Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 9th International Conference on Endocrinology and Diabetes Summit Singapore.

Day 1 :

Keynote Forum

Juan C Calderon

University of Antioquia, Colombia

Keynote: The new endocrine role of skeletal muscle myokines

Time : 12:05-12:50

OMICS International Endocrinology Summit 2017 International Conference Keynote Speaker Juan C Calderon photo

There has been a recent change in the way scientists understand skeletal muscle functions. It is not only a tissue that generates force and movement, but a one that regulates its own functions and others by means of myokines secretion. Myokines are small peptides or proteins with autocrine, paracrine and endocrine functions. Some of them have long been known, such as cytokines and growth factors, but others are new such as musclin, myostatin, myonectic, apelin and irisin. They are regulated by exercise, muscle fiber type, caloric intake and several humoral stimuli. Their structure and receptors are now been sought. These molecules have regulatory effects on immune (inflammation), metabolic (insulin resistance/sensitivity and fat metabolism) and cardiovascular (blood pressure and angiogenesis) systems. They are important to understand the complex crosstalk between muscle-exercise-adaptations and muscle-sedentarism-chronic diseases. New myokines as well as their regulation and functions are likely to be discovered in the near future. Also, their therapeutic use is expected. Our research groups (PHYSIS and GRINMADE) have been exploring the relationships between muscle mass, fiber types and myokines in several populations in Colombia. We have found a protective effect of thigh muscle mass on metabolic disease, but not a direct relationship between musclin and insulin resistance in patients with metabolic syndrome. Preliminary results also show a regulation of musclin by a high intensity exercise bout in these patients. In conclusion, the skeletal muscle works too as an endocrine organ, whose study will help us understand the pathophysiology of some chronic diseases and also envision diagnostic and therapeutic tools to tackle them.


Juan C Calderon is a Medical Doctor, completed his PhD in Physiology, devoted to understand different functions of skeletal muscle. His work has been related to excitation-contraction coupling, calcium signaling and muscle fatigue.

Keynote Forum

Lynn Ge-Zerbe

Boise Thyroid & Endocrinology PC

Keynote: What do we know about artificial sweetener and its relationship with obesity and diabetes epidemic?

Time : 09:30-10:15

OMICS International Endocrinology Summit 2017 International Conference Keynote Speaker Lynn Ge-Zerbe photo

Lynn Ge-Zerbe is a recipient of the Leading Physician of the World and Pinnacle Professional of the Year 2017 award. She is board certified in Endocrinology and Internal Medicine, the Owner of Boise Thyroid & Endocrinology PC, a concierge endocrinology and weight loss practice, the Principle Investigator of Advanced Clinical Research, a Consultant Endocrinologist with RubiconMD and Video Medicine. She has earned her MD at PUMC, MPH of Epidemiology at University of Pittsburgh, Post-doctoral Fellowship in Molecular Medicine at NIH, Residency in Internal Medicine at Leigh Valley Hospital, Penn State University, Fellowship in Endocrinology at Vanderbilt University as well as Age Management Certification by AMMEF. She is passionate in combining east and west medicine to cure and prevent endocrinology disorders.


Obesity is among the most common and costly chronic disorders worldwide. The new epidemic is in Asia countries. Growing evidence suggests that obesity is a disorder of the energy homeostasis system. Weight control is important for reducing the risk of metabolic disease such as diabetes. Obesity and diabetes epidemic coincides with an increase in the widespread use of artificial sweetener in modern diet for weight control by retaining sweet taste without increase caloric intake. However, research studies suggest that artificial sweetener may contribute to weight gain instead of weight loss. Artificial sweetener caused weight gain may have multiple etiology. The new study shows that sweetness helps to determine how calories are metabolized and signaled to the brain. When sweetness and calories are matched, the calories are metabolized and this is registered by brain reward circuits. However, when a mismatch occurs, the calories fail to trigger the body’s metabolism and the reward circuits in the brain fail to register that calories have consumed. As a result, artificial sweetener triggers food seeking behavior and may contribute to obesity. Calories are only half of the equation; sweet taste perception is the other half. A sweet-tasting low calorie drink can trigger a greater metabolic response than drinks with higher calories, explaining the association between artificial sweeteners and diabetes discovered in earlier studies. Studies found artificial sweetener intake can induce excess activation of sweet taste receptor and evoke GLP-2 release, in turn, increase SGLT1 expression and mucosal growth. SGLT1 as a prime intestinal glucose transporter plays important role in intestinal glucose sensing and incretin secretion. So, artificial sweeteners encourage sugar craving and sugar dependence as well as alter glucose tolerance. Studies also showed that consumption of artificial sweetener drives the development of glucose intolerance through induction of compositional and functional alterations of the intestinal microbial. Numerous studies have indicated an important role of the gut microbiome in body weight control and glucose metabolism and regulation.




Keynote Forum

S Chhabra

Mahatma Gandhi Institute of Medical Sciences

Keynote: Hypertensive disorders during pregnancy: A disease of dilemmas and dangers

Time : 10:15-11:00

OMICS International Endocrinology Summit 2017 International Conference Keynote Speaker S Chhabra photo

S Chhabra is a Director Professor of Obstetrics and Gynecology in the College of Mahatma Gandhi Institute of Medical Sciences, India and CEO of Akanksha Shishu Kalyan Kendra and OSD in Dr. Sushila Nayar Hospital, Sewagram.


Hypertensive disorders during pregnancy (HDsP) disease of dilemmas with dangers to mother/baby are difficult to predict with limitations to prevention. Some studies have revealed blood/urinary calcium inverse relationship to HDsP, so researchers believe calcium has a role, others refute. Problem seems to be at cellular level, needs to be investigated. Extra calcium as program needs more research. Concept of early onset (EO HDsP), late onset (LO HDsP), two entities with different etiologies, pathologies, effects on baby, mother, long term sequel is modern. LOHDsP are believed to be related to maternal constitution, EO HDsP probably have placental origin with interplay between maternal constitution, placental factors, inappropriate adaptive changes in pregnancy, predominantly involving cardiovascular, inflammatory system. EO is believed to be associated with increased arterial stiffness that extends beyond pregnancy with adverse vascular outcomes. Studies are being done about genetic variations, immune system association between HCG, a variety of thrombophilic disorders and EOHDP. In one of studies, HDsP contributed to 11.6% obstetric admissions. 17.8% births, 212 (5.6% of 3780 HDsP) were severely ill, case fatality was 0.5% of HDsP, 9% of severely ill (19 of 212), 43% (9 of 21) of severely ill with HELLP. Another study of 1046 cases HDsP represented 11.73% of 8920 births. Mean gestation at birth in HDsP of 20 to <28 weeks (A) was 30±1 weeks, between >28 to <34 weeks, (B) 32±6, between >34 to <37 weeks (C) 35±4 weeks, 37 weeks (D) 38±4 weeks. Mean birth weight in very early gestation cases was 1741.54 gms, in >28 to <34 weeks 1936.31 gms, >34 to 37 weeks 2633.38 gms and >37 weeks 2677.30 gms. Perinatal deaths in very early HDsP were 45%, >28 to <34 weeks 25.13%, >34 to <37 weeks 14.32%, >37 weeks 14.00%. Most of EO HDsP was primigravida of younger age with severe rapidly progressive disease with significantly higher multiorgan disorders, liver dysfunction, HELLP, renal failure. Placental abruption occurred in 25% in A, 14.66% B, 3.79% C, 2.67% D. Conservative management improved fetal outcome, but maternal mortality morbidity is concerned. LO HDsP also could become dangerous. Around 34 weeks survival was similar to term. Role of aspirin, calcium has been documented for prevention but continues to be surrounded by controversies. Studies are also being done about vitamin C and E for prevention of HDsP, some shown benefits, others not. Low-molecular-weight heparin has also been studied with no effect on outcome of EO HDsP.


Keynote Forum

Kriz-Ann R Hernandez

Jose R Reyes Memorial Medical Center, Philippines

Keynote: Prediction model of mortality among patients with diabetic ketoacidosis

Time : 11:20-12:05

OMICS International Endocrinology Summit 2017 International Conference Keynote Speaker Kriz-Ann R Hernandez photo

Kriz-Ann R Hernandez has completed her Doctor of Medicine degree from University of Santo Tomas, Faculty of Medicine and Surgery in Manila, Philippines. She has completed her 3 year’s Residency training in Internal Medicine at Jose R. Reyes Memorial Medical Center in Manila, Philippines. She has served as the Chief Resident from 2011-2012. Her research interests are diabetes mellitus and its related complications. Currently, she serves as a Telemetry Senior House Officer in Asian Hospital and Medical Center since March 2017.


Background & Aim: Diabetes Mellitus (DM) is a major cause of premature mortality globally. One of its acute complications is Diabetic Ketoacidosis (DKA). DKA is a medical emergency wherein abrupt and correct management could prevent patient mortality. Prediction of mortality from DKA could be done using patient’s demographics, clinical profile and laboratory parameters. However, locally, there is no prediction model developed yet to predict mortality. This study aims to create an assessment tool that could accurately predict the risk of mortality among DKA patients within the first 24 hours of admission and correlate patient’s demographics, clinical profile and laboratory parameters with improvement of survival rate.


Methods: This is a retrospective, cohort study which included 129 admitted adult DKA patients. Statistical analysis used was logistic binary regression. Receiving operating characteristic (ROC) curve was done to validate prediction models.

Results: 6 variables identified to predict mortality are patient’s age ≥60 years, severe DKA, non- insulin dependent status, GCS<15, non-normal platelet count and non-normal estimated creatinine clearance. Prediction models developed included and omitted age profile. Cut-off scores of prediction models were validated with the ROC curve. Cut-off score with age was 5 with sensitivity of 73.91% and specificity of 74.70% and the area under the curve is 0.751 which is significant (p=0.0001). On the other hand, cut-off score of the prediction model without age is 4 with sensitivity of 65.22% and specificity of 67.47% and the area under the curve is 0.719 which is significant (p=0.0001).

Conclusion: This study was able to prove that mortality in DKA can be predicted within the first 24 hours of admission using patient’s demographics and significant clinical profile in the prediction models developed.