Insulin and glucagon release in the diabetic Chinese hamster: Differences among inbred sublines

Frankel, Barbara J.; Heldt, Anneliese; Grodsky, G M

doi:10.1007/bf00281309

Cited by 13 publications

(5 citation statements)

References 22 publications

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“…Older ACsubline diabetic hamsters showed clearly elevated pancreatic glucagon levels and somewhat elevated plasma glucagon levels [7]. Excessive glucagon release from the perfused pancreas in vitro is a characteristic in some, but not all, diabetic sublines [23] and from the present data, the excessive glucagon release appears to develop later than the insulin secretory defect.…”

Section: Discussionsupporting

confidence: 52%

Insulin, glucagon, and somatostatin release from the prediabetic Chinese hamster

et al. 1984

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Diabetes mellitus in the adult Chinese hamster is characterized by subnormal pancreatic insulin release in vitro, decreased insulin content, and lack of obesity. The cause of the islet B-cell failure is not clear. We measured insulin, glucagon, and somatostatin release from in vitro perfused pancreases of young (mean age 10 and 20 weeks), genetically diabetic animals (subline AC, mean plasma glucose 8.0 and 16.6 mmol/l, respectively). Compared to age- and sex-matched normal hamsters (subline M, mean plasma glucose 5.3 mmol/l), the younger diabetic animals had a significantly elevated mean plasma glucose level, but net in vitro pancreatic release of insulin, glucagon, and somatostatin was normal. Pancreatic content of insulin and glucagon was also not significantly different from normal. At age 20 weeks, when the plasma glucose of the diabetic animals was even more elevated, pancreatic content and release of insulin were significantly subnormal, whereas glucagon and somatostatin release were normal, and pancreatic content of glucagon was normal. In a similar group of young (mean age 10 weeks) diabetic animals, non-fasting plasma insulin levels were within the normal range, but the corresponding glucose levels were excessive in most of the animals (13 out of 19). In conclusion, 10-week-old diabetic hamsters show mild hyperglycaemia which cannot be accounted for directly by decreased pancreatic release in response to a glucose plus arginine stimulus in vitro. Decreased ability of the B cell to respond in vivo to hyperglycaemia or peripheral resistance to insulin may contribute to later B-cell failure in the older diabetic hamster.

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Section: Discussionsupporting

confidence: 52%

Insulin, glucagon, and somatostatin release from the prediabetic Chinese hamster

et al. 1984

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“…In previous morphological studies the changes in the pancreatic islets and the destruction of the beta cells during the development of diabetes have been documented [7,9,18,19]. The degenerative beta cell lesions are accompanied by a deterioration of glucose-induced insulin secretion [6].…”

Section: Introductionmentioning

confidence: 97%

Loss of GLUT2 glucose transporter expression in pancreatic beta cells from diabetic Chinese hamsters

Jörns

Tiedge

Sickel³

et al. 1996

Vichows Archiv A Pathol Anat

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The diabetic Chinese hamster is a well-established animal model for NIDDM with a defective glucose-induced insulin secretory response. In the pancreas of nondiabetic hamsters, the GLUT2 glucose transporter was localized in the plasma membrane of insulin-positive beta cells. At variance with the rat, immunoreactivity was also detected in the cytoplasm. Other islet cell types were not GLUT2 positive. GLUT2 immunoreactivity was already significantly reduced in beta cells from mildly diabetic animals in spite of a normal insulin immunoreactivity. In severely diabetic animals the majority of the beta cells had lost GLUT2 immunostaining. This observation was confirmed in a Western blot analysis of the GLUT2 protein in isolated pancreatic islets. Only beta cells that were densely immunostained for insulin were still GLUT2 positive. However, around 40% of the beta cells devoid of GLUT2 immunoreactivity were still insulin immunoreactive. Thus, the loss of GLUT2 immunoreactivity, which is an important component of the glucose recognition apparatus of the pancreatic beta cell, is an early indicator of beta cell dysfunction before the development of degenerative lesions or the loss of insulin immunoreactivity. GLUT2 loss may be important in the deterioration of glucose-induced insulin secretion in the diabetic Chinese hamster.

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“…D iabetes mellitus spontaneously develops in certain sublines of nonobese Chinese hamsters, and the diabetic animals show many sequelae similar to those found in human diabetics (1)(2)(3)(4)(5). Mor-phological studies reveal decreased size of pancreatic islets, fewer p-cells, glycogen accumulation, and p-cell degranulation (6)(7)(8)(9)(10)(11)(12).…”

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confidence: 87%

Abnormalities in Glucose-Stimulated Insulin Release, 45Ca Uptake, and 86Rb Efflux in Diabetic Chinese Hamster Islets

Frankel

Sehlin

1987

Diabetes

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We loaded islets from normal and diabetic Chinese hamsters with 86Rb (an analogue for K+) and measured 86Rb efflux during stimulation with 20 mM D-glucose. Genetically diabetic Chinese hamsters were selected from a subline (L) known for subnormal pancreatic insulin release and excessive pancreatic glucagon release in vitro. 86Rb accumulation in 1 mM glucose was normal in the diabetic islets. Similar to the pattern of 86Rb efflux previously seen from normal rat and mouse islets, 20 mM glucose suppressed 86Rb efflux within 1-2 min, and efflux remained suppressed until return to 1 mM glucose in both normal and diabetic hamster islets. After the first 2 min of 20 mM glucose, suppression of 86Rb efflux was somewhat greater in the diabetic hamster islets than in the normals. In addition, glucose-stimulated insulin release and 45Ca uptake were significantly reduced in the diabetic islets. Therefore, in the diabetic hamster islets, there is at least no impairment in the initial suppression of 86Rb efflux by glucose. This suggests that the diabetic beta-cells recognize glucose and carry out the initial steps in the stimulus-secretion coupling sequence normally. The later, excessive suppression of 86Rb efflux may be due to impaired Ca2+-induced changes in 86Rb efflux, suggesting that defective regulation of intracellular Ca2+ activity, rather than defective regulation of K+ permeability, may lead to the impaired insulin secretion.

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Insulin and glucagon release in the diabetic Chinese hamster: Differences among inbred sublines

Cited by 13 publications

References 22 publications

Insulin, glucagon, and somatostatin release from the prediabetic Chinese hamster

Insulin, glucagon, and somatostatin release from the prediabetic Chinese hamster

Loss of GLUT2 glucose transporter expression in pancreatic beta cells from diabetic Chinese hamsters

Abnormalities in Glucose-Stimulated Insulin Release, 45Ca Uptake, and 86Rb Efflux in Diabetic Chinese Hamster Islets

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