HIGH LEVELS OF PANCREATIC INSULIN COEXISTENT WITH HYPERPLASIA AND DEGRANULATION OF BETA CELLS IN MICE WITH THE HEREDITARY OBESE-HYPERGLYCEMIC SYNDROME¹

Reporter islets in the eye reveal the plasticity of the endocrine pancreas

“…Because direct inspection of these islets is obstructed due to the fact that they are deeply embedded and scattered within the pancreas, we propose the use of "reporter islets" transplanted into the anterior chamber of the eye, serving as optically accessible indicators of islet plasticity in the pancreas and as a tool to individually assess effectiveness of specific treatment regimens. in apparent degranulation (10), and the development of insulin resistance.…”

“…In addition, leptin receptors are expressed in beta cells and are involved in an adipo-insular feedback loop inhibiting insulin expression and release after food intake (8,9). The lack of leptin in the ob/ob mouse thus results in a rapid increase in body weight and, in an effort to compensate for the increased demand for insulin, beta cell hyperplasia (10). As a result the islet cell population is altered in the ob/ob mouse; the percentage of beta cells compared with other endocrine cells is particularly high, accounting for more than 90% of the total islet cells (11).…”

Pancreatic Islets in Mice with the Obese-hyperglycemic Syndrome: Lack of Effect of Carbutamide

“…have been recorded), hypercholesterolemic, show high blood glucose levels generally further increased by the administration of growth hormone, 1 an increased lipogenesis even when fasted, 2 increased glycogen turnover, 3 increased liver phosphorylase,* and a number of other nutritional, endocrine and behavioral idiosyncrasies. 5 Of particular interest from the etiological point of view is the fact that the islets of Langerhans are grossly hypertrophied, 6 " 8 that the insulin content of the pancreas is increased, 7 that the insulin-like activity of their serum is greater than that of the nonobese animals, 9 that diethyldithiocarbamate, which Kadota and Midorikawa found to be alphacytotoxic, 10 decreases blood sugar and eliminates the hyperglycemic reaction to growth hormone 11 and that the pancreatic glucagon content appears increased after growth hormone administration. 13 It has also been found that carbutamide did not correct the defects in carbohydrate metabolism 13 and in fat metabolism 14 found in these animals.…”

Obesity, Diabetes and Leptin: Lessons Learned from Obese Hyperclycemic Mice

“…32 The obese hyperglycemic syndrome is characterized by an increase in the extractable insulin of pancreas in both young (2 months old) and mature (4 months old) ob/ob mice than their lean littermates. 37,41 Whereas the pancreatic content of glucagon and pancreatic polypeptide are higher in ob/ob mice [42][43][44][45] the somatostatin content of, and release from, pancreatic islets is approximately 6 times lower than that in islets of the lean mice. 46 …”

“…There are signs of β-cell degranulations in islets from obese mice with increased nuclear and nucleolar size. 1,[37][38][39] The islets of the obese mice are remarkably hyperemic; 30,39,40 pseudocysts, dilated ducts and dilated capillaries are also common findings in ob-mouse islets. 32 The obese hyperglycemic syndrome is characterized by an increase in the extractable insulin of pancreas in both young (2 months old) and mature (4 months old) ob/ob mice than their lean littermates.…”