Experimental diabetes mellitus induced by diet in the sand rat

Haines, Howard; Hackel, Donald B.; Schmidt‐Nielsen, Knut

doi:10.1152/ajplegacy.1965.208.2.297

Cited by 85 publications

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“…The sand rat is a unique model for evaluating the interplay between nutrition and genetics in the pathophysiology of NIDDM since development of diabetes in this rodent is not predetermined but rather dependent on caloric intake (3)(4)(5)(6)(7). Food restriction can revert the diabetic sand rat back to a normoglycemia and normoinsulinemia (7).…”

Section: Discussionmentioning

confidence: 99%

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Hyperinsulinemia induces a reversible impairment ininsulin receptor function leading to diabetes in the sand rat model ofnon-insulin-dependent diabetes mellitus.

Kanety

Moshe

Shafrir

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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The insulin receptor was evaluated at different disease stages in the sand rat (Psammomys obesus), a model for nutrition-induced diabetes. Nondiabetic sand rats showed markedly low receptor number in liver compared with albino rats. Their receptor had an intact tyrosine kinase activity but a higher K. for ATP in the phosphorylation reaction of exogenous substrates. The initial effects of overeating (i.e., development of hyperinsulinemia without hyperglycemia) were associated in the sand rat with a dramatic decrease in in vitro and in vivo insulin-induced receptor tyrosine kinase activity in both liver and muscle. In muscle, this coincided with a decrease in receptor number and an increase in basal tyrosine kinase activity. Similar canges were observed upon development of hyperinsulinemia with hyperglycemia. Upon recovery from the diabetic state by diet restriction, the impaired receptor kinse activation was corrected. Complete restoration occurred only in animals that fully recovered from the diabetic state and became normoinLinemic. These observations indicate that loss and gain of receptor tyrosine kinase activity were dependent on insulin levels. Thus, overeating may lead to the development of hyperinsulinemia through ineffective extraction of excess insulin by the scarce liver receptors. Hyperinsulinemia, in turn, causes a reversible reduction in receptor kinase activity, leading to insulin resistance. This sequence of events may be relevant to diet-related changes in human non-insulin-dependent diabetes mellitus.The development of non-insulin-dependent diabetes mellitus (NIDDM) in the majority of patients occurs in parallel to weight gain (1). Overeating is initially followed by hyperinsulinemia and insulin resistance, which gradually develop into pronounced hyperglycemia. This diabetogenic process may be reversed by diet restriction and weight loss (2). Since both hyperinsulinemia and insulin resistance coincide with weight gain in humans, it is not feasible to determine which is the primary event mediating the effect of obesity. We have addressed this query in an animal model of NIDDM. The sand rat is a desert-adapted gerbil that in its natural habitat is nondiabetic (3-7). In captivity, on an ad libitum rodent diet, it develops obesity and hyperinsulinemia without or with hyperglycemia (6,7). Through control of the animals' diet, it is possible to discern several stages of development of glucose intolerance, as well as reverse them, thus addressing the sequence of events that lead to induction of diabetes. We studied the insulin receptor (IR) function in these wellcharacterized animals and found alterations that may be relevant to human nutrition-induced diabetes. ['t-32P]ATP was from Amersham. ATP, CTP, Hepes, Tween 20, poly(Glu8Tyr20), bovine serum albumin (insulin free), N-acetyl-D-glucosamine, leupeptin, aprotinin, soybean trypsin inhibitor, and phenylmethylsulfonyl fluoride were from Sigma. Wheat germ agglutinin (WGA) and Con A coupled to agarose were from Bio-Makor (Rehovot, Israel). Reagen...

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Section: Discussionmentioning

confidence: 99%

“…We have addressed this query in an animal model of NIDDM. The sand rat is a desert-adapted gerbil that in its natural habitat is nondiabetic (3)(4)(5)(6)(7). In captivity, on an ad libitum rodent diet, it develops obesity and hyperinsulinemia without or with hyperglycemia (6,7).…”

mentioning

confidence: 99%

Hyperinsulinemia induces a reversible impairment ininsulin receptor function leading to diabetes in the sand rat model ofnon-insulin-dependent diabetes mellitus.

Kanety

Moshe

Shafrir

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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“…In all but one of these play a role, e.g. in sandrats [9,10], KK-mice [13], and Wellesley hybrid mice [8]. Desert regions are the natural habitat of the Mongolian gerbil.…”

Section: Discussionmentioning

confidence: 99%

Obesity and pancreatic islet hyperplasia in the Mongolian gerbil

Boquist

1972

Diabetologia

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Summary. In a colony of Mongolian gerbils maintained on a standard laboratory diet, occasional obese animals were found. Obesity developed in animals of both sexes and was either transitory or permanent. The mean fasting blood glucose level in non-obese and obese gerbils was 83 and 105 rag/100 ml, respectively. Glucosuria and hyperglycemia were found only in a few obese animals, whereas the glucose tolerance was decreased in most obese gerbils. --The endocrine pancreas of the obese animals was morphologically either normal or more often hyperplastic, sometimes with the appearance of adenomatous islets. The fl-eells possessed prominent Golgi complex and endoplasmic reticulum, and sparse granulation. Large, granule-poor cells and mitotic figures were seen in the islets. Degenerative changes occurred in the fl-cells of diabetic animals. --It is suggested that the maintenance of the gerbils under laboratory conditions with free access to laboratory diet plays a majo r role in the development of obesity and that the endocrine pancreas of these animals has a good capacity for hyperplasia that often is sufficient to maintain normo-glycemia in obese animals, although the glucose tolerance is decreased. Obdsit@ et hyperplasie des ilots du panerdas chez la gerbille mongolienneRdsumd. Dans un 61evage de gerbilles mongoliennes soumises ~ un r@gime standard de laboratoire ont dr@ parfois trouvds des animaux ob@ses. L~ se dgveloppait chez les animaux des deux sexes et 6tait tantSt transitoire, tant6t permanente. Le taux moyen de glucose du sang, ~ jefin, ehez les animaux non ob@ses et ob~-ses 6tait respectivement de 83 et 105 mg/100 ml. La glyeosurie et l'hyperglycdmie n'dtaient trouvdes que ehez peu d'animaux ob6ses, tandis que la toldrance au glucose 6tait rdduite ehez la plupart des animaux ob@ses. --Le pancrdas endocrine des animaux ob@ses dtait, morphologiquement, normal ou plus souvent hyperplasique avec parfois l'apparition d'ilots adgnomateux. Les eellules /~ poss@daient un eomplexe de Golgi et un rdticulum endoplasmique pro@minents et une granulation faible. De grosses eellules pauvres en granules et des figures mitotiques se montraient dans les ilots. Des changements d@gdndratifs se produisaient dans les cellules fl des animaux diab6tiques. --On sugg~re que le maintien des animaux darts les conditions de laboratoire avec libre acc@s au r@gime de laboratoire joue un r61e prddominant darts le d@veloppement de I'ob@sit@ et que le pancr@as endocrine de ces animaux a une excellente eapaeit6 d'hyperplasie qu! suffit souvent ~ maintenir la normoglycdmie ehez les ammaux ob@ses, malgr6 la r6duction de la tol6rance au glucose. ~]bergewieht und Hyperplasie der Pankreasinseln bei der mongolischen RennmausZusammenfassung.

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“…[2][3][4][5] Many recent works on diabetes mellitus in animals, especially on diabetic rodents, 2,[6][7][8][9][10][11][12] have described hyperglycemia, decreased glucose tolerance, glycosuria, and sometimes, ketoacidosis, as major features of diabetic syndrome. Hence, similar changes were pos tulated to occur in Sekoke disease.…”

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confidence: 99%

Sekoke Disease, Spontaneous Diabetes in Carp Found in Fish Farms-II

Yokote¹

1970

NIPPON SUISAN GAKKAISHI

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In the previous paper,1) the writer has reported that microscopical findings in Sekoke carp were very similar to those ever described for diabetes mellitus in mammals.2-5) Many recent works on diabetes mellitus in animals, especially on diabetic rodents,2,6-12) have described hyperglycemia, decreased glucose tolerance, glycosuria, and sometimes, ketoacidosis, as major features of diabetic syndrome. Hence, similar changes were pos tulated to occur in Sekoke disease.Present investigation was undertaken to put Sekoke carp to the basic tests for dia gnosing diabetes; determination of blood sugar level, glucose tolerate test, and analysis of blood pH.As the results of the present study, it was revealed that hyperglycemia, decreased glucose tolerance, glycosuria, and acidosis developed in Sekoke carp examined. These findings are considered to lend support to the conclusion of the histopathological study on the disease.

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Experimental diabetes mellitus induced by diet in the sand rat

Cited by 85 publications

References 0 publications

Hyperinsulinemia induces a reversible impairment ininsulin receptor function leading to diabetes in the sand rat model ofnon-insulin-dependent diabetes mellitus.

Hyperinsulinemia induces a reversible impairment ininsulin receptor function leading to diabetes in the sand rat model ofnon-insulin-dependent diabetes mellitus.

Obesity and pancreatic islet hyperplasia in the Mongolian gerbil

Sekoke Disease, Spontaneous Diabetes in Carp Found in Fish Farms-II

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