examined. Included persons were from 18 to 65 years old with at least a 1 year history of disease, the condition of which met the criteria of schizophrenia according to ICD-10. The Basis map of sociodemographic and clinical-dynamic signs for patients with schizophrenia was filled in, PANSS in the adapted Russian version – SCI-PANSS, noninvasive bioimpedancemetry, measurement of growth, transversethoracic, biacromial and bicrystal diameter, with calculation of body mass indexes, Tanner and Rees – Eysenk and definition of integral morphophenotypic indicators were carried out. Statistical processing was performed using Student’s t-test with a preliminary estimate of Pearson’s χ2 normal distribution, the Mann – Whitney U test to compare independent samples, the Spearman correlation analysis, the two-sided Fisher test.Results.There were no significant differences in both subgroups in terms of bioimpedancemetry. The correlation between the level of visceral fat and the Rees – Eysenk index in patients receiving risperidone was a moderate inverse: the greater the value of the Rees – Eysenk index, the lower the level of visceral fat (r= –0.73381,t= –4.70833,p= 0.00015). The correlation between the Tanner index and the level of visceral fat in the quetiapine subgroup was strong: the larger the Tanner index, the higher the visceral fat level (r= 0.7763,t= 4.08481,p= 0.00181); in the risperidone subgroup, there was an average direct correlation (r= 0.48133,t= 2.39356,p= 0.02716).Conclusion.The magnitude of the Rees – Eysenk index of schizophrenic patients can be considered among other factors in the management of risperidone in individuals with asthenic physique. The determination of the Tanner index at the beginning of treatment can play the role of a prognostic factor in the development of visceral obesity in patients with schizophrenia in the planned use as a basic therapy for quetiapine.

Abstract P467: Urocortin 2 Levels and Metabolic Profile in Patients With Primary Hypertension

Objective: Urocortin 2 (UCN 2) has powerful hemodynamic and neurohormonal actions. Some recent studies suggest that ucn2 may also decrease the steroid production. The aim of this study was to assess the relationship between the serum concentration of UCN 2 and metabolic parameters in patients with primary hypertension. Methods: We examined 65 participants with essential hypertension treated with at least 3 antihypertensive medications. The evaluation included anthropometric measurements (BMI, WHR) and ambulatory blood pressure monitoring (ABPM). Moreover we evaluated metabolic parameters in blood serum: glucose, total cholesterol , low-density cholesterol (LDL-C), high density cholesterol (HDL-C), triglycerides (TG), HbA1c, insulin, cortisol, hsCRP. For the analysis of UCN 2 serum level we used ELISA Kit. We divided the surveyed subjects into two groups according to the urocortin’s median value. The comparative analyses between the groups were based on the student’s T-test, U Mann-Whitney and Chi 2 . To examine the relationships between selected parameters we used Pearson and Spearman correlations. Conclusion: Subjects with higher level of UCN 2 have lower concentration of total cholesterol and LDL-C, however changes in UCN 2 concentration were not associated with others metabolic parameters. Ucn2 may play a protective role in cardiovascular morbidity through reduction of cholesterol synthesis and development of visceral obesity in patients with arterial hypertension.

Teneligliptin improves metabolic abnormalities in a mouse model of postmenopausal obesity.

A decrease in serum estrogen levels in menopause is closely associated with the development of visceral obesity and the onset of type 2 diabetes in women. In the present study, we demonstrated the therapeutic effects of the novel DPP4 inhibitor, teneligliptin, on the features of postmenopausal obesity in mice. In the control group, female C57BL/6 mice were sham-operated and maintained on a standard diet. In the postmenopausal obese group, ovariectomized (OVX) mice were maintained on a high-fat diet, and were referred to as OVX-HF. In the treated group, teneligliptin at 60 mg/kg per day was administrated to OVX-HF, and were referred to as Tene. After a 12-week food challenge, the metabolic phenotypes of these mice were analyzed. Body weight, fat accumulation, and glucose intolerance were greater in OVX-HF than in control, while these abnormalities were markedly improved without alterations in calorie intake in Tene. Teneligliptin effectively ameliorated the characteristics of metabolic abnormalities associated with postmenopausal obesity. Regarding chronic inflammation in visceral adipose tissue, the numbers of F4/80(+)CD11c(+)CD206(-) M1-macrophages in flow cytometry, crown-like structure formation in immunohistochemistry, and proinflammatory cytokine expression were significantly attenuated in Tene. Hepatic steatosis was also markedly improved. Furthermore, decreased energy consumption in the dark and light phases, reduced locomotor activity in the dark phase, and lowered core body temperature in OVX-HF were ameliorated in Tene. Since obesity and reduced energy metabolism are a common physiology of menopause, teneligliptin appears to be beneficial as a treatment for type 2 diabetes in postmenopausal obesity.

Resveratrol prevents hyperleptinemia and central leptin resistance in adult rats programmed by early weaning.

We have previously shown that early weaning in rats increases the risk of obesity and insulin resistance at adulthood, and leptin resistance can be a prime factor leading to these changes. Resveratrol is reported to decrease oxidative stress, insulin resistance, and cardiovascular risk. However, there is no report about its effect on leptin resistance. Thus, in this study we have evaluated resveratrol-preventing effect on the development of visceral obesity, insulin, and leptin resistance in rats programmed by early weaning. To induce early weaning, lactating dams were separated into 2 groups: early weaning (EW)--dams were wrapped with a bandage to interrupt lactation in the last 3 days of lactation and control (C)--dams whose pups had free access to milk during throughout lactation period (21 days). At 150 days-old, EW offspring were subdivided into 2 groups: EW+res--treated with resveratrol solution (30 mg/kg BW/day) or EW--receiving equal volume of vehicle solution, both given by gavage during 30 days. Control group received vehicle solution. Resveratrol prevented the higher body weight, hyperphagia, visceral obesity, hyperleptinemia, hyperglycemia, insulin resistance, and hypoadiponectinemia at adulthood in animals that were early weaned. Leptin resistance, associated with lower JAK2 and pSTAT3 and higher NPY in hypothalamus of EW rats were also normalized by resveratrol. The present results suggest that resveratrol is useful as therapeutic tool in treating obesity, mainly because it prevents the development of central leptin resistance.

The common polymorphism Val109Asp in the omentin gene is associated with daily energy intake in the Central-European population

BackgroundOmentin is an adipokine expressed predominantly in visceral adipose tissue, with adipose tissue stromal cells being the main source. Very little is known about the relationship between the genetic variability of the omentin gene and pathophysiology of obesity, although omentin is believed to play an important role in visceral obesity development. The aim of the study was to investigate two common polymorphisms in the omentin gene (rs2274908 and rs2274907) and dietary composition and anthropometric parameters of obesity in the Central European population.Material and methodsA total of 495 subjects were included into the study, they were further dividend into the non-obese, obese, and morbidly obese cohorts. Dietary habits were established using the 7-day food records and selected anthropometric parameters were measured.ResultsThere were significant differences in genotype distributions of rs2274907 between the obese and morbidly obese cohorts (P = 0.01). In the multivariate modelling, the rs2274907 polymorphism expressed independent prediction role for the daily energy intake, independently on the age and gender (P = 0.03); the TT genotype associated with the lowest (7877 ± 2780 J/day) and the AA genotype with the highest (8764 ± 2467 J/day) average energy intake. The rs2274907 also significantly associated with the daily consumption of fat and proteins.ConclusionThis is, so far, the first study to investigate the polymorphisms in the omentin gene in a large population cohort of obese and non-obese individuals. Based on our results, the rs2274907 polymorphism is associated with the daily energy intake as well as daily intake of fat and protein.

Metabolic profile and morpho-functional state of the liver in rats with glutamate-induced obesity

The aim of our study was to investigate effects of monosodium glutamate (MSG) neonatal treatment on metabolic profile and liver morpho-functional state in rats at 16-weeks of age. Our study confirms previously reported data that neonatal treatment with MSG, administered by subcutaneous injection, is able to induce obesity without hyperphagia, which is diagnosed by high Lee index and characterized by small corporal weight and naso-anal length. It was established that MSG neonatal treatment induced metabolic changes at 16 weeks of age, which manifested as disproportional laying of fat deposits with the development of visceral obesity. The level of adiponectin was decreased after MSG neonatal treatment. Also, we showed development of dyslipidemia and non-alcoholic fatty liver disease and impairment sensitivity of peripheral tissue to insulin.

Gender features of metabolic syndrome in old age: Literature review

This review is devoted to one of the urgent issues in medicine—the problem of metabolic syndrome (MS) in elderly people. Special attention is paid to its higher frequency of occurrence in aged people. The updated records on pathogenesis of the basic MS components potentiating the development of cardiac diseases and pancreatic diabetes of the second type are given. It is pointed out that the hormonal changes arising with age create conditions for development of visceral obesity, insulin resistance, dislipidemy, and subclinical inflammation, i.e., those pathological changes that make the MS basis. Measures to prevent the cardiovascular complications consisting in changes in the way of life for people suffering MS are considered.

Interleukin-1 beta: a potential link between stress and the development of visceral obesity

BackgroundA disproportionate amount of body fat within the abdominal cavity, otherwise known as visceral obesity, best predicts the negative health outcomes associated with high levels body fat. Growing evidence suggests that repeated activation of the stress response can favor visceral fat deposition and that visceral obesity may induce low-grade, systemic inflammation which is etiologically linked to the pathogenesis of obesity related diseases such as cardiovascular disease and type 2 diabetes. While the obesity epidemic has fueled considerable interest in these obesity-related inflammatory diseases, surprisingly little research is currently focused on understanding the functions of inflammatory proteins in healthy, non-obese white adipose tissue (WAT) and their possible role in modulating stress-induced shifts in body fat distribution.HypothesisThe current review presents evidence in support the novel hypothesis that stress-evoked interleukin-1 beta (IL-1β) signaling within subcutaneous adipose tissue, when repeatedly induced, contributes toward the development of visceral obesity. It is suggested that because acute stressor exposure differentially increases IL-1β levels within subcutaneous adipose relative to visceral adipose tissue in otherwise healthy, non-obese rats, repeated induction of this response may impair the ability of subcutaneous adipose tissue to uptake energy substrates, synthesize and retain triglycerides, and/or adapt to positive energy balance via hyperplasia. Consequently, circulating energy substrates may be disproportionately shunted to visceral adipose tissue for storage, thus driving the development of visceral obesity.ConclusionsThis review establishes the following key points: 1) body fat distribution outweighs the importance of total body fat when predicting obesity-related disease risk; 2) repeated exposure to stress can drive the development of visceral obesity independent of changes in body weight; 3) because of the heterogeneity of WAT composition and function, an accurate understanding of WAT responses requires sampling multiple WAT depots; 4) acute, non-pathogenic stressor exposure increases WAT IL-1β concentrations in a depot specific manner suggesting an adaptive, metabolic role for this cytokine; however, when repeated, stress-induced IL-1β in non-visceral WAT may result in functional impairments that drive the development of stress-induced visceral obesity.

INFLUENCE OF TAURINE-CONTAINING DRUG ON THE DEVELOPMENT OF VISCERAL OBESITY IN OVARIECTOMED RATS WITH SYNDROME INSULIN RESISTANCE INDUCED BY A HIGH FAT DIET

The effect of taurine-containing drug on the development of visceral obesity in rats was studied
 with the syndrome of insulin resistance on the background of estrogen deficiency, which was kept on a high-fat diet. It was found that oral administration of taurine-containing drug, in the absence of
 stimulating effect on proliferative processes in the uterus, improves tolerance to
 carbohydrates and sensitivity to insulin, inhibits the development of abdominal obesity, weight gain
 body. The obtained results substantiate the prospects of using taurine-containing drug for pharmacological correction of the main components of postmenopausal metabolic
 syndrome.

A rodent model for visceral obesity development evaluated by MRI

A rodent model for visceral obesity development evaluated by MRI

Nature of obesity and the rate of aging in women with reproductive disorders

Anthropometric and metabolic features of obesity and the rate of aging were determined in young women (mean age of 25.5 years) with infertility as a result of polycystic ovary syndrome, chronic anovulation, and other reproductive noninflammatory disorders. These parameters were compared to data for women of different age groups with obesity who had already realized their reproductive potential prior to the survey. Women with infertility due to increased visceral fat content which started to accumulate in the pre- and pubertal periods were shown to have metabolic disturbances that are typical for mature-aged women. These women showed the highest aging rate coefficient, resulting in a higher biological chronological age. Thus, early development of visceral obesity combined with reproductive disorders is associated with the increase of aging rate in young women.

The role of the tissue renin-angiotensin-aldosterone system in the development of metabolic syndrome, diabetes mellitus and itsvascular complications

Renin-angiotensin-aldosterone system (RAAS) is a major system of the human body playing a key role in the regulation of most physiological andpathological conditions, such as vascular tone, AD level, myocardial and vascular wall remodeling, development of atherosclerosis, glomerulosclerosis,and other pathologies. The discovery of local (tissue) RAAS in the late XX century gave evidence of direct synthesis of all components of this system,from renin to aldosterone, in target tissues and organs. Activation of tissue RAAS was shown to play a leading role in the evolvement of diabetic complicationsincluding cardiovascular diseases, diabetic nephropathy (DN), and retinopathy. Recent studies revealed the presence of RAAS componentsin fat and pancreas. This system is involved in the development of visceral obesity, pre-diabetes, and Type 2 diabetes. These findings are confirmedby a reduced risk of CDM2 in subjects receiving long-term therapy with RAAS blockers.

Impact of ecology on development of NIDDM

Diabetes has become a global epidemic. The increased incidence of NIDDM is seen all over the world but there is geographical variation. Certain population groups show increased susceptibility to develop diabetes. The prevalence is lowest in Caucasian whites and highest in Pima Indians and Naurans. Iceland has a particularly low incidence whereas Bahrain is among the countries with highest prevalence. The highest prevalence of diabetes in 2000 was found in Papua New Guiana (15.5%), Mauritius (15%), Bahrain (14.8%), Mexico (14.2%), Trinidad and Tobago (14.1%). Most of the hypotheses developed to explain this trend concerned mainly on dietary and nutritional factors. Man had to struggle against harsh climatic conditions for survival. It has been observed that people who have been adapted to cold environment for generations demonstrate some resistance to develop diabetes. It is hypothesized that presence of thick subcutaneous fat, reactivation of brown adipose tissue in cold environment and effective mitochondrial enzyme systems for heat generation act as adaptive mechanisms for survival in cold environment and retard the development of visceral obesity. Mitochondrial defects have been found in patients with NIDDM and NAFLD. Changes of nuclear genes which encode mitochondrial enzyme systems involved in thermo genesis could be the cause for development of visceral obesity and NIDDM.