Psammomys obesus and the albino rat - two different models of nutritional insulin resistance, representing two different types of human populations

Animal models for insulin resistance and type 2 diabetes are required for t he study of the mechanism of these phenomena and for a better understanding of diabetes complications in human populations. Type 2 diabetes is a syndr ome that affects 5-10% of the adult population. Hyperinsulinaemia, hypertri glyceridaemia, 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 s yndrome or syndrome X. The gerbil, Psammomys obesus is characterized by pri mary insulin resistance and is a well-defined model for dietary induced typ e 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 de termine the development of metabolic changes leading to diabetes. Feeding P sammomys on HE diet resulted in hyperglycaemia (303 +/- 40 mg/dl), hyperins ulinaemia (194 +/- 31 muU/ml) and a moderate elevation in body weight, obes ity and plasma triglycerides. Albino rats on HE diet demonstrated an elevat ion in plasma insulin (30 +/- 4 muU/ml), hypertriglyceridaemia (170 +/- mg/ dl), an elevation in body weight and obesity, but maintained normoglycaemia (98 +/- 6 mg/dl). Psammomys represent a model that is similar to human pop ulations, with primary insulin resistance expressed in young age, which lea ds to a high percentage of adult type 2 diabetes. Examples for such populat ions 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 ad vantage of its capacity for a constant accumulation of adipose tissue that will serve for maintenance and breeding in periods of scarcity. This metabo lism known as 'thrifty metabolism', is compromised at a high nutrient intak e.