Atherosclerosis and insulin in primates with diabetes mellitus.
The most commonly available primate models of diabetes mellitus are of the insulin-dependent type and are attained through beta cell ablation techniques. Noninsulin-dependent primate models are less common since the animals must have a genetic predisposition to diabetes. Few studies have been conducted on lipid or vascular abnormalities associated with diabetes in primates. Diabetes develops spontaneously in Macaca nigra as the result of a lesion in the islets of Langerhans. As secretory cells are gradually lost, mild to moderate hyperglycemia, impaired glucose clearance, acute insulin release, hyperglucagonemia, and chronic hypoinsulinemia develop. Overtly diabetic monkeys require insulin therapy and thus alternate between hypoinsulinemia and hyperinsulinemia. The development of aortic atherosclerosis correlates positively with the severity of metabolic impairment. Lipid deposition is primarily extracellular and there is a paucity of foam cells. The very low density and intermediate-density lipoprotein fractions increase significantly, the low-density lipoprotein fraction increases slightly, and the high-density lipoprotein fractions remain essentially unchanged. Because these monkeys are maintained on a nonatherogenic chow ration, the effects of diabetes, per se, on vascular sclerosis can be evaluated.
D000818:Animals; D001161:Arteriosclerosis / Q000150:complications / Q000662:veterinary; D003920:Diabetes Mellitus / Q000473:pathology / Q000662:veterinary*; D003922:Diabetes Mellitus, Type 1 / Q000662:veterinary; D003924:Diabetes Mellitus, Type 2 / Q000662:veterinary; D003925:Diabetic Angiopathies / Q000662:veterinary; D004195:Disease Models, Animal; D007328:Insulin / Q000627:therapeutic use*; D007515:Islets of Langerhans / Q000473:pathology; D008074:Lipoproteins / Q000378:metabolism; D008251:Macaca
D007328:Insulin; D008074:Lipoproteins