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Dr. Grasso's major area of investigation is focused on the molecular mechanisms by which synthetic peptide leptin mimetics influence energy expenditure, glucose homeostasis, serum lipids, and cognitive function. Our laboratory has recently shown that oral administration of synthetic peptides representing discreet domains of mouse leptin, reduces food intake, body weight gain, and serum glucose levels, normalizes serum lipid profiles, increases tissue sensitivity to insulin peripherally and in the brain, and improves episodic memory.  These observations indicate that the entire leptin molecule is not required for its metabolic and neurologic effects, and that smaller peptides encompassing one or more active domains of leptin may contain sufficient information to (a) compensate for endogenous leptin deficiency or defective transport across the blood-brain barrier, (b) induce satiety, (c) stimulate weight loss, (d) regulate blood glucose and serum lipid levels, and improve episodic memory.  Alzheimer’s Disease (AD) has been called “Type 3 diabetes” because of its association with insulin resistance in the brain, suggesting a very strong metabolic influence on cognitive function.  We are currently investigating the effects of leptin mimetics on this link in mouse models of AD, vascular dementia, and Down syndrome.