Glucagon and insulin from lean rats and genetically obese fatty rats: Studies by radioimmunoassay, radioreceptorassay and bioassay

Laburthe, Marc; Rançon, F; Freychet, P; Rosselin, G

doi:10.1007/bf01222101

Cited by 19 publications

(7 citation statements)

References 39 publications

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“…As with the kidneys, there were pancreatic morphological abnormalities of Zucker fatty control rats, changes that were ameliorated or prevented by rosiglitazone. Islet (3-cell hyperplasia (12), an elevated pancreatic insulin content (37,38), and a disseminated distribution of a-cells throughout the islet (12) have each been described previously in fatty rats and were prominent features here. The signature of work hypertrophy (i.e., Golgi hypertrophy, hyperplasia of rough endoplasmic reticulum, and dilation of endoplasmic reticulum) was also apparent at the ultrastructural level of the (3-cell.…”

Section: )mentioning

confidence: 75%

Peroxisome Proliferator-Activated Receptor-γ Agonist, Rosiglitazone, Protects Against Nephropathy and Pancreatic Islet Abnormalities in Zucker Fatty Rats

et al. 1998

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Rosiglitazone (BRL 49653), a peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist and potent insulin action-enhancing agent, was given in the diet (50 micromol/kg of diet) to male Zucker rats ages 6-7 weeks for 9 months (prevention group). In this treatment mode, rosiglitazone prolonged the time to onset of proteinuria from 3 to 6 months and markedly reduced the rate of its subsequent progression. Progression was also retarded when treatment was commenced (intervention group) after proteinuria had become established (4 months; ages 24-25 weeks). In either treatment mode, rosiglitazone normalized urinary N-acetyl-beta-D-glucosaminidase activity, a marker for renal proximal tubular damage, and ameliorated the rise in systolic blood pressure that occurred coincidentally with the development of proteinuria in Zucker fatty control rats. The renal protective action of rosiglitazone was verified morphologically. Thus in the prevention group there was an absence of the various indexes of chronic nephropathy that were prominent in the Zucker fatty control group, namely, glomerulosclerosis, dilated tubules containing proteinaceous casts, a loss of functional microvilli on the tubular epithelium, and varying degrees of chronic interstitial nephritis. An intermediate pathology was observed in the intervention group. Also, pancreatic islet hyperplasia, ultrastructural evidence of beta-cell work hypertrophy, and derangement of alpha-cell distribution within the islet were prominent features of Zucker fatty control rats, but these adaptive changes were ameliorated (intervention group) or prevented (prevention group) by rosiglitazone treatment. These data demonstrate that treatment of Zucker fatty rats with rosiglitazone produced substantial protection over a prolonged period against the development and progression of renal injury and the adaptive changes to pancreatic islet morphology caused by sustained hyperinsulinemia.

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confidence: 75%

Peroxisome Proliferator-Activated Receptor-γ Agonist, Rosiglitazone, Protects Against Nephropathy and Pancreatic Islet Abnormalities in Zucker Fatty Rats

et al. 1998

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“…Binding of [12-r'I]GIP to the anti-GIP serum was expressed as the percentage of initial binding (B/Bo 100, where Bo represents the binding of [125I]GIP in the absence of unlabelled GIP). Logit transformation of the results, regression lines and comparison of the slopes of paired regression lines were obtained as described elsewhere (Laburthe et al 1975).…”

Section: Methodsmentioning

confidence: 99%

Ontogeny and Distribution of Immunoreactive Gastric Inhibitory Polypeptide (Ir-Gip) in Rat Small Intestine

Gespach¹,

Bataille²,

Jarrousse³

et al. 1979

Acta Endocrinologica

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The ontogeny and distribution of immunoreactive gastric inhibitory polypeptide (IR-GIP) has been studied in the rat duodenum and jejunoileum between day 20 post-coitum and day 150 post-partum by radioimmunoassay following tissue extraction. In foetuses on day 20 of gestation, the content of IR-GIP was 2.0 \ m=+-\0.2 ng/duodenum and 18 \ m=+-\ 2.0 ng/jejuno-ileum. The IR-GIP content increased during the whole period investigated and a peak of concentration was observed in the first post-natal week in both the duodenum (860 \m=+-\150 ng/g) and jejunoileum (650 \m=+-\135 ng/g). In the duodenum, the main increase in IR-GIP content (ng per organ) occurred in the 3rd week of life and the same phenomenon was observed 2 weeks later in the jejuno-ileum. The highest GIP concentration was found in the duodenum and in the proximal jejunum, indicating that the upper small intestine is the major site of IR-GIP storage. It is concluded that the ontogeny of IR-GIP further supports the concept that this hormone is involved in the endocrine regulation of metabolism and suggests that this regulatory process takes place at an early stage of rat development.

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“…In fatty rats, pathological changes in the pancreatic islet, such as islet ␤-cell hyperplasia (12), elevated pancreatic insulin content (13,14), and a disseminated distribution of ␣-cells in the islet (12), have been described. These adaptive changes could be ameliorated or prevented by RSG treatment (15).…”

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confidence: 99%

Rosiglitazone (BRL 49653) Enhances Insulin Secretory Response via Phosphatidylinositol 3-Kinase Pathway

Yang

Chang

et al. 2001

Diabetes

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To elucidate the direct effect of rosiglitazone (RSG), a new thiazolidinedione antihyperglycemic agent, on pancreatic insulin secretion, an in situ investigation by rat pancreatic perfusion was performed. At a basal glucose concentration of 6 mmol/l, RSG (0.045-4.5 mol/l) stimulated insulin release in a dose-dependent manner. In addition, 4.5 mol/l RSG potentiated the glucose (10 mmol/l)-induced insulin secretion. Both the first and second phases of glucose-induced insulin secretion were significantly enhanced by RSG, by 80.7 and 52.4%, respectively. The effects of RSG on insulin secretion were inhibited by a phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002. In contrast, the glucose-stimulated insulin secretion was not affected by LY294002. The potentiation effect of RSG on glucose-stimulated insulin secretion, in both the first and second phases, was significantly blocked by LY294002. These results suggest that RSG has a direct potentiation effect on insulin secretion in the presence of 10 mmol/l glucose, mediated through PI3K activity. The inability of LY294002 to inhibit glucose-induced insulin secretion suggests that different pathways are responsible for glucose and RSG signaling.

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Glucagon and insulin from lean rats and genetically obese fatty rats: Studies by radioimmunoassay, radioreceptorassay and bioassay

Cited by 19 publications

References 39 publications

Peroxisome Proliferator-Activated Receptor-γ Agonist, Rosiglitazone, Protects Against Nephropathy and Pancreatic Islet Abnormalities in Zucker Fatty Rats

Peroxisome Proliferator-Activated Receptor-γ Agonist, Rosiglitazone, Protects Against Nephropathy and Pancreatic Islet Abnormalities in Zucker Fatty Rats

Ontogeny and Distribution of Immunoreactive Gastric Inhibitory Polypeptide (Ir-Gip) in Rat Small Intestine

Rosiglitazone (BRL 49653) Enhances Insulin Secretory Response via Phosphatidylinositol 3-Kinase Pathway

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