Preliminary studies on food and water consumption of prediafoetic chinese hamsters

Gerritsen, G. C.; Blanks, M. C.

doi:10.1007/bf01212226

Cited by 18 publications

(14 citation statements)

References 15 publications

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“…Fasting alone reduced blood glucose, 14 and reduction of caloric intake of either a high or low-fat diet decreased blood glucose. 4 -18 Offspring from two ketonuric parents were prediabetic 18 and hyperphagic, 78 since they ate 40% more than nonprediabetics. Normalization of food intake of these hyperphagic prediabetics significantly retarded onset of glycosuria, prevented ketonuria, and normalized life span.…”

Section: Nutrition and Environmentmentioning

confidence: 99%

“…33 Prediabetics with two ketotic parents were hyperphagic. 78 However, in prediabetics from nonketonuric diabetic parents who were not hyperphagic, 4 -25 diet limitation delayed onset of glycosuria and hyperglycemia. 33 -39 Furthermore, nonhyperphagic prediabetics appear to have hyperinsulinemia prior to onset of hyperglycemia, 33 and this hyperinsulinemia can be eliminated by diet limitation.…”

Section: Nutrition and Environmentmentioning

confidence: 99%

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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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Section: Nutrition and Environmentmentioning

confidence: 99%

Section: Nutrition and Environmentmentioning

confidence: 99%

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

Gerritsen¹

1982

Diabetes

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“…When any two of these genes are homozygous recessive, the animals become diabetic [3]. The syndrome is characterized by hyperphagia [4,5], early but variable onset of hyperglycemia and glycosuria and the unique absence of obesity [1,7]. Hepatic and renal gluconeogenesis are elevated [6] and peripheral adipose tissue and skeletal muscle are normally responsive to insulin in vitro [7].…”

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confidence: 99%

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

Gerritsen

Dulin

et al. 1974

Diabetologia

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Summary. Light microscopic and autoradiographie studies were performed in normal genetic nondiabetie and diabetic Chinese hamsters after the administration of thymidine-aH and correlated with levels of blood glucose (BG) and plasma insulin (IRI). Pancreatic islets of normal hamsters contained well granulated beta cells; rare islet ceils incorporated thymidine-3H and the IRI/BG ratio (I/G) was = 1.91. l~ecent onset diabetics revealed hyperglycemia and hyperinsulinemia (I/G = 1.97), beta cell degranulation and increased islet cell labelling. With progression of diabetes, I/G ratios decreased (Non-ketotie animals: 1.08, Ketotic hamsters: 0.17), beta cell numbers declined and islet labelling was infrequent. Hamsters with spontaneous remission from diabetes showed normoglycemia, hyperinsulinemia (I/G = 2.84) and beta cell hyperplasia. Glucoeortieoid administration to normal hamsters induced marked BG elevations, beta cell hyperplasia and increased thymidine-3H incorporation. The absence of increased beta cell labelling among most diabetics treated with glueoeorticoids may be a manifestation of a genetically defined defect of beta cell replication that is in part responsible for the declining beta cell mass and insulin synthetic capacity of the diabetic Chinese hamsters.

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“…The syndrome is, at least in part, genetically determined, and its spectrum ranges in severity from intermittent glucosuria to ketoacidosis. Although prediabetic hamsters are hyperphagic (and may be mildly obese) when young (9,10), the adults are the only spontaneously diabetic laboratory animals that are not obese (11,12). They develop neuropathy…”

Section: Introductionmentioning

confidence: 99%

“…1-17); glucagon measurements from normals (nos. [6][7][8][9][10][11] and diabetics (nos. [13][14][15][16][17], as designated in Table I.…”

Section: Introductionmentioning

confidence: 99%

Abnormal Secretion of Insulin and Glucagon by the In Vitro Perfused Pancreas of the Genetically Diabetic Chinese Hamster

Frankel¹,

Gerich²,

Hagura³

et al. 1974

J. Clin. Invest.

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Therefore, to characterize pancreatic islet function, dynamic insulin and glucagon release from normal and nonketotic diabetic hamster pancreases in response to glucose (300 mg/100 ml) and theophylline (10 mM), infused singly and together, was studied in vitro.20-min glucose infusions of normal hamster pancreases caused biphasic insulin release, consisting of a rapid first peak and a gradually rising second phase, similar to that reported for man in vivo. Both phases were significantly reduced in the diabetic pancreases. Theophylline alone stimulated similar nonphasic insulin release in both the normal and the diabetic pancreases. Glucose and theophylline together caused greater insulin release than either stimulant alone in both normals and diabetics; however, the diabetic response was still subnormal.Glucose suppressed glucagon release from normal pancreases; suppression was significantly impaired in diabetics. Theophylline stimulated nonphasic glucagon release in both the normals and diabetics. Glucose partially suppressed the theophylline-stimulated release in both groups.Insulin/glucagon molar ratios of the diabetics were consistently subnormal, although individual hormone levels often overlapped into the normal range.This work was presented in part at the Western Section of the American Federation for Clinical Research, Carmel, Calif., 2 February 1973 (Clin. Res. 21: 273)

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Preliminary studies on food and water consumption of prediafoetic chinese hamsters

Cited by 18 publications

References 15 publications

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

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

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

Abnormal Secretion of Insulin and Glucagon by the In Vitro Perfused Pancreas of the Genetically Diabetic Chinese Hamster

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