Dr. Ben B. Yaspelskis, III
(818) 677-7509

Long term objectives:

To determine if chronic leptin administration improves skeletal muscle insulin resistance, due in part to an alteration in visceral fat deposition.

Background:

Obesity, especially extensive visceral adipose deposition , is associated with resistance to insulin-stimulated skeletal muscle glucose uptake and may ultimately lead to the development of non-insulin-dependent diabetes.  Chronic administration of leptin, the product of the ob gene has been shown to reduce fat mass, foot intake, hyperglycemia  hyperinsulinemia.

Importance:

Individuals who exhibit a compensatory elevation their blood insulin levels for maintenance of glucose homeostasis may become predisposed to develop a number of metabolic abnormalities.  These include elevated triglycerides, reduced high-density lipoproteins, elevated apolipoprotein B levels and hypertension, which are collectively said to comprise syndrome X or "insulin resistance syndrome".

As it has been shown that skeletal muscle insulin resistance is the first step in developing abnormalities in the metabolic pathways which may ultimately lead to the development of non-insulin-dependent diabetes then it is of importance to ascertain whether the administration of leptin may reverse the development of skeletal muscle insulin resistance.  Thus, the overall goal  of the proposed investigations are to determine if chronic leptin treatment improves insulin-stimulated glucose uptake and transport in insulin-resistant skeletal muscle and to identify the cellular adaptation that account for the improved insulin responsiveness.

Summary:

Experimental Methods:

Muscle metabolism analyses
Blood and muscle substrate analyses
Muscle enzymatic analyses
Bradford protein analysis
SDS-PAGE
Subcellular fraction procedures

Computer Analyses (PC Based):

MAC and IBM based MS Work, Excel and Power Point
Statview, NIH Image

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Report Writing:

Journal format