B.Sc. (Summa Cum Laude)
Faculty of Life Sciences
Tel Aviv University
Tel Aviv, Israel.
M.Sc.
Department of Physiology
Faculty of Medicine
University of Toronto
Toronto, Ontario, Cananda.
Ph.D. Candidate
Department of Immunobiology
School of Medicine
Yale University
New Haven, CT, USA
Project Title: Leptin and The Hypothalamo-Pituitary-Adrenal Axis (HPA) in Streptozotocin
(STZ) Diabetic Rats.
Research:
Hypoglycemia is a major complication of type 1 diabetes mellitus, and is the predominant limiting factor in the improvement of glycemic control. In type 1 diabetes, hypoglycemia arises from the interplay of excess insulin and deficient counterregulation. Leptin per se or in combination with insulin treatment may normalize the basal HPA activity and the counterregulatory. Furthermore, leptin’s ability to increase insulin sensitivity can lead to a decrease in exogenous insulin, thus minimizing the possibility of antecedent hypoglycemia and the impaired counterregulatory responses to acute hypoglycemia in Type I diabetes.
I have shown that leptin normalization without insulin treatment can increase HPA activity and epinephrine (EPI) release while decreasing norepinephrine levels in STZ-diabetic rats. Most interestingly, following leptin normalization STZ-diabetic rats demonstrated a decreased diabetes-associated hyperphagia. Paradoxically, even though rat treated with leptin showed a decrease in food consumption when compared to vehicle-treated diabetic rats, both groups showed similar weight gains throughout the treatment period. On the other hand, pair feeding per se resulted in severe weight loss in diabetic rats. Corticosterone levels and rhythmicity, lost in diabetic rats, were normalized after leptin administration. Radioimmunoassays, brain sectioning and molecular analysis were conducted to evaluate the physiological changes in the HPA axis and catecholamines among the different groups.
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