Day 2 :
Keynote Forum
Omo Ojo
Keynote: The Role of Exenatide in Managing Cardiovascular Risks and Complications in Patients with Type 2 Diabetes
Time : 10:00-10:30
Biography:
Dr Ojo has a PhD in nutrition, a post graduate diploma in diabetes and a graduate certificate in Higher Education. He is a Senior Lecturer in Primary Care and teaches across a range of courses and programmes in the school. His key interest and areas of expertise are diabetes and nutrition which form the focus of his research and teaching activities. Dr Ojo leads the school Diabetes Specialist Interest Group and co-ordinates the Diabetes Care and Management course for post registration nurses and Patient Pathways of Care for pre-registration participants.rnHe supervises both undergraduate and postgraduate research students including PhD students. His research interests are reflected in his 25 publications in reputed journals and 9 conference presentations. His work is recognised both nationally and internationally and he has been a keynote speaker at the NNNG conference, a reviewer for Journals and sits on the Editorial Board on a number of International Journals. rn
Abstract:
The aim of this systmatic review is to examine the role of exenatide BID in managing cardiovascular risks and complications in patients with type 2 diabetes.rnMethod: This involved a literature search including a general scoping of the data bases which found previous reviews relevant to the population and intervention of interest, but these were either more than 4 years old, were narrative reviews or included liraglutide and studies which were not randomised. The current systematic review is based only on randomised controlled studies. rnrnThe literature search strategy for the review relied on previously published guidelines for reviews and was based on the Population (P), the Interventions (I), Comparative interventions (C) and Outcomes (O) (PICO) framework. A number of databases including EBSCO host, encompassing Academic search premier, Medline, Psychology and Behavioural sciences collection, PSYCINFO, SPORTDISCUSS and Cumulative Index to Nursing and Allied Health Literature (CINAHL) Plus were accessed.rnIn addition, ‘Boolean’ search strategy allowing the combination of search terms such as ‘Exenatide’ AND ‘Diabetes’ AND ‘cardiovascular diseases’; ‘Exenatide’ AND ‘Diabetes’ AND ‘glycaemic control’; ‘GLP–1’ AND ‘Diabetes’; ‘GLP–1’ AND ‘Diabetes’ AND ‘cardiovascular diseases’; ‘GLP–1’ AND ‘Diabetes’ AND ‘macrovascular diseases’; ‘Exenatide’ AND ‘Cardiovascular risks’; ‘Exenatide’ AND ‘Cardiovascular complications’; Exenatide’ AND ‘ glycaemic control’ was used.rnThe quality of the studies selected were evaluated using the checklists for quantitative studies.rnTen (10) randomised controlled studies which met the inclusion criteria were selected for the current review. rnThe outcome measures included in the search were; Cardiovascular risks, Cardiovascular complications, glycaemic control.rnAll the studies reviewed except 1 showed that the use of exenatide BID as a monotherapy or in combination with other medications was associated with reduction in most cardiovascular risks and complications such as weight, blood pressure, glycated haemoglobin which are associated with type 2 diabetes compared with control.rnrn
Keynote Forum
Belma Turan
Ankara University, Turkey
Keynote: Cardiac β-adrenoceptor subtypes in diabetes: Regulation of cardiac β3-adrenergic receptors
Time : 10:00-10:30
Biography:
Belma Turan has completed her PhD at the year of 1982 from Ankara University and postdoctoral studies from INSERM France and University of Ottawa School of Medicine. She is Professor and the Head of Biophysics Department in Ankara University Faculty of Medicine. She has published more than 100 papers in reputed journals and has been serving as an editorial board member of more than 10 international journals. She is also fellow of International Academy of Cardiovascular Sciences since 2005. She has been supervised over 20 PhD and MSc thesis. Her research interest is focused on cardiac electrophysiology, calcium and zinc ion regulations, oxidant stress, antioxidants, diabetic cardiomyopathy
Abstract:
Positive inotropic action of catecholamines is mediated through their interaction with beta-adrenergic receptors (β-ARs), while they can also mediate some deleterious effects, such as cardiac arrhythmias. The β-ARs are members of the G protein-coupled receptors and play important roles in the regulation of heart function. Cellular signaling associated with cardiac β-ARs is composed of coupled mechanism between β1-/β2-AR and Gs proteins with contribution of constitutive β3-AR coupling to Gi proteins. This coupled mechanism further leads to the activation of adenylyl cyclase, and thereby increases in intracellular cAMP level. However, recent studies have emphasized the contribution of constitutive β3-AR coupling to Gi proteins, thereby initiating additional signal transduction pathways, particularly under physiopathological conditions such as hyperglycemia. Diabetic cardiomyopathy, as a distinct entity, is recognized due to its diminished responsiveness to β1-AR agonist stimulation in the heart from diabetic rats with no important changes in the responses mediated with β2-AR. Furthermore, an upregulation of β3-AR has been shown in diabetic rat heart with a strong negative inotropic effect on left ventricular function. Experimental data provide evidences that the mechanisms for the negative inotropic effect with β3-AR activation appears to involve activation of a nitric oxide synthase pathway. On the other hand, we have shown that although insulin resistance and cardiomyopathy are developed under high-carbohydrate diet-induced metabolic syndrome (MetS), compared to type 1 diabetes, MetS-associated cardiac dysfunction seems not to be associated with any change in β3-AR system, with similar ultrastructural changes into the myocardium
Keynote Forum
Vladimir Strbak
Slovak Medical University ,Slovakia
Keynote: Insulin Regulatory Secretory Pathway: Role of Thyrotropin Releasing Hormone
Time : 10:00-10:30
Biography:
Vladimír Strbak,MD and DSc., has completed his study in Bratislava. He was Director of the Inst. Exp. End.SAS, Head of Pathological Physiology, Slovak Med. Univ., president of the Slovak Physiological Society, Council Member FEPS, chair of the Scientfic Board of the Slovak Academy of Sciences for Medical Sciences, Council Member of the International Society for Pathophysiology. Published 118 PuBMed papers. Organized series of symposia on Hormones in Milk (5) and Cell volume and function (2) and FEPS meeting in Bratislava. He served as Organizing Committee member of the 6th Global Diabetes Summit and Medicare Expo in Dubai (2015).rn
Abstract:
Thyrotropin-releasing hormone (TRH) was found in various locations. Pancreatic TRH is colocalized with insulin in the secretory granules of ï¢ cells. High TRH expression in the pancreatic islets in perinatal rat coincides with maturation of the insulin secretory responsiveness to glucose. Prepro-TRH gene disruption in mice results in hyperglycemia, accompanied by impaired insulin response to glucose. We showed that secretion of TRH from islets is stimulated by glucose and inhibited by insulin or somatostatin. These data indicate specific relation between TRH and glucose-induced insulin secretion To induce acute shortage of TRH we blocked the terminal step of the post-translational TRH maturation in adult rat in vivo by disulfiram (DS, 5 day i.p. 200 mg/kg pretreatment) and tested insulin secretion from isolated islets in vitro. TRH in physiological concentration (1 nM) did not affect basal or glucose stimulated insulin secretion. Release of insulin from DS-treated pancreatic islets under basal (unstimulated) conditions was four times higher compared to controls and could not be further stimulated by high-glucose. Addition of 1nM TRH in the incubation medium decreased basal insulin secretion to control levels and normalized response to 16.7 mM glucose of islets from DS treated rats. We conclude that TRH is essential for insulin direction from constitutional to regulatory secretory pathway. This function might be disturbed in diabetes mellitus 2.
Keynote Forum
Udaya Kabadi
University of Iowa, USA
Keynote: Diabetes Mellitus: Disorder of cellular dysfunction due to lack of entry into cell of glucose; the most efficient fuel for cellular function.
Time : 11:20 - 11:50
Biography:
Dr. Udaya M Kabadi completed general medicine residency at KEM Hospital and obtained post graduate degree MD from Mumbai University, Mumbai, India. He continued his post graduate training in internal medicine and fellowship training in New York, NY, USA. He is Board certified in Internal Medicine, Endocrinolgy and Metabolism and Geriatric Medicine by American Board of Internal Medicine. He is Fellow of American College of Physicians, American College ofr Endocrinolgy and Royal College of Physicians of Canada. He is an Adjunct Professor of Medicine at Des Moines University, Des Moines,rnrnIowa and University of Iowa, Iowa, USA. He has authored over 190 papers in peer reviewed medical journals and 2 books. He has conducted over 500 CME presentations and chaired symposia at Regional. National and International Meetings. He serves as a member of Editorial Board of many Medical Journals. He has also been elected ' Teacher of The Year' by undergraduate students and postgraduate trainees on several occasions during his career.
Abstract:
Traditionally, diabetes Mellitus has been deemed to be a chronicrnrnhyperglycemic disorder secondary to altered glucose metabolism. Alternatively, hyperglycemia may be one of several manifestations inrnrnsubjects with type 1 and type 2 diabetes Mellitus. Almost all tissuesrnrnrequire insulin for entry of glucose, the possible exceptions being redrnrnblood cells, renal medulla as well as central and peripheral nervousrnrnsystems. Hyperglycemia in intravascular compartment and otherrnrnextra cellular milieu may be attributed to impaired glucose entry intornrnendothelial cells of the vessel wall and almost all other cells includingrnrnhepatocytes, myocytes of all varieties, adipocytes and individual cellsrnrnin most other organs respectively due to absence of insulin in type1rnrnand both the insulin resistance as well as the decline in both phasesrnrnof insulin secretion in type 2 Diabetes. Albeit, the decline in bothrnrnphases of insulin secretion are induced by lack of glucose entry intornrnpancreatic beta cells. Finally, hyperglycemia is perpetuated byrnrnincreased hepatic glucose production caused by into sustainedrnrncirculating hyperglucagonemia secondary to lack of glucose entryrnrninto the pancreatic alpha cells. Alternatively, both the decline inrnrninsulin secretion by the beta cells and the rise in glucagon release byrnrnthe alpha cells are enhanced by fall in GLP1 and GIP caused byrnrndysfunction of L cells and K cells respectively secondary to lack ofrnrnglucose entry in both type 1 and type 2 diabetes. Similarly, increasedrnrnprevalence of infections and thromboembolic micro andrnrnmacrovascular events may be attributed to dysfunction of leukocytesrnrnand platelets respectively due to impaired glucose entry. Finally,rnrnalterations in several other metabolemics including serumrnrnconcentrations of Adiponectin (Adipose cells), TNF alpha,rnrnPlasminogen inhibitor factor 1, Homocysteine, CRP, Lipids etc (rnrnHepatocytes) as well as dysfunction of several organs ( liver, heart,rnrnkidney, adrenal, pituitary, lungs etc) in both type 1 and type 2 diabetesrnrnmay also be attributed to the lack of glucose entry into these specificrnrncells. This hypothesis is validated by improvement in metabolemicsrnrnand organ function on facilitation of glucose entry into cells by insulinrnrnadministration and / or improvement in insulin sensitivity. Therefore,rnrnin conclusion, diabetes mellitus is a disorder manifesting dysfunctionrnrninvolving almost all organs and cells induced by lack of entry ofrnrnglucose, the most efficient substrate for cellular function.
Keynote Forum
Gaurav Sharma
DrG Wellness, India
Keynote: The Future of Type 2 Diabetes Management- Today and what to expect tomorrow
Time : 11:50 - 12:35
Biography:
Dr. Gaurav Sharma is a renowned Diabetologist and a lifestyle doctor who is credited with changing the entire wellness industry across the globe. He is one of the illustrious personalities known for his contribution towards society & making people aware about the perpetual dominance of a number of lifestyle related disorders. A visionary by approach & innovator by default his urge of giving back to society inspired him to launch DrG Wellness, a company which has motto of constant innovation in terms of pathbreaking food supplement & products. Dr. G Wellness has dedicated R & D team which is headed by Dr. G Sharma himself. After completion of his post graduation (M.D) from St. Petesburg state medical academy, he heralded a profound need for people to lead a healthy lifestyle by adopting the right diet plans. He was always keen towards working for the benefits for those suffering from most prevalent lifestyle related disorders like diabetes, arthritis, obesity. He has been practicing for more than 14 years in preventing and managing such disorders through his world famous lifestyle modification programs. He was recently awarded at the 4th M.T India health care awards held in 2014 to become the most admired Diabetologist and lifestyle doctor. Dr. G feels “Impossible is equal to opportunity” & this is what has inspired him to innovate products which have reversed diabetes and arthritis of thousands of patients. Dr. G Sharma has been featured numerous times on the leading national television discussing how to reverse the symptoms of most lifestyles related disorders naturally
Abstract:
Diabetes mellitus (DM) is a metabolic disorder in the endocrine system with a defect in the insulin secretion or action or both which leads to increase in blood sugar in the body. At present, Type 2 diabetes mellitus (T2DM) is the predominant form of DM that accounts for 90–95% of diabetic patients globally. The standard therapy for T2DM includes balanced diet, appropriate exercise, and more importantly, the use of oral hypoglycaemic drugs, and/or subcutaneous insulin injections. Use of anti- diabetic drugs have lead to concerns about their potential toxicity and side effects such as weight gain, bone loss, and increased risk of cardiovascular events.rnNutraceutical supplement is one of the upcoming approaches towards the control and reversal of diabetes worldwide. Diabetall & Diabetplus are magical supplements that work as a sure shot adjuvant with no side effects. They not only regulate and maintain the blood sugar levels through various pathways but also reverses the effect of T2DM which is evident through our in house clinical trials.rnHere we emphasize on how the use of natural therapy that includes supplements with botanical extracts, dietary modifications and exercise programs and counselling help to reverse the effect of diabetes and also promote a sense of well being in individuals.rn
- Genetics and Transplantation of Diabetes, Therapy for Diabetes
Location: Birmingham, UK
Chair
Lixin Li
Central Michigan University, USA
Co-Chair
Haobo Li
The University of Hong Kong, Hong Kon
Session Introduction
Jae Woong Sull
Eulji University School of Health Science, South Korea
Title: Effects of fasting glucose levels on the association between CDH13 (rs4783244) and adiponectin among Korean population
Biography:
Dr. Jae Woong Sull (MHS, Ph.D.) is an Assistant Professor at Eulji University. He obtained both his Ph.D. degree in the Genetic Epidemiology and Master of Health Science degree in Epidemiology from Yonsei University in Korea. He was also trained as a postdoctoral fellow in genetic epidemiology at Johns Hopkins Univiersity in USA. He has published over 50 papers in peer-reviewed journals.
Abstract:
Adiponectin is associated with obesity and insulin resistance. Several genome-wide association studies of adiponectin levels have identified candidate genes, including the CDH13 gene. The study objective was to examine the association of serum adiponectin levels (or hypoadiponectinemia) with SNP rs4783244 in CDH13 gene considering fasting blood glucose levels. This study included 2,005 subjects. Hypoadiponectinemia was defined as the lowest quartile of adiponectin. The CDH13 gene SNPs were genotyped via the TaqMan reaction. The multivariate linear regression models and multiple logistic regression analysis were performed. The majority of individuals were middle-aged. Subjects with the GG genotype had a 2.44-fold (range 1.97–3.03-fold) higher risk of hypoadiponectinemia than subjects with the TG/TT genotype. When analyzed by fasting blood glucose levels, the CDH13 association was much stronger in male subjects with pre-diabetes (odds ratio, 10.96; 95% confidence interval, 4.31–27.88; P < 0.0001). Our results suggested that the association between CDH13 and adiponectin can be modified by fasting blood glucose levels.
Hande Ozge Altunkaynak
Baskent University School of Medicine, Turkey
Title: The Impact of adipose tissue hypoxia on insulin sensitivity
Biography:
Hande Ozge Altunkaynak (PhD) is pharmacologist and currently works in Baskent University, Faculty of Medicine, Department of Medical Pharmacology. Her research work involves the cardioprotective mechanisms on the response of hearts against ischemia reperfusion injury, particularly, of diabetic hearts.
Abstract:
A growing body of evidence indicates that adipose tissue could become hypoxic in the obese state. The response to hypoxia is mainly regulated by oxygen-sensitive transcription factors also known as hypoxia-inducible factors (HIFs). Among these, three members of the family are described as HIF-1, HIF-2 and HIF-3. Despite HIF-1α and HIF-2α target many common gene expression, HIF-1α is rather associated with glycolytic gene expression and hence participates different roles in the regulation of insulin sensitivity and glucose tolerance. In addition, it is clear from recent studies by using genetically modified mice that HIF-1α is also involved in the insulin signalling pathway and insulin secretion.Therefore, the present part focuses the impact of hypoxic signalling pathway driven by HIFs in adipose tissue on insulin sensitivity and glucose tolerance.
Sunita Singh
Banaras Hindu University, India
Title: KCNJ11 gene polymorphism E23K (rs5219): An Association study in Type 2 diabetes mellitus in Indian population of eastern Uttar Pradesh
Biography:
Sunita Singh, Ph.D. is Associate Professor in Banaras Hindu University, India. She did her Ph.D. in Biochemical and Evolutionary Genetics and postdoctoral studies in Population Genetics from Banaras Hindu University. Dr. Singh’s current research work involves genetics of complex diseases, including genetics of Type 2 Diabetes and molecular pathology of multiple cancers. Dr. Singh has authored/co-authored 23 papers in the field of Molecular evolution, Type 2 Diabetes and Carcinogenesis.
Abstract:
Despite a very large burden of type 2 diabetes in India, insight into the genetic architecture of Type 2 Diabetes (T2D) in Indian population of eastern Uttar Pradesh is currently lacking. Genome-wide association scan studies (GWASs) have led to the discovery of several novel genetic markers associated to Type 2 diabetes (T2D). Multiple studies have demonstrated reproducible association of several genetic markers (SNPs) with T2D risk, each making a modest contribution to the overall risk mainly in European populations. Only a few investigations for T2D susceptibility genes have been reported in South Asians. Recent studies suggest that the KCNJ11 gene, which encodes the Kir6.2 subunit of the ATP-sensitive potassium (KATP) channel, may also be a candidate diabetogenic gene. The E23K KATP channel polymorphism has received much attention recently due to its higher frequency in the Caucasian type-2 diabetic population. The variant E23K (rs5219) of KCNJ11 has been demonstrated to have modest association with T2D in European, Japanese and North Indian populations. In the present investigation, we have studied the association of KCNJ11 (E23K) (rs5219) gene polymorphism to T2D in the Indian population of eastern Uttar Pradesh in 240 cases and 229 ethnically matched control subjects. Our data show weak association to T2D with odds ratio 1.086 (95% CI 0.832-1.416; P = 0.544). Our data also show association to T2D under co-dominant model only.
Zipeng Liu
The University of Hong Kong, Hong Kong
Title: Combining genomic and genetic knowledge to discover the underlying mechanism of diabetic cardiac dysfunction
Biography:
Zipeng LIU, MSc and PhD in Bioinformatics and Pharmacogy at the University of Hong Kong. His research interest lies in the application of bioinformatic approaches to study diabetic cardioprotection. He has published related research as either first author or co-authors on peer-reviewed journals such as Nucleic Acids Research, Diabetes and Cardiovascular Diabetology.
Abstract:
Myocardial infarction (MI) is a major cause of sudden death and one of the most common perioperative complications prevalent in diabetes mellitus. The underlying biological process is different from that in non-diabetes partially due to increased oxidative stress in diabetes. Cardioprotective interventions that are effective in non-diabetic patients loss their effectiveness in diabetic patients, which exacerbates the susceptibility of diabetic hearts to myocardial ischemia reperfusion injury (IRI). However, the mechanism is still largely unclear. The rapid evolution of genomic and genetic approaches, such as microarray and genome-wide association study (GWAS), provides additional insights into complex disease studies. Here, by combining gene co-expression network analysis from a set of microarray profiling and MI/type 2 diabetes (T2D) associated gene sets from GWAS, we built a transcription factor (TF) based regulatory network to explore the pathological behavior. The resulting network using this combination method was validated by high enrichment in several well-documented pathways of diabetic cardiac pathology (e.g. PI3K/Akt and Jak/Stat3 signaling pathway) and was also significantly improved than that using only genomic or genetic data individually. This TF-based network also revealed numbers of previously unreported protein interactions linking distinct pathways, among which we verified a relation between Stat3 and Hif-1α in diabetic myocardial IRI models. Thus, our study showed potency of combining knowledge from genomic and genetic studies in discovering the hidden mechanism in diabetic cardiac dysfunction.
Biography:
Gopeshwar Narayan has completed his Ph.D. from Banaras Hindu University in 1994; and postdoctoral studies from Institute of Human Genetics, Frei University, Berlin, Germany and Columbia University, New York, USA. Currently he is working as Professor in the Department of Molecular and Human Genetics, Banaras Hindu University, Varanasi, India. He has published more than 50 papers in reputed journals in the fields of Animal Genetics, Cancer Genetics and Type 2 Diabetes.
Abstract:
Type 2 diabetes (T2D) has become a major health problem throughout the world. Compared with European populations, Asians develop diabetes at younger age, at lower degrees of obesity, and at much higher incidence rates given the same amount of weight gain. Recent Genome Wide Association studies (GWAS) in populations of European descent have identified several single nucleotide polymorphisms (SNPs) associated with T2D. The variants have been identified to be differentially associated with T2D in different ethnic groups. The reasons for these ethnic variations towards the risk of T2D have to be understood in order to delineate the role of ethnicity in the background of same genetic elements. We have investigated the association of TCF7L2 rs12255372 (G/T) and PPARγ rs1801282 (C/G) gene polymorphism (SNPs) with T2D in Indian population of eastern Uttar Pradesh. Genomic DNA was extracted from peripheral blood of 434 cases and 292 controls for TCF7L2 (rs12255372) and PPARγ (rs1801282) genes. Gene polymorphisms were analyzed by PCR-RFLP. We compared the genotype distributions and allelic frequencies of each variant in the studied population between cases and controls. Odds ratio (OR) at 95% confidence interval (CI) was determined to describe the strength of association by 2x2 and 2x3contingency table. We report that while allele frequency distribution for TCF7L2 polymorphism is statistically significant (OR = 1.33, 95% CI 1.029- 1.738, P=0.03), it is not significantly different for PPARγ (OR-0.98, 95% CI 0.7O59-1.366, P=0.98) between Type2 diabetic patient and the control groups. Our findings suggest that while TCF7L2 gene polymorphism increases susceptibility to T2D, the PPARγ polymorphism does not show significant association with T2D in the Indian population of eastern Uttar Pradesh. To our knowledge this is the first report in this population and provides valuable information for comparison with other ethnic groups as well as in determining disease susceptibility in this population.
Khalid K Alharbi
King Saud University, Saudi Arabia
Title: Obesity and the incidence of apolipoprotein E polymorphisms in an assorted population from Saudi Arabia population
Biography:
Khalid K Alharbi has completed his PhD in 2004 from University of Southampton. He is a professor and chairman of Saudi society for clinical labaoratory sciences in college of Applied Medical Sciences at King Saud University. He has published more than 50 papers in reputed journals and has been serving as an editorial board member of repute. He is actively involved in Deanship of Scientific Research and National Plan for Scince and Technology projects. His area of interest was type 2 diabetes, obesity, familial hypercholesterolemia and consanguineous problems.
Abstract:
Obesity is known to be a complex disorder caused by both genetic and environmental factors. Patients with obesity tend to develop cardiovascular disease and type 2 diabetes. Earlier studies have revealed that obesity is associated with genetic variations like those found in apolipoprotein E (APOE), a genetic determinant of obesity-related factors and lipid profiles. Hence, in the present study we aimed to perform a molecular characterization of APOE gene polymorphisms found in obese patients within a Saudi population. A case-control study was performed on 198 cases and 198 controls, selected from participants at the King Saud University. TaqMan genotyping was performed to investigate polymorphisms in the APOE gene. The present study identified that APOE polymorphisms were significantly associated with obesity in a Saudi population with the ɛ4 allele (p=0.0001). We found a statistically significant difference in the genotype distribution between cases and controls [for E3/E4: OR, 2.16 (95% CI: 1.19-3.91); p=0.009]. A significant difference was observed in the lipid profile parameters like triglycerides, low-density lipoprotein, and APOE alleles (p<0.001). Our results confirm that APOE variants are associated with obesity in a Saudi population.
Yuliia Klitsunova
Zaporizhia Medical Academy, Ukraine
Title: Sitagliptin as combination therapy in the treatment of inadequately controlled type 2 diabetes
Biography:
Klitsunova Yuliia, PhD is assistant professor of State Institution “Zaporizhia Medical Academy of Post-Graduate Education Ministry of Health of Ukraine”, Zaporizhzhia, Ukraine, where she covers endocrinology and cardiology projects. She holds B.S. and M.S. degrees in medicine from the Zaporizhzhia State Medical University. She is a member of EASD (reg.# 360234) and she has more than 9 years of experience in medicine. She is the author of more than 35 scientific articles and 1 guidelines for daily monitoring of blood pressure.
Abstract:
The purpose of this study was to evaluate the effects of sitagliptin 100 mg in the treatment of participants with type 2 diabetes mellitus who have inadequate glycemic control on metformin ≥1500mg/day. Materials and methods: Outpatients aged 52-72 years with type 2 diabetes. Patients were on metformin monotherapy (>=1500 mg/day) for >=8 weeks with a A1C >=7.5% and <=11.0% before treatment with sitagliptin. Glycemic efficacy endpoints were included the changes from baseline in A1C and FPG at week 26 and also Percentage of Participants Achieving a HbA1c of <7%. Other efficacy endpoints that were assessed include changes from baseline at week 26 in body weight, and some safety endpoints such as hepatic safety tests ALT and AST, total and direct bilirubin, renal failure tests - serum creatinite calculated using the CKD-EPI formula, urinary albumin/creatinine ratio. The efficacy and safety were retrospectively evaluated by comparison of laboratory values before and after the administration of sitagliptin and by review of adverse events after treatment.