Insulin Release in Rats 1 and 5 Days after Hypophysectomy

Heinze, E.; Kleinert, W.; Voigt, Karlheinz

doi:10.1159/000179394

Cited by 12 publications

(4 citation statements)

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“…These findings might be interpreted as a reflection of reduced translational efficiency together with a blunted insulin response to glucose due to the lack of GH. Several studies have shown that the insulin response to glucose is delayed and/or reduced in hypox-rat-isolated islets (Parman 1975) or in hypox rats in vivo (Penhos et al 1971;Heinze et al 1981). In another study, the first and second phase of insulin secretion in the perfused pancreas of hypox rats have been found to be depressed (Curry and Bennett 1973).…”

Section: Discussionmentioning

confidence: 93%

The effect of hypophysectomy on pancreatic islet hormone and insulin-like growth factor I content and mRNA expression in rat

Jevdjović

Maake

Zwimpfer³

et al. 2005

Histochem Cell Biol

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The growth arrest after hypophysectomy in rats is mainly due to growth hormone (GH) deficiency because replacement of GH or insulin-like growth factor (IGF) I, the mediator of GH action, leads to resumption of growth despite the lack of other pituitary hormones. Hypophysectomized (hypox) rats have, therefore, often been used to study metabolic consequences of GH deficiency and its effects on tissues concerned with growth. The present study was undertaken to assess the effects of hypophysectomy on the serum and pancreatic levels of the three major islet hormones insulin, glucagon, and somatostatin, as well as on IGF-I. Immunohistochemistry (IHC), in situ hybridization (ISH), radioimmunoassays (RIA), and Northern blot analysis were used to localize and quantify the hormones in the pancreas at the peptide and mRNA levels. IHC showed slightly decreased insulin levels in the b cells of hypox compared with normal, age-matched rats whereas glucagon in a cells and somatostatin in d cells showed increase. IGF-I, which localized to a cells, showed decrease. ISH detected a slightly higher expression of insulin mRNA and markedly stronger signals for glucagon and somatostatin mRNA in the islets of hypox rats. Serum glucose concentrations did not differ between the two groups although serum insulin and C-peptide were lower and serum glucagon was higher in the hypox animals. These changes were accompanied by a more than tenfold drop in serum IGF-I. The pancreatic insulin content per gram of tissue was not significantly different in hypox and normal rats. Pancreatic glucagon and somatostatin per gram of tissue were higher in the hypox animals. The pancreatic IGF-I content of hypox rats was significantly reduced. Northern blot analysis gave a 2.6-, 4.5-, and 2.2-fold increase in pancreatic insulin, glucagon, and somatostatin mRNA levels, respectively, in hypox rats, and a 2.3-fold decrease in IGF-I mRNA levels. Our results show that the fall of serum IGF-I after hypophysectomy is accompanied by a decrease in pancreatic IGF-I peptide and mRNA but by partly discordant changes in the serum concentrations of insulin and glucagon and the islet peptide and/or mRNA content of the three major islet hormones. It appears that GH deficiency resulting in a ''low IGF-I state'' affects translational efficiency of these hormones as well as their secretory responses. The maintenance of normoglycemia in the presence of reduced insulin and elevated glucagon serum levels, both of which would be expected to raise blood glucose, may result mainly from the enhanced insulin sensitivity, possibly due to GH deficiency and the subsequent decrease in IGF-I production.

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Section: Discussionmentioning

confidence: 93%

The effect of hypophysectomy on pancreatic islet hormone and insulin-like growth factor I content and mRNA expression in rat

Jevdjović

Maake

Zwimpfer³

et al. 2005

Histochem Cell Biol

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“…They were housed under controlled conditions with constant temperature (24-26 C), constant humidity (50-60%), and a 14-h light, 10 pellet food (Type R3, Ewos, Sodertalje, Sweden) ad libitum. This diet consisted of 21% protein, 52% carbohydrates (starch), 6% fat, 11% water, 3.5% fibers, and 6.5% minerals and salts.…”

Section: Animalsmentioning

confidence: 99%

“…Recent studies have indicated that insulin might be an important long term regulator of the glucose transport capacity of adipose tissue (8). The insulin levels are low in hypophysectomized animals (9)(10)(11). To investigate the role of insulin in the changes in glucose metabolism and hormone responsiveness of adipose tissue of hypophysectomized animals, we examined the effects of additional glucose in the drinking water or insulin treatment of hypophysectomized rats on the responsiveness of adipose tissue to insulin and GH.…”

mentioning

confidence: 99%

Effect of Insulin Treatment of Hypophysectomized Rats on Adipose Tissue Responsiveness to Insulin and Growth Hormone*

et al. 1985

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The effects of insulin treatment and dietary glucose on the responsiveness of adipose tissue to insulin and GH after hypophysectomy were studied. Male rats, 130-150 g, were hypophysectomized. Glucose metabolism was measured by determining the production of CO2 from [14C]glucose and the incorporation of glucose into lipids in the epididymal fat pad. Basal levels of glucose oxidation as well as the response to insulin were markedly decreased 7 days after hypophysectomy. In hypophysectomized animals given drinking water containing 10% glucose, insulin responsiveness was partially restored, and an enhanced response to the insulin-like effect of GH was observed. Plasma insulin levels decreased after hypophysectomy. Additional glucose caused a significant increase in plasma insulin levels, but these levels were still lower than those in sham-operated animals. To examine the possibility that endogenous insulin levels are important for the capacity of adipose tissue to metabolize glucose and respond to insulin and GH, hypophysectomized rats were injected with different, progressively increasing doses of insulin for 7 days, beginning on the day after the operation. Basal levels of glucose oxidation were decreased in hypophysectomized control animals and gradually increased in a dose-dependent manner in insulin-treated animals. Basal levels were normalized when the total dose of insulin injected was 16.5 U. In these animals, the response to insulin was enhanced, and there was an increase in the magnitude of the response to GH. Similar results were obtained when glucose incorporation into lipids was determined. The decrease in basal and insulin-stimulated glucose oxidation levels after hypophysectomy were most pronounced when measured at a high glucose concentration (50 mM), when glucose transport is not rate limiting. The results indicate that the changes in glucose metabolism and hormonal responsiveness of adipose tissue after hypophysectomy are, at least in part, dependent upon the decrease in endogenous insulin levels.

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“…The concentration of insulin in the blood is increased relative to normal and relative to glucose concentrations in acromegalic patients (137, 378,402,673,694), in rats harboring GH-secreting tumors (518, 523, 642, 645), and in transgenic mice (845), pigs (664), or sheep (679) that overexpress GH. Conversely, insulin levels in blood are usually low in hypophysectomized animals (200,208,249,358,516,663,863). In GH-deficient humans, fasting insulin levels may be lower (28, 59), un-changed (546,734), or higher than normal (548,734), depending on the degree of obesity (733).…”

Section: Pancreatic Beta Ce/hmentioning

confidence: 99%