Studies in the diabetic Chinese hamster: Light microscopy and autoradiography of pancreatic islets

Like, Arthur A.; Gerritsen, G. C.; Dulin, W. E.; Gaudreau, Pierrette

doi:10.1007/bf01221980

Cited by 21 publications

(13 citation statements)

References 25 publications

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“…The majority of the intact beta cells represents the group of the functionally active beta cells that have lost GLUT2 immunoreactivity. Confirming previous studies [9,18,19], these intact beta cells showed a well-developed Golgi complex and a large amount of rough endoplasmic reticulum with a marked reduction of secretory granules at the light-and electron-microscopical levels, as well as morphological signs of high insulin biosynthesis and secretory activity. Thus, expression of GLUT2 alone is not a sufficient indicator of glucose responsiveness, as was previously considered in animal models for diabetes [32].…”

Section: Discussionsupporting

confidence: 86%

“…The islet periphery, which is called its mantle, was mainly composed of glucagon (alpha) and somatostatin (delta) cells, whereas the beta cells were mostly localized in the centre of the islet. This confirms earlier observations in this species [9,18,19]. In parallel with the development of diabetes in Chinese hamsters, the morphology of the islet changed.…”

Section: Histology Of the Islets Of Langerhanssupporting

confidence: 89%

“…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: 96%

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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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Section: Discussionsupporting

confidence: 86%

Section: Histology Of the Islets Of Langerhanssupporting

confidence: 89%

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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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“…Pancreatic islet hypertrophy and hyperplasia reported in spontaneous diabetes of other animal species 96 are not found in the diabetic Chinese hamster. However, hypertrophy of the pancreatic beta-cell, 86 increased size of beta-cells, 42 and neoformation of islets from duct cells 16 have been reported in diabetic Chinese hamsters. Replication as measured by 3 Hthymidine incorporation of preexisting beta-cells in diabetic Chinese hamsters has been reported 87 ' 97 though no proof of cell division has been presented in the published literature.…”

Section: Morphologic Changes and Complicationsmentioning

confidence: 99%

The Chinese Hamster as a Model for the Study of Diabetes Mellitus

Gerritsen¹

1982

Diabetes

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Selection for and against diabetes and subsequent inbreeding of Chinese hamsters started in 1963. Currently there are six inbred sublines that have greater than 85% incidence of glycosuria and two control inbred nondiabetic sublines that are essentially free of glycosuria. At birth, hamsters from inbred sublines are considered prediabetic. There is phenotypic variation between diabetic sublines. Onset time, incidence of ketonuria, blood glucose, plasma insulin, glucagon and glycohydrolase levels vary from subline to subline, but pancreatic insulin and glucagon levels are consistently low and high, respectively, in all diabetic sublines compared with nondiabetics. Experimental breeding data suggest a minimum of two homozygous recessive genes for diabetes. It is not known if the inbred lines are similar diabetic genotypes, but the probability is high that modifier background genes vary from subline to subline.Chinese hamsters have diabetes ranging from mild to severe. Animals weighing 25 g can excrete up to 75 ml of urine containing 3 g of glucose per day. Fasting blood glucose as high as 500 mg/dl and 10 /nmol/ml of beta-hydroxybutyrate have been reported. Gluconeogenesis is elevated, and some glycolytic enzymes are decreased in severe diabetes. Low levels of renal acid glycohydrolase enzymes may contribute to glomerular capillary loop basement membrane thickening in diabetic hamsters. Caloric restriction per se or reduction of dietary fat prevented onset of hyperglycemia and hyperinsulinemia in prediabetics. Morphologic changes have been observed in pancreatic islets, kidney, nerve, blood vessels, eyes, brain, and genitourinary systems of diabetic Chinese hamsters. Pathogenesis of diabetes in this animal appears to be related to an increased demand for insulin. Initially there is a positive response to this demand by beta cells, but exhaustion occurs. This is followed by a decrease in beta-cell mass and relative or absolute insulin deficiency. DIABETES 37 (Suppl.

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“…Like et al [18] have previously published semiquantitative data from autoradiography of pancreatic islets after 'H-thymidine labeling of 3 normal and 9 mild-to-severely diabetic hamsters at different stages of the syndrome. Due to the low number of animals studied and the semiquantitalive technique used for determinations of the labeling frequency, it is difficult to draw firm conclusions from their results.…”

Section: Discussionmentioning

confidence: 99%

DIMA Replication in Pancreatic Islets and Adrenals in Diabetic Chinese Hamsters

Frankel

Korsgren²,

Andersson³

1993

Horm Res

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The diabetic syndrome in Chinese hamsters is progressive and there is a decrease in the size of the pancreatic islets. To what extent this is due to impaired DNA replication in their islet cells is unknown. Therefore ³H-thymidine incorporation into islet cells was studied in genetically diabetic (subline L) male hamsters aged 17-20 days, 6 weeks, 3, 6 and 12 months. Because adrenal weight was decreased at almost all ages, studies of adrenal morphology and function were also performed. Age- and sex-matched normal (subline M) hamsters served as controls. Autoradiography showed progressively falling labeling with increasing age in both normal and diabetic animals in both islets and adrenals. At the earliest age studied, the diabetic subline animals were normoglycemic but showed hyperinsulinemia. DNA replication was reduced both in the islet cells and the adrenal cortex. From 6 weeks of age and onwards, the diabetic hamsters were hyperglycemic and usually hyperinsulinemic but DNA replication in both islets and adrenals was not different from that in normals. Histomorphometry showed reduced volume in both the adrenal medulla and cortex in 3-month-old diabetic hamsters. In 12-month-old male and female diabetic hamsters plasma cortisol and aldosterone and 24-hour urinary epinephrine were normal, but urinary norepinephrine and dopamine levels were excessive. Thus, in contrast to what is found in the obese-hyperglycemic mouse, there was no increased islet cell DNA replication in response to the increased functional demand in the diabetic Chinese hamster. The transiently decreased DNA replication in the youngest animals may contribute to the reduced islet volume later in life. Also, in contrast to the findings in obese-hyperglycemic mice, adrenal weights were decreased and adrenal-cortex function appeared to be normal in the diabetic hamsters. Perhaps this lack of adrenal enlargement is one significant factor for the lack of adaptive islet growth in the diabetic hamster.

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Studies in the diabetic Chinese hamster: Light microscopy and autoradiography of pancreatic islets

Cited by 21 publications

References 25 publications

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

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

The Chinese Hamster as a Model for the Study of Diabetes Mellitus

DIMA Replication in Pancreatic Islets and Adrenals in Diabetic Chinese Hamsters

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