Novel research indicates that the global non alcoholic fatty liver disease (NAFLD) epidemic is critical to the induction of the obesity epidemic. In man dietary and drug interventions in obesity have failed to correct the defect in the adipose tissue-liver interaction with the induction of NAFLD and NAFLD to effect between 20-40% of the global population. In various studies in obese animals dietary restriction has improved the adipose tissue-liver interaction with increased hepatic metabolism of lipids. Mitochondrial apoptosis is now a major concern in NAFLD with defective lipid metabolism in adipocytes related to adiposity and NAFLD. Specific genes have been identified that regulate the adipose tissue-liver interaction with calorie sensitive genes essential to maintain the interaction with the prevention of obesity. Global populations include various racial groups with consumption of anti-aging gene nutrients that may vary considerably between Caucasians, Africans, Europeans, Hispanics, Pacific Islanders and Asians. Nutritional and environmental epigenetics now identify the calorie sensitive gene Sirtuin 1 (Sirt 1) to be critical to the reversal of NAFLD and obesity. Sirt 1 is important to mitochondrial biogenesis with Sirt 1 repression responsible for the adipose tissue-liver defect. Nutritional diets that contain Sirt 1 activators reverse NAFLD with relevance to obesity and various global chronic diseases. ONLINE REFERENCE 1. Unhealthy Nutrigenomic Diets Accelerate NAFLD and Adiposity in Global communities. J Mol Genet Med. 2015; 9:1-8. 2. Defective Inter¬play between Adipose Tissue and Immune System Induces Non Alcoholic Fatty Liver Disease. Updates Nutr Disorders Ther. 2017; 1: 3.1. 3. Induction of NAFLD with Increased Risk of Obesity and Chronic Diseases in Developed Countries. OJEMD. 2104;4:90-110. 4. Nutrition increases Survival and Reverses NAFLD and Alzheimer's disease Ian J Martins First Edition edited by Alina Berdos, 01/2015; LAP LAMBERT. 5. Single Gene Inactivation with Implications to Diabetes and Multiple Organ Dysfunction Syndrome. J Clin Epigenet. 2017;3:24. 6. Caffeine with Links to NAFLD and Accelerated Brain Aging. Chapter: Non-Alcoholic Fatty Liver Disease - Molecular Bases, Prevention and Treatment. InTech - Open Science Open Minds | InTechOpen. 2017. 7. Avasimibe and Sirt 1 Activators Reverse NAFLD and Obesity. Nov Appro Drug Des Dev. 2017; 1: 555561. 8. Drug Therapy for Obesity with Anti-Aging Genes Modification. Ann Obes Disord. 2016;1: 1001. 9. Appetite dysregulation and obesity in Western Countries Ian J Martins • First edited by Emma Jones; LAP LAMBERT Academic Publishing.
Biography Dr. Ian James Martins is an Editor/Reveiwer for Open Acess Pub/MDPI journals and various other international journals. Advisory Board Member for Photon Journal. Fellow of International Agency for Standards and Ratings (IASR). Chief Editor for International Journal of Diabetes Research (2014-2018), Research and Reviews: Neuroscience (2016-2018) and Journal of Diabetes and Clinical Studies (2017-2018). He is a BIT Member (BIT Congress. Inc) with an H-index of 43, (ResearchGate STATs (23), Mendeley STATS (20). Scientist for The Science Advisory Board (USA) and an Academic with Academia.edu. The total citations over the past 27 years of scientific research has accumulated to >3300. ResearchGate’s analysis available on google, Tweet, Facebook, Lindekin under Ian James Martins’ name places publication Stats RG score higher than 96% of the international SCIENTISTS.
Abdominal obesity is a major risk factor for type 2 diabetes (T2D). Glucagon-like peptide-1 (GLP-1) stimulates the proliferation of β-cells and increases insulin secretion, maintaining normal glucose levels. The aim of the research was to study the rs6923761 SNP in GLP1R gene association with an increased risk of developing T2D and serum insulin and C-peptide level. The study sample included 87 patients with a diagnosis of obesity with T2D (body mass index (BMI) = 45.6±10.3 kg/m2). The control group included 109 healthy volunteers with normal anthropometric and biochemical parameters. The matching the distribution of genotype frequencies of rs6923761 SNP in GLP1R gene to Hardy-Weinberg equilibrium has been determined in group of healthy volunteers (χ2=0.16, p=0.69) and obesity patients with T2D (χ2=0.68, p=0.06). The association of A allele and AA genotype with an increased risk of development of T2D (OR=1.69, 95%CI:1.04–2.73, р=0.03; OR=2.92, 95%CI:1.10–7.79, р=0.02) has been established. The study of serum insulin and C-peptide levels in patients with obesity and T2D depending on genotypes of rs6923761 SNP in GLP1R gene has revealed an increase in this indicator in patients with AA genotype as compared with carriers of GA and GG genotypes. Thus, the allele A and genotype AA of rs6923761 SNP associated with increased risk of T2DM in patients with obesity and T2DM affects the increase in serum insulin and C-peptide levels.
Biography Maria Vulf has completed his PhD from Institute of Experimental Medicine, St. Petersburg, and postdoctoral studies from Immanuel Kant Baltic Federal University, Kaliningrad. I am a research fellow at the basic laboratory of immunology and cellular biotechnology. She has published about 20 papers in reputed journals.
Cardiometabolic risk is defined as a risk for development of type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). Metabolic syndrome (MS) is a cluster of factors that increase cardiometabolic risk. Central obesity and insulin resistance are considered as the core defects of the MS. Consequently dietary or pharmacologic approach that promote weight loss and decrease insulin resistance could reduce cardiometabolic risk. We investigated the effect of metformin on central obesity, insulin resistance, hyperinsulinaemia, dyslipidaemia and arterial hypertension in normal glucose tolerant persons with MS according to the IDF definition, who represent a high-risk group for development of type T2DM and CVD. Metformin was applied at a mean dose of 2.55±0.2 g daily on an usual diet and physical activity. Body weight, body mass index and waist circumference decreased significantly at 6 month of metformin treatment and this effect continued to the end of the observation and it was no more pronounced at 1 year compared to the 6 month. The mean body weight reduction was 7.7 kg at 6 month and 12.1 kg at 1 year. Fasting serum insulin and homeostasis model assessment of insulin resistance significantly reduced at 6, 9 month and at 1 year. Triglycerides, LDL cholesterol, systolic and diastolic blood pressure significantly decreased at 9 month and at 1 year. HDL cholesterol significantly increased at 1 year of metformin treatment. In conclusion: metformin reduces cardiometabolic risk factors in normal glucose tolerant persons with central obesity and MS and could be considered as a therapeutic alternative for reduction of cardiometabolic risk. Petya Kamenova-MD, PhD is an Assistant Professor at the Department of Diabetology of Clinical Center of Endocrinology and Gerontology, Medical University, Sofia. She is an author of above 90 papers and scientific presentations, specialist on internal diseases, endocrinology and diseases of metabolism and educator of students, trainee doctors, spcializing doctors and general practitioners.
Obesity is an epidemic of the 21st century. Visceral obesity is associated with cardiovascular diseases, affects the quality and duration of life. Adipose tissue regulates glucose homeostasis by regulating lipid metabolism. Disorders of lipid metabolism can lead to systemic dysregulation of carbohydrate metabolism and the formation of insulin resistance. The aim of the study was to study the production of various types of adipose tissue mediators with metabolic and pro-inflammatory activity in obese patients. The study included 155 patients diagnosed with obesity. Participants in the study were divided into groups, depending on the extent of (obesity) obesity (by BMI) and the presence of diabetes mellitus 2. The control group included 43 healthy volunteers with normal anthropometric and biochemical parameters. To study the expression of genes in adipose tissue, a comparison group of 30 patients was included. It was found that the maintenance of serum glucose levels within the norm in obese patients (BMI <40 kg / m2) is due to the cooperative action of mediators: adiponectin, adipsin, chimerin and IL-6, and in patients with morbid obesity depends on the plasma chimerin content (correlation with the level of expression of the RARRES2 gene in adipose tissue of the small intestine mesentery) and adiponectin (correlations with the level of ADIPOQ gene expression in the subcutaneous adipose tissue).We assume that, with obesity, a significant role in the pathogenesis of insulin resistance is played by an increase in the functional activity of adipose tissue in the mesentery of the small intestine. This is confirmed by the high level of expression of LEP, SERPINA12, RARRES2, IL-6 and TNFα (encoding leptin, vaspin, chimerin, IL-6 and TNFα, respectively) in its biopsy specimens, as well as the involvement of adipose tissue in the formation of plasma levels of these mediators directly associated with insulin resistance (glucose, glycated hemoglobin, HOMA-IR index).
Natalya Gazatova research fellow at the basic laboratory of immunology and cellular biotechnology Immanuel Kant Baltic Federal University, Kaliningrad. She has published about 15 papers in reputed journals.
The problem of diabetes mellitus 2 (DM 2) is one of the most priority and socially significant. In the pathogenesis of DM 2, hormones of the gastroduodenal zone and adipokines, adipokine mediators that regulate serum glucose are important. The aim of the study was to analyze the pathogenetic significance of polymorphic variants of incretin receptor genes (GIPR, GLP-1R) in the development of insulin resistance in obese patients with DM 2. The study included 191 patients suffering from abdominal obesity. Of these: 90 obese patients with DM 2 (BMI = 43.70 ± 9.32 kg / m2, age 46.5 ± 10.1 years) - group 2; 101 patients with obesity without violations of carbohydrate metabolism (BMI = 36.13 ± 6.72 kg / m2, 43.93 ± 8.35 years) - group 3. The control group (group 1) included 137 conditionally healthy donors with normal anthropometric and biochemical indicators (22.6 ± 2.7 kg / m2, 39.5 ± 7.6 years). As a result of the study, polymorphisms of the GIPR gene (rs2302382, rs1800437) and the GLP-1R gene (rs1042044, rs6923761 and rs10305420) are associated with the risk of developing DM 2 in obesity in the East Slavic population of the North-West region of Russia. In patients with obesity with DM 2, the observed increase in plasma levels of the C-peptide, insulin after the test breakfast, and the presence of correlation interrelations between them, indicate the preservation of the functional activity of β-cells of the pancreas. The position of the polymorphisms of the GLP-1R gene within the transcript shows that they can influence the signal transmission from GLP-1 to its receptor, mediating the changes in the mature translated protein. Thus, replacing leucine with phenylalanine (Leu260Phe) in the GLP-1R gene in the amino acid sequence in the amino acid sequence is likely to cause conformational changes that exert effects on receptor binding to the ligand and thus contribute to the development of DM 2 in obesity. Changes in signaling from the receptor to GLP-1 regulates the secretion of hormones into adipokines. Thus, with the increase in GLP-1 signaling, the plasma level of insulin, resistin, and ghrelin increased and glucagon, leptin, visfatine and glucose levels were reduced, indicating its positive effect on carbohydrate metabolism.
Elena Kirienkova, Ph.D., a researcher at the basic laboratory of immunology and cell biotechnology. Immanuel Kant Baltic Federal University in Kaliningrad.Published about 35 papers in reputed journals.