Effects of long-term restricted insulin production in obese-hyperglycemic (genotype ob/ob) mice.
Primary hypersecretion of insulin has been suggested as one possibility for the genetic fault of ob/ob mice. To test this hypothesis, streptozotocin (SZO) was used to reduce permanently insulin secretion in young lean and obese mice. After establishment of hyperglycaemia and weight reduction in treated obese mice (obese-SZO), daily insulin replacment was begun in some (obese-SZO-Ins). Obese-SZO mice maintained insulin levels and body weights similar to lean controls, though they were shorter and fatter, while food intake and blood sugar levels exceeded lean values. Obese-SZO-Ins mice with reduced islet hyperplasia, but great insulin resistance, gained more weight than obese-SZO mice; had high serum insulin and controlled blood glucose; and exhibited hyperphagia. These results suggest that primary hypersecretion of insulin cannot be the genetic defect, as ob/ob mice are hyperphagic, hyperglycaemic, insulin resistant, and "obese" even when insulin levels are restricted.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D003920:Diabetes Mellitus / Q000378:metabolism / Q000473:pathology / Q000662:veterinary*; D005247:Feeding Behavior / Q000187:drug effects; D006029:Glycosuria / Q000139:chemically induced; D006128:Growth / Q000187:drug effects; D007328:Insulin / Q000502:physiology*; D007333:Insulin Resistance; D007515:Islets of Langerhans / Q000473:pathology; D051379:Mice; D008820:Mice, Obese; D009765:Obesity; D012376:Rodent Diseases / Q000378:metabolism* / Q000473:pathology; D013311:Streptozocin / Q000494:pharmacology
D001786:Blood Glucose; D007328:Insulin; D013311:Streptozocin