ISSN:
1432-0428
Keywords:
Mutation ob/ob
;
obese mouse
;
streptozotocin
;
insulin resistance
;
hyperphagia
;
spontaneous diabetes
;
diabetes in mice
;
obesity in mice
;
hereditary obesity
;
obese-hyperglycaemic mice
;
B-cells
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary 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 replacement 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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00428986
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