PSAMMOMYS OBESUS AND THE ALBINO RAT — TWO DIFFERENT MODELS OF NUTRITIONAL INSULIN RESISTANCE, REPRESENTING TWO DIFFERENT TYPES OF HUMAN POPULATIONS

R. Kalman, Hebrew University of Jerusalem

 Animal models for insulin resistance and type 2 diabetes are required for the study of the mechanism of these phenomena and for better understanding of diabetes complications in human populations. Type 2 diabetes is a syndrome affecting 5-10% of the adult population. Hyperinsulinemia, hyperglyceridemia, decreased high-density lipoprotein (HDL) cholesterol levels, obesity and hypertension, all form a cluster of risk factors that increase the risk of coronary artery disease, and are known as insulin resistance syndrome or syndrome X. The gerbil, Psammomys obesus is characterized by primary insulin resistance and is a well-defined model for dietary induced type 2 diabetes. Weanling Psammomys and Albino rats were held individually for several weeks on High Energy (HE) and Low Energy (LE) diets in order to determine the development of metabolic changes leading to diabetes. Feeding Psammomys on HE diet resulted in hyperglycemia (303±40 mg/dl), hyperinsulinemia (194±31 µU/ml) and moderate elevation in body weight, obesity and plasma triglycerides. Albino rats on HE diet demonstrated elevations in plasma insulin (30±4 µU/ml), hyperglyceridemia (170±11 mg/dl), elevation in body weight and obesity, but maintained normoglycemia (98±6 mg/dl). Psammomys represents a model that is similar to human populations with primary insulin resistance expressed in juveniles, which leads to a high percentage of adult type 2 diabetes. Examples of such populations are the Pima Indians, Australian Aborigines and many other third world populations. The results indicate that the metabolism of Psammomys is well adapted towards life in a low energy environment, where Psammomys takes advantage of its capacity of constant accumulation of adipose tissue that will serve it for maintenance and breeding in periods of scarcity. This metabolism is known as thrifty metabolism and is compromised at a high nutrient intake.

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