Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 11th World Congress on Endocrinology and Metabolic Disorders Auckland, New Zealand.

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Day 1 :

Keynote Forum

Joseph Fomusi Ndisang

Associate Professor, University of Saskatchewan College of Medicine, Canada

Keynote: Heme oxygenase is an important switch-box that ameliorates cardio-renal complications in diabetes

Time : 10:00-10:50 am

Conference Series Endocrinology Congress 2018 International Conference Keynote Speaker Joseph Fomusi Ndisang photo
Biography:

Dr. Joseph Fomusi Ndisang is an Associate Professor in the University of Saskatchewan College of Medicine, Department of Physiology. He received postdoctoral training in Physiology at the University of Saskatchewan College of Medicine from 2000-2005. He obtained a PhD in Pharmacology & Toxicology from the University of Florence, Italy, 2000. He obtained a Doctor of Pharmacy degree from University of Florence, Italy in 1995. He has received several distinguished awards and distinctions including: (i) Fellow of the Canadian Cardiovascular Society (FCCS) in 2016, (ii) Fellow of the American Heart Association (FAHA) in 2011; (iii) Fellow of the International College of Angiology (FICA) in 2007; (iv) Young Investigator Award by International College of Angiology (2007); (v) Young Investigator Award by the American Society of Pharmacology & Experimental Therapeutics-Division for Drug Discovery, Development & Regulatory Affairs (2005); (vi) Young Investigator Award by the Society of Experimental Biology and Medicine (2005); (vii) Caroline tum Suden/Frances A Hellebrandt Professional Opportunity Award for Meritorious Research by the American Physiological Society (2005); and (viii) Recognition Award for Meritorious Research by a Young Investigator by the American Physiological Society (2004). Top 5% of cited authors in journals of Biology and Biochemistry in 2011, by Thomson-Reuters. Currently, Dr. Ndisang is an Editor for Frontiers in Bioscience (impact factor 3.8) and Executive Guest Editor for Current Medicinal Chemistry (impact factor 3.7) He has published more than 64-full length manuscripts in peer-reviewed journals and more than 80 abstracts. Dr. Ndisang has served as external PhD examiner for several universities in Canada, has given more than 30-invited talks, and has also served as peer-reviewer for several reputed journals and granting agencies in United States, United Kingdom, Canada, New Zealand and Poland.

Abstract:

Impaired insulin signaling and deregulated glucose metabolism are associated with the progressive alterations in structure and function of vital organs like the heart and kidneys in diabetic patients.  Our recent studies indicate that upregulating the heme oxygenase (HO) system with HO-inducers like hemin and heme-arginate potentiates insulin signaling and improve glucose metabolism in different animal models of type-1 and type-2 diabetes including (i) streptozotocininduced diabetic rats, (ii) Zucker diabetic fatty rats (ZDF), (iii) obese Zucker rats, (iv) GotoKakizaki rats (lean type-2 diabetic model) as well as other models that display glucose intolerance like spontaneously hypertensive rats and uninephrectomized DOCA-salt hypertensive rats, suggesting a universal role of the HO-system in regulating insulin signaling and glucose metabolism.  The administration of HO-inducers (i) attenuated inflammatory mediators including cytokines like TNF-α, IL-6, IL-1β that in turn stimulate chemokines such as MCP-1 and MIP-1α to promote macrophage-M1 infiltration, (ii) suppressed oxidative stress including NF-κB,  activating-protein (AP)-1, AP-2, and c-Jun-N-terminal-kinaseand 8-isoprostane, (iii) enhanced fundamental proteins implicated in the insulin signal transduction  pathway like IRS-1, PI3K and PKB, (iv) reduced insulin/glucose intolerance (IPITT), (v) increased insulin sensitivity and the inability of insulin to enhance GLUT4 was overturned. These were associated with improved cardiac hemodynamics and the attenuation of cardiac hypertrophy, collagen deposition in cardiomyocytes and the reduction of left ventricular longitudinal muscle fiber thickness, a pathophysiological feature of cardiomyocyte hypertrophy. Similarly, HO  reduced renal histological lesions such as glomerulosclerosis, tubular necrosis, tubular vacuolization, interstitial macrophage infiltration and abated pro-fibrotic/extracellular-matrix proteins like collagen and fibronectin that deplete nephrin, an important transmembrane protein which forms the scaffolding of the podocyte slit-diaphragm allowing ions to filter but not massive excretion of proteins, hence proteinuria.  Thus, diabetic complications such as cardiomyopathy and nephropathy were markedly improved.  Taken together, these studies suggest that the HO-system could be considered and important switch box that when potentiated adequately can rescue organ damage in diabetes.  

Keynote Forum

Christo John Frederick Muller

Biomedical Research and Innovation Platform, South Africa

Keynote: Effects of Rooibos on microbiota dysbiosis: implications for diet-induced metabolic dysfunction

Time : 11:05-11:55

Conference Series Endocrinology Congress 2018 International Conference Keynote Speaker Christo John Frederick Muller photo
Biography:

Prof. Christo J.F. Muller is Chief Specialist Scientist, Biomedical Research and Innovation Platform (BRIP), South African Medical Research Council. He has 2 International patents (USA and Europe) for the prevention of diabetes and has authored and co-authored 81 peer–reviewed articles and two book chapters. He has graduated 5 MSc, 3 PhD and supervised 2 postdoctoral fellows. Currently he is supervising 3 PhD’s and 4 MSc students and acts as a reviewer for many international journals. Prof Muller focuses his research on the potential role of phenolic compounds in the prevention and treatment of metabolic conditions such as insulin resistance, dysbiosis, obesity and type 2 diabetes. He is also involved with a proteomics study to identify early markers for type 2 diabetes. These markers are currently being tested in human subjects.
 

Abstract:

Recent research indicates that the gut microbiota plays a crucial role in maintaining health or promoting metabolic diseases such as obesity and diabetes. Modulation of the gut microbiome composition by enhancing the polyphenol content of the diet has potentiality in health improvement and even disease prevention. Rooibos (Aspalathus linearis) is known to exhibit such preventive effects against metabolic diseases such as diabetes. We propose that a major factor mediating these effects is through the regulation of gut microbiota by Rooibos polyphenols. We used a high fat and sugar diet-induced non-human diabetic primate model (n=6) to elucidate the effects of Rooibos on GUT microbiota. In the study, we evaluated the effect of 4 weeks of supplementation (90 mg/kg body weight) with a pharmaceutical grade aspalathin-enriched green rooibos extract (Afriplex GRT) containing ca. 12.8% aspalathin, on the gut microbiota of high fat diet-induced diabetic and normal vervet monkeys (Chlorocebus aethiops).  Stools collected before and during treatment were analyzed by Microbial DNA qPCR array. The 28-day treatment of the monkeys with GRT extract, improved glucose tolerance, lowered cholesterol, specifically LDL-cholesterol in the blood. In addition, Afriplex GRT significantly affected bacteria deemed to be characteristic of the microbiota phenotype harmful to the metabolism as seen in the shifts between normal monkeys on a maize diet compared to diabetic monkeys on a high fat and sugar diet. The Firmicutes to Bacteroidetes (F/B) ratio, increased in the diabetic monkeys, was reduced by the treatment, that correlated with improved blood glucose and lipid parameters. Key bacterial species increased by the GRT treatment, include: Akkermansia muciniphila, Bacteroides intestinalis, Desulfovibrio piger and Bifidobacterium adolescentis. Supplementation of the diabetic animals Afriplex GRT treatment improved several microbial species relevant to human metabolic diseases in high fat and sugar fed diabetic vervet monkeys. 

Conference Series Endocrinology Congress 2018 International Conference Keynote Speaker Sermin Kesebir  photo
Biography:

Born in Germany in 1972. She completed his specialist education at Ege University. During his professional life, she worked as a psychiatric specialist in a general medical hospital, as a associate professor of psychiatry in the second largest mental health hospital in the Turkey. Since 2014, as a professor of psychiatry she has taught at Üsküdar University and has been worked with bipolar disorder in NPIstanbul Brain Hospital. Another area of interest is psychoanalytic psychotherapies. 
sermin

Abstract:

Temperament originates in the brain structure, and individual differences are attributable to neural and physiological function differences (Kesebir et al. 2005a). Affective temperament is a suggested endophenotype for BD as well. It has been suggested that temperament is associated with metabolic syndrome (MetS) markers, which may be partly mediated by lifestyle and socioeconomic status. Altınbaş et al. suggest that depressive temperament profiles may predispose an individual to the development of MetS in the winter (2013). In their study the proportions of MetS were 19.2, 23.1, 34.6, and 38.5% in the summer, fall, spring, and winter, respectively. Only depressive temperament scores were higher during the winter in patients  with MetS. Neuroticism and openness were confirmed as factors linked to seasonal mood variability (Oginska and Oginska-Bruchal, 2014). Additionally, the study revealed an association between susceptibility to mild winter depression and an avoidanceoriented coping style. The avoidance coping style was correlated positively with all the aspects of seasonality described by SPAQ (correlation coefficients from 0.21 to 0.34). Both sub-types of avoidance-oriented style, i.e. distraction and social diversion, were associated with marked subjective seasonal changes in sleep length, mood and the energy level. While the subjective amplitude of circadian rhythm proved to be connected with seasonality, the subjective acrophase of the rhythm (morningnesseveningness preference) did not. Temperamental factors were related cross-sectionally to, as well as predicted for, the MetS precursors over the 3-year period (Ravaja et al. 1995). Mental vitality and positive emotionality were likely to be related and positive emotionality were likely to be related to a low MetS risk level, whereas hyperactivity, negative emotionality, responsivity to others, and cooperativeness were related to a high level of MetS risk. Same group’s results showed that a temperament profile characterized by a high level of persistence and reward dependence, an average level of novelty seeking, and a low level of harm avoidance was related to a high level of MetS risk factors (Keltikangas-Järvinen 1999). In a systematic review with thirteen cross-sectional analyses, and ten longitudinal analyses, hostility, anger, type A behavior and neuroticism and type D personality were associated with an increased prevalence of metabolic syndrome and its development over time (Mommersteeg and Pouwer 2012). In our study, two types of affective temperament were differantiated between MetS (+) and (-) subjects: Anxious and irritable temperaments (Kesebir et al. 2017). Hyperactivity, high level of persistence and reward dependence, average level of novelty seeking, and low level of harm avoidance which were reported in earlier studies are similar to the features defined for irritable temperament. Additionally, negative emotionality, responsivity to others and cooperativeness are features consistent with the properties defined for the anxious temperament. Irritable temperament was associated with mixed episodes in patients with BD (Kesebir et al. 2005b). According to McIntyre, obesity may affect the symptomatic presentation of BD, by increasing the likelihood that these patients will present with mixed episodes (McIntyre 2013). I think this is applicable not only to obesity but also to MetS. Inappropriate psycopharmacological antidepressant use may contribute to this situation directly by increasing the risk of mixed episode and indirectly by increasing the risk of MetS. On the other hand, there was no clear association between temperament measures and the occurrence and development of the metS. In our last study, triglyceride levels were found to be correlated with hyperthymic, irritable and anxious temperament scores (Kesebir et al. 2016f). There was a inverse correlation between HDL levels and irritable and anxious temperament scores. Blood pressure was found to be correlated with irritabl and anxious temperament scores. There was a strong correlation between waist circumference and cyclothymic and anxious temperament scores. There was not found to be any relation between blood fasting glucose levels and affective temperament scores. There is, however, a cluster of risk factors that include the presence of the metabolic syndrome, as well as a more negative prone temperament profile, that both predispose to the development of coronary heart disease and diabetes.

 

Conclusion: In conclusion, there is multidimensional explanation for bipolar disorders that is coherent, comprehensive, and explanatory. The presence of MetS seems to be correlated with the onset and progression of BD. Previous depressive episode, seasonality, negative family history and childhood trauma are determined as the predictors of MetS. Anxious and irritable temperament scores were higher in MetS (+) patients. This link could provide an interesting new paradigm for the study of the "systemic" nature of mood disorders. This may also contribute to the discovery of biological markers, increase in our diagnostic tools, development of protective and individual-spesific treatment options. At this point, some endocrinological drugs may be effective in the treatment of mood disorders. Use of Allopurinol and Tamoxifen was determined as antimanic treatment in guidelines for the treatment of mood disorder (Kesebir et al. 2014, Yıldız et al. 2008). 

  • Thyroid Disorders | Advancements in Treatment & Prevention | Thyroid Cancer | Endocrinology & Diabetes
Location: Wink @ Naumi Hotel Auckland Airport
Speaker

Chair

Christo John Frederick Muller,

Biomedical Research and Innovation Platform, South Africa

Session Introduction

Dr Shaheena Banu

Senior lecturer Healthcare management, Research & Training Auckland, New Zealand

Title: Genetic and Epigenetic Markers of Low Density Lipoprotein-cholesterol Receptors in Management of Type2 Diabetes Mellitus and Newer Treatment Options

Time : 13:45-14:15

Speaker
Biography:

Dr Shaheena Banu has completed his PhD in 2005 from Rajiv Gandhi University of Health Sciences,India and postdoctoral studies at Jayadeva Institute of Cardiovascular Sciences and Research Bangalore. She is currently Senior Lecturer at Aspire2 International, a category-1 PTE of New Zealand. She has published more than 25 papers in reputed journals and has been serving as Guest editor for special issue of Bentham Publications “Endocrine, Metabolic & Immune Disorders-Drug Targets with Impact Factor 1.897). 

Abstract:

The global rise of Type-2 Diabetes Mellitus(T2DM) and its complications, primarily Coronary Artery Disease (CAD) are enormous. Application of genetic knowledge of T2DM polymorphisms to clinical use is limited. Genetic markers of T2DM based on genome-wide association scan (GWAS) findings yield inconclusive results. The burden of CAD in T2DM is high, increased levels of Low-Density Lipoprotein cholesterol remains prevalent. This paper evaluates the genetic variants of Low-Density Lipoprotein receptor(LDLR), review inheritable changes in gene expression caused by epigenetic regulations and discuss newer therapeutic options. For the purpose of literature review, the systematic search was conducted with the use of Medline and Cochrane library.  Data collected from 2013 through to 2018 published in English alone was analyzed. The role of LDLR polymorphisms in T2DM is discussed. Analysis of LDLRrs688 TT genotype and T alleles associated are compared with similar studies and linked to dyslipidemia in T2DM. Epigenetic changes that are reported, following diet and exercise. are reviewed. Further, the diabetogenic effect of statins on T2DM and emerging treatment options are reviewed2.    The research identifies uncommon variants, structural variation and gene-environment interactions of LDLR that contribute to CAD in T2DM. LDLR rs688 TT genotype and T alleles indicate susceptibility to CAD in Indians within a small study. Individual statins differ with respect to their diabetogenic property. Underlying genetic mutation of LDLR can be used as a predictor of response.   LDLR polymorphism can be approached in a holistic manner, considering newer treatments for dyslipidemia of T2DM, applying genetically guided personalized therapies. 

Hyun-Chul Kim

E & M Psychiatry Clinic, Republic of Korea

Title: Dysthyroidism : Is this one of suicide squads?

Time : 14:15-14:45

Speaker
Biography:

HyunChul Kim is Graduated from Gyeong Buk Medical University (1999) Degree of Master/Post Graduate diploma/School of psychiatry, Hallym University (2004) A doctor for compulsory military service (2004-2007) Director of Mental Health Promotion Center, Daegu Suseong District (2007-2011) EMDR therapist course completed (2011). Member of the International Association of Self Psychology (IASP) (2011) International Member of American Psychiatric Association (2018) Corresponding Member of the European Congress of Neuropharmacology (2018).
 

Abstract:

For a decade S. Korea has the highest suicide rate among OECD countries even with fabulous medical check-ups and insurances. But unfortunately, Thyroid Function Test(TFT) has not been included in routine check-ups. Even if asked, blood sampling and follow-up is relatively ignored compared with expensive ultrasonography to rule out cancer, which threatens to everyone . Many symptoms of psychiatric disorder are known to be interfered by dysthyroidism. But in the case of subclinical dysthyroidism, treatment strategies are controversial. We’ve found how many psychiatric outpatients are suffered from subclinical dysthyroidism and their relation with autonomic nerve system activity and clinical improvement.
 
METHODS: The 335 outpatients in this study were recruited and 244 subjects who meet diagnostic criteria of Schizophrenia spectrum disorder, Affective spectrum disorder, Panic disorder. Heart Rate Variability(HRV) Tests and blood sampling to check Thyroid hormone were performed to all patients, both of which results are not interfered by any intention. Clinical Global Improvement Scale was used to know the effect of thyroid treatment in subclinical dysthyroidism. Descriptive statistics were used to check how many patients recognized dysthyroidism for the first time and ANCOVA was used to evaluate the differences between euthyroid and dysthyroid group in symptoms and autonomic nerve system activities. Partial correlation and Multiple regression analysis were conducted to determine thyroid hormone as a predictive value.
 
CONCLUSION: CGI score (not shown above) in dysthyroid group after administration of T4 showed significant improvement (p<0.01),especially co-morbid addiction pathology with panic disorder and with Depressive disorder. This Study has successfully proved via HRV test that Thyroid Hormone, which relates with oxidative stress and neuronal degeneration, can be one of major predictive factors in planning treatment strategy and assuming prognosis. Repeated multi-centered study will be required to validate this result, so as to be one of references in planning national suicide prevention program.
 

Sermin Kesebir

NPIstanbul Brain Hospital, Turkey

Title: Metabolic Syndrome and Psychotropic Drugs

Time : 14:45-15:15

Speaker
Biography:

Born in Germany in 1972. She completed her specialist education at Ege University. During his professional life, she worked as a psychiatric specialist in a general medical hospital, as a associate professor of psychiatry in the second largest mental health hospital in the Turkey. Since 2014, as a professor of psychiatry she has taught at Üsküdar University and has been worked with bipolar disorder in NPIstanbul Brain Hospital. Another area of interest is psychoanalytic psychotherapies. 

Abstract:

According to Vancampfort et al.’s meta-analysis, antipsychotic use significantly explained higher MetS prevalence estimates in major depressive disorder (MDD), (2013b). Differences in MetS prevalences were not mediated by age, gender, geographical area, smoking, antidepressant use, presence of psychiatric co-morbidity. In another study, there was some mediating role for tricyclic and non-selective serotonin-reuptake inhibitor antidepressant use but overall, the mediating role of clinical differences were limited (Luppino et al. 2014). When Margary et al. evaluated 83 psychiatric inpatients diagnosed with schizophrenia, bipolar disoreder and MDD they found a positive association between antidepressant drug treatment with triglycerides, and triglycerides/HDL ratio levels and antipsychotics drugs with the HOMA and Framingham index (2013). In Perugi et al.’s study, duration of pharmacological treatment and age at onset of first major episode were associated with the presence of comorbid MetS (2015). Time of onset for affective disorders and medical conditions were relatively concurrent. When comorbidity of medical conditions were evaluated in terms of phases of bipolar disorder, possibly they are more prevalent at onset and earlier episodes. This is because early mortality is observed more in patients with earlier onset (Goldstein et al. 2009). Comorbid medical conditions that emerge in middle stages of bipolar disorder would possibly be related to the effect of treatment and effects of patient’s habits and lifestyle. However it was showed that even in these circumstances they emerge one decade earlier than the age-matched subjects without bipolar disorder. When all these findings are taken together, it seems that MetS is one of the variables which is in a position as both an initiator and an outcome of bipolar disorder.
 

Neda Seyedsadjadi

University of New South Wales, Australia

Title: Visceral fat mass: Is it the link between uric acid and diabetes risk?

Time : 15:15-15:45

Biography:

Neda Seyedsadjadi has her expertise in evaluation and passion in improving the health and wellbeing. She is a PhD student at University of New South Wales working on how lifestyle behaviors are associated with subclinical changes in biomarkers associated with non-Communicable Diseases (NCDs) such as diabetes. This will assist in on time and appropriate prevention of this prevalent disease.
 

Abstract:

Uric acid (UA) has been suggested as a novel risk factor for diabetes. However, as it is also accompanied with other major risk factors such as obesity and high visceral adiposity, its definite role in this area is still the subject of discussion. Therefore, in this study we aimed to investigate the associations between plasma UA and fasting plasma glucose, HbA1c, lipid profile and inflammatory markers after accounting for the contribution of other diabetes risk factors such as BMI and VAT fat mass. In a cross-sectional study, 100 non-diabetic middle-aged males and females were recruited. Central fat distribution measures including android to gynoid fat ratio, VAT and Subcutaneous Adipose Tissue (SAT) fat mass were determined using Dualenergy X-ray Absorptiometry (DXA). Biochemical analysis was done using methods well established for clinical and research laboratories. Multiple linear regression analysis was performed to do statistical analysis. UA was positively associated with body mass index (BMI) (r(98)=0.42, P≤0.001), android to gynoid fat ratio (r(98)=0.62, P≤0.001) and VAT fat mass (r(96)=0.55, P≤0.001). UA was also positively associated with plasma glucose (r(98)=0.33, P≤0.001), HbA1c (r(93) =0.25, P=0.014), triglyceride (rs(95)=0.40, P≤0.001), HDL-cholesterol (r(98)=−0.61, P≤0.001) and CRP (rs(98)=0.23, P=0.026). However, these associations were no longer significant after accounting for BMI or/and VAT f vat mass. No significant association was observed between UA and SAT fat mass (r(97)=0.02, P≥0.05), Total cholesterol (r(98)=0.03, P≥0.05), LDL-cholesterol (r(98)=0.13, P≥0.05), TNF-α (r(97)=0.12, P≥0.05) and IL-6 (r(96)=−0.02, P≥0.05). Our results suggest, for the first time, that VAT fat mass plays a major role in linking plasma UA and glucose in a non-diabetic population.
 

Biography:

Mennatallah A. Ali is currently a Lecturer at Pharmacology & Therapeutics Department, Faculty of Pharmacy & Drug Manufacturing, Pharos University in Alexandria since 2008. He obtained my Ph.D. degree in Pharmacology from Faculty of Pharmacy, Cairo University in 2015. The Master degree of Pharmacology and Experimental Therapeutics was obtained from Medical Research Institute, Alexandria University in 2012. Bachelor degree in Pharmaceutical Sciences was from Faculty of Pharmacy, Ain Shams University in 2007. He worked as a community pharmacist since her graduation as he was keen on patient counseling and advising. My research motivation is to explore the underlying molecular mechanisms that potentiate the therapeutic beneficial effects of any antidiabetic agent and to discover any new compounds that can be used as adjuvants to treat diabetes mellitus

Abstract:

There has been a recent explosion of interest in the notion that metaflammation and activation of the innate immune system are closely involved in the pathogenesis of type 2 diabetes mellitus (T2DM). Hence, we assessed the potential antidiabetic effect of leflunomide (10 mg/kg every other day) and sulfasalazine (100 mg/kg/day), in a comparison with pioglitazone (5 mg/ kg/day) as a reference drug, using neonatal STZ animal model. All treatments were gavaged for 8 weeks. Leflunomide and sulfasalazine lowered significantly the n5-STZ-induced elevation in body weight, blood glucose, and HOMA index. Moreover, they amended successfully serum lipid profile and increased serum insulin level. Additionally, leflunomide and sulfasalazine showed antioxidant (Nrf2, keap1), anti-inflammatory (NF-κB, TNF-α) and anti-apoptotic (caspase-3, cytochrome c) capabilities. Both drugs showed comparable effects on almost all the parameters, however, pioglitazone effect was superior to both. On the molecular level, drugs have improved the hepatic insulin (glucokinase, p-insulin receptor, p-Akt, IRS-1), lipogenic (SREBP-1c, PGC-1α) and Wnt/β-catenin (p-GSK-3β, β-catenin, FOXO) signaling pathways. All treatments also showed decreases in the hepatic 8-oxoguanine content. The present results clearly proved that altered immune responses play a key role in T2DM and that the immunomodulatory drugs can gain insights as prospective antidiabetic agents.
 

Biography:

Abstract:

Background: Metformin is a standard therapy, most commonly prescribed oral hypoglycemic agent for individuals with type2 diabetes (T2DM). Many studies also documented the association between long-term metformin use and low vitamin B12 levels among individuals with T2DM.To the best of our knowledge, studies on the association between long term metformin use and low vitamin B12 levels among individuals with T2DM are scarcely found in Ethiopia.

Objective: To determine the status of vitamin B12 deficiency and associated risk factors in type 2 diabetes mellitus patients taking metformin treatment attending diabetic clinic of the Tikur Anbesa Specialized Hospital (TASH), Addis Ababa, Ethiopia.

Methods: Institutional based cross-sectional study was conducted from March 01/ 2017 to June 30/2017 at diabetic clinic of TASH. The study participants were all patients with a diagnosis of T2DM on follow up at the clinic during the study period and having a baseline data. Blood samples were collected and Vitamin B12 levels were determined by cobas e411 analyzer by electro chemiluminescence immunoassay. Neuropathy Total Symptom Score-6 questionnaire (NTSS-6 scores) was used to compare severity of PN in both groups. Finally data was entered and analyzed through SPSS version 20 computer software packages. Results: Serum B12 levels were low in 15 patients (21.1%) on metformin as compared to 2 patients (4.0%) without metformin treatment. Mean B12 level on metformin were found to be 331.58 pg/ml(± 134.48) as compare to those without metformin 482.23pg/ml(± 235.24), the difference was statistically significant with p value 0.000. A strong negative correlation between serum B12 levels and the duration of metformin use (r = -0.608; P = 0.000) was seen.

Conclusion: Among patients with T2DM treated with metformin had low serum B12 levels than patients not treated by metformin with significant effect of metformin dose and duration on B12 levels. The deficiency was not associated with peripheral neuropathy.

Speaker
Biography:

Lakshmi M L is currently employed in Cancer Research Program Lab at Rajiv Gandhi Center for Biotechnology, India. She is a Senior Research Fellow of University Grants Commission (UGC), Government of India. She is having 4 years of research experience and is currently working on the elucidation of mechanistic regulation of ezrin in in Estrogen Receptor (ER) positive thyroid carcinoma cells

Abstract:

Thyroid carcinoma is 3-4 times more prevalent in women than in men and this preponderance can be linked to age, sex, iodine deficiency, and diet and radiation exposure. Certain factors like genetics, sex hormones and environment are reckoned to predispose a person to thyroid carcinoma. These data suggests the role of the sex steroid estrogen in the pathogenesis of thyroid carcinoma. It is clearly demonstrated that like breast and ovary, thyroid is also an estrogen responsive tissue. So in this study we checked the effect of 17-β Estradiol in the invasion of thyroid carcinoma. Cancer cell metastasis involves the formation of lamellipodia and filopodia. The formation of these structures is related to rapid activation of Ezrin/Radixin/Moesin (ERM) family of proteins. It is reported that ezrin was highly overexpressed in metastatic cancer cell lines when compared to poorly metastatic counterparts. We investigated influence of genomic and nongenomic actions of 17-β estradiol on ezrin. Genomic pathway is a long delayed process. Beyond the conventional genomic pathway, the nongenomic pathway of 17-β Estradiol is a transient process which lasts for few minutes. The phosphorylated ezrin can interacts and activates many signaling molecules which are important for cancer cell proliferation, invasion and metastasis. Further we have to investigate the upstream kinase causing the phosphorylation of ezrin and various expression patterns of ezrin and phosphoezrin ex vivo. Genomic pathway which is a long delayed process through ER alpha increased the expression of ezrin in a time dependent and dose dependent manner we observed a transient phosphorylation of ezrin by17-β Estradiol which lasts only for a few minutes. This process was sensitive to inhibitors. We observed that 17-β Estradiol can cause both the increased expression and activation of ezrin which occurs through the estrogen receptors suggesting that thyroid is also a target for estrogenic action. Such studies may lead to a new understanding of the pathogenesis of thyroid cancer and its female bias.