Insulin Biosynthesis and Release in Isolated Islets from Hyperglycemic Male Rats

Heinze, E.; Hagele, U; Rd, Fussgänger; Pfeiffer, Ernst-Friedrich

doi:10.1055/s-2007-996239

Cited by 4 publications

(3 citation statements)

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“…[15][16][17][18][19] Sustained hyperglycemia shown in the present study was induced by refeeding a nutritionally balanced diet. Therefore, hyperphagia by refeeding may be an important factor in an induction of hyperglycemia.…”

Section: Discussionmentioning

confidence: 99%

Sustained Hyperglycemia and Insulin Resistance Induced by Dietary Restriction

Maeda

Sakita

Kaihatsu

et al. 2001

Biological & Pharmaceutical Bulletin

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Hyperglycemia is a persistent symptom in diabetes mellitus. The complex pathogenesis of type 2 diabetes, its most common form, involves the progressive development of insulin resistance and defective insulin secretion, which leads to overt hyperglycemia.1) Genetic and environmental factors such as extraordinary nutritional conditions contribute to the development of insulin resistance and a defect in insulin secretion.2) However, the molecular basis for development of insulin resistance has not been documented. Patients with type 2 diabetes have elevated blood levels of glucagon, cortisol, fatty acids, protein, glucose and possibly acute phase reactants. Provonsha et al., have suggested the possibility that this can occur with meals, resulting a multilevel, multiorgan interference with glucose handling, and can also be caused by the release of the endogenous substance during starvation. 3)There are many studies concerning the effects of refeeding on plasma glucose and insulin levels. [4][5][6][7] Insulin is thought to play a major role in the physiological adaptation of tissues to fasting and refeeding. Insulin secretion diminishes during starvation and increases upon refeeding. 8,9) Insulin-stimulated glucose uptake in adipose tissue was decreased by fasting and its overshoot was caused by refeeding. 10) Penicaud et al., have used euglycemic-hyperinsulinemic clamps on rats to show that insulin resistance is induced by 3-d fasting and is restored by 3-d refeeding.11) Insulin resistance was induced by fasting and it contributes to the glucose intolerance in human.12) However the ability to stimulate glucose metabolism in rat skeletal muscle was enhanced by fasting.13) It seems that influences of fasting to insulin sensitivity depends on the tissues.The aim of our study is to examine whether defects in insulin secretion and in insulin action are induced by fasting and/or refeeding. In the present study, we found that the sustained hyperglycemia induced by refeeding mice standard chow pellets after the 48 h fasting was caused by defective insulin secretion in the early phase, and by the resulting insulin resistance in the late phase. MATERIALS AND METHODSAnimal Care Six week-old male ddY mice were purchased from Japan SLC Inc. (Hamamatsu). The mice were maintained on 12 h light/dark cycles for two weeks with free access to the standard chow pellets (MF diet, Oriental Yeast Co., Ltd.) and water. Mice weighing 36-38 g were then used.Experimental Design Fasting was started by removing the chow pellets from their home cages at 9:00 p.m. After 24 or 48 h, the mice were refed standard chow pellets, blood was obtained at the indicated time for glucose and insulin assays. Control mice were fed the standard chow pellets ad libitum. Glucose levels were determined by using the assay kit, Glucose-B Test Wako (Wako Pure Chemical Industries, Ltd., Osaka, Japan) on serum separated by centrifuging blood obtained from the caudal vein. The insulin level was determined using the Insulin Assay Kit (Seikagaku Corporation, Tokyo) on ser...

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Section: Discussionmentioning

confidence: 99%

Sustained Hyperglycemia and Insulin Resistance Induced by Dietary Restriction

Maeda

Sakita

Kaihatsu

et al. 2001

Biological & Pharmaceutical Bulletin

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“…The infusion system was described previously [6], Briefly, under general anesthesia (Nembutal®, 40 mg/lOOg body weight), the right external jugular vein was cannulated with a polyethylene catheter terminating with a 3-cm intravenous tip o f soft Silastic® tubing. The cannula was drawn under the skin o f the back to the proximal part o f the tail.…”

Section: Methodsmentioning

confidence: 99%

Insulin Release in Rats 1 and 5 Days after Hypophysectomy

Heinze¹,

Kleinert²,

Voigt³

1981

Horm Res

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In the present experiments the effect of an intravenous glucose (0.5 g/kg body weight) and an intravenous glibenclamide (1 mg/kg body weight) injection on insulin release was studied in conscious rats shortly after hypophysectomy. 1 and 5 days after removal of the pituitary gland both the fasting blood glucose and the serum insulin concentrations were significantly lower when compared with control rats as was the insulin response to the stimulation by glucose or glibenclamide. In order to elucidate the contribution of the lower fasting blood glucose to the decreased insulin release, the effect of a continuous glucose infusion (2 ml/h of a 40% glucose solution) was studied in hypophysectomized rats. The artificial hyperglycemia for 4½ days did not alter the low glucose-induced insulin release in these animals. The results clearly show that under appropriate in vivo conditions the diminished B-cell function can be detected very shortly after hypophysectomy. Furthermore, it appears that the depressed insulin release in hypophysectomized rats is not related to the lower blood glucose concentration.

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“…For the glucose infusion studies the pregnant rats were anesthetized with Nembutal® (40 mg/100 g of body weight) on day 15 post-concep tion, and the right jugular vein was cannulated as pre viously described [10].…”

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Interrelationship of Insulin and Somatomedin Activity in Fetal Rats

Heinze¹,

Thi²,

Vetter³

et al. 1982

Neonatology

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The effects of glucose and glibenclamide on fetal body weight and fetal serum somatomedin activity were studied. From day 18 to day 20 post-conception, pregnant rats were continuously infused with saline or 40 % glucose, which raised the maternal blood sugar to about 200 mg/dl. On day 21 of gestation, fetal body weight was not different, while fetal serum somatomedin activity was significantly elevated in the hyperlycemic animals. Glibenclamide, 1 mg/kg body weight, was injected on day 20 of gestation to the rat mother. The sulfonylurea crossed the placenta. A daily glibenclamide injection from day 16 to day 20 post-conception did not change the fetal body weight, but it significantly augmented the fetal serum somatomedian activity. The results suggest that insulin stimulated the generation of somatomedian activity in the fetus. Both insulin and somatomedian may act as fetal growth factors.

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Insulin Biosynthesis and Release in Isolated Islets from Hyperglycemic Male Rats

Cited by 4 publications

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Sustained Hyperglycemia and Insulin Resistance Induced by Dietary Restriction

Sustained Hyperglycemia and Insulin Resistance Induced by Dietary Restriction

Insulin Release in Rats 1 and 5 Days after Hypophysectomy

Interrelationship of Insulin and Somatomedin Activity in Fetal Rats

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