Carrick Institute

ISCN 2016 – Endocrinologist & Diabetes Expert Dima Abdelmannan, M.D.

 

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Dr DimaWe are proud to announce the addition of DimaAbdelmannan to our speaker list for this years ISCN.

Dr. Dima Abdelmannan is Professor of Medicine and Dean of Clinical Medicine at the Dubai Medical College in Dubai. U.A.E . She is also a Consultant Endocrinologist at the Dubai Diabetes Center at Dubai Health Authority. Dr. Abdelmannan completed her post-graduate education in the UK then the USA . In the USA, She completed her internal medicine training at Cleveland Clinic Health System and then completed fellowship training in Endocrinology, Diabetes and Metabolism at Case Western Reserve University, in Cleveland, OH. Dr. Abdelmannan continued to do clinical and research work at the same institution for several years before returning to Dubai, UAE.  Her research work is in the field of Pituitary and Adrenal diseases as well as Diabetes.  Dr. Abdelmannan has been interested in Medical Education besides clinical endocrinology and research, and therefore accepted a faculty position at the medical school in Dubai in order to contribute to improving the standards of medical education globally. Dr. Abdelmannan is a clinical scholar at Harvard Medical School and is also a scholar of the Harvard Macy Institute where she is actively involved in implementing efficient ways in medical pedagogy including simulation and e-learning.

Her presentation is an exciting look at her research and clinical applications specific to Type 2 Diabetes.  She will explore her research involving the identification of risk factors for this disorder and provide insights into further diagnosis and treatment using a nonpharmacologic approach.  Her presentation is in 2 parts as follows:

Nonpharmacologic Treatment for Type 2 Diabetes
Type 2 Diabetes Mellitus (T2DM) encompasses two key pathophysiologic defects: increased insulin resistance and relative or absolute insulin secretory deficiency. Focusing on these two abnormalities to normalize glucose levels in someone with T2DM, one must either decrease insulin resistance or increase the amount of available insulin to compensate for a given degree of insulin resistance. Non-pharmacological treatments have been proven effective in the treatment of T2DM.

The major components of non-pharmacologic therapy of blood glucose in type 2 diabetes are dietary modification , exercise and weight reduction. Dietary modification is the process by which the dietary plan is tailored for people with diabetes, based on medical, lifestyle, and personal factors. It is an integral component of diabetes management and diabetes self-management education. Weight reduction for patients with type 2 diabetes who are overweight (BMI ≥25 to 29.9) and obese (BMI ≥30), major emphasis should be placed on lowering caloric intake, increasing physical activity, and behavior modification to achieve weight loss. Exercise and muscle metabolism: As in normal individuals, exercise has both short (e.g. Improves insulin sensitivity) and long-term (e.g. improving exercise capacity) effects on carbohydrate metabolism in diabetic patients as it does in nondiabetics.

Can we identify people at risk for T2DM earlier using a single dose of Dexamethasone? –
Type 2 Diabetes (T2DM) is an on-going process that develops over the span of many years. Several risk factors are known to predispose non-diabetic individuals to diabetes. Family history and obesity are the best predictors among the other known risk factors (diet, life style, impaired glucose tolerance (IGT), impaired fasting glycemia (IFG), etc.). Yet, not all subjects with the mentioned risk factors become diabetic. Because the genetic predisposition to T2DM causes impaired insulin secretory response to insulin resistance, it follows that, induction of insulin resistance in an insulin sensitive individual and monitoring the beta cell response to this insulin resistance will unveil the genetic predisposition of T2DM. Dexamethasone (DEX), a glucocorticoid, causes insulin resistance in skeletal muscle and liver and results in increased rate of hepatic glucose production. We characterized the dynamic changes in plasma glucose and insulin concentration in normal glucose tolerant individuals in response to acute exposure to DEX. We have demonstrated that normal glucose tolerant individuals manifest a dose response increase in insulin secretion during the OGTT 24 hours following DEX administration. Looking at a high-risk non-diabetic patient ( e.g. offspring of two diabetic parents), insulin resistance caused by single DEX administration, similar to that caused by elevation of plasma FFA concentration, will result in a decrease in insulin secretion and beta cell function. The results of these studies will demonstrate that “metabolic stress by single DEX administration” produces a differential response in insulin secretion that will distinguish between subjects who are genetically predisposed to develop T2DM and subjects without genetic predisposition to T2DM, and therefore, the former group is at an increased risk of future T2DM. Early identification of people who will develop type 2 DM through a cost-effective test that can be potentially applied to the community is the main potential significance of this study.

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