Diabetes Mellitus in the Sand Rat Induced by Standard Laboratory Diets

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

doi:10.1126/science.143.3607.689

Cited by 132 publications

(47 citation statements)

References 2 publications

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“…These points include the need to manipulate caloric intake prospectively over an extended period of time to establish desired levels of obesity and hypertriglyceridemia and the lack of universal agreement re- (8,9). The sand rats used in this study were trapped in Egypt and transported to Seattle, Wash., where they were maintained in a clean environment which utilized a laminar flow unit.…”

Section: Introductionmentioning

confidence: 99%

Accelerated Triglyceride Secretion A METABOLIC CONSEQUENCE OF OBESITY

Robertson¹,

Dj²,

Jd³

et al. 1973

J. Clin. Invest.

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A new animal model was developed to determine the effect of obesity upon endogenous triglyceride secretion. Desert sand rats (Psammomys obesus), rodents which become spontaneously obese and hyperinsulinemic when given ad lib. chow, were given intravenous Triton to allow in vivo measurement of triglyceride secretion rates (TGSR). In a group of 18 fasted animals of varying body weight and degrees of obesity, TGSR correlated significantly with body weight (r = 0.68, P < 0.01) indicating that obesity was associated with accelerated endogenous release of triglyceride. In these same animals, basal plasma insulin levels correlated significantly with body weight (r = 0.78, P < 0.001) and TGSR correlated significantly with mean plasma insulin levels (r = 0.73, P <0.001), suggesting that hyperinsulinemia may have been the mechanism through which obesity enhanced TGSR. No correlation was found between basal triglyceride level and either body weight, basal insulin, or TGSR which suggested that individual triglyceride removal rates among the animals may have been variable. To test this hypothesis, seven animals were studied prospectively before and after induction of obesity. There were significant increases (P < 0.02) in all parameters, i.e., weight, plasma insulin level, TGSR, and basal triglyceride level. Thus, when each animal was used as its own control, thereby minimizing the postulated factor of variable individual triglyceride removal, increments in basal triglyceride were shown to accompany the development of obesity, hyperinsulinemia, and accelerated triglyceride secretion.These data from studies in the sand rat offer in vivo evidence that obesity leads to accelerated triglyceride

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Section: Introductionmentioning

confidence: 99%

Accelerated Triglyceride Secretion A METABOLIC CONSEQUENCE OF OBESITY

Robertson¹,

Dj²,

Jd³

et al. 1973

J. Clin. Invest.

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“…1B). P. obesus has emerged as a model for research into diet-induced type II diabetes because, if provided with high carbohydrate diets, the majority of individuals become obese and develop classic diabetes symptoms, in the most extreme cases leading to pancreatic failure and death (1)(2)(3)(4).…”

mentioning

confidence: 99%

Genome sequence of a diabetes-prone rodent reveals a mutation hotspot around the ParaHox gene cluster

Hargreaves

Zhang

Christensen

et al. 2017

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

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The sand rat Psammomys obesus is a gerbil species native to deserts of North Africa and the Middle East, and is constrained in its ecology because high carbohydrate diets induce obesity and type II diabetes that, in extreme cases, can lead to pancreatic failure and death. We report the sequencing of the sand rat genome and discovery of an unusual, extensive, and mutationally biased GC-rich genomic domain. This highly divergent genomic region encompasses several functionally essential genes, and spans the ParaHox cluster which includes the insulin-regulating homeobox gene Pdx1. The sequence of sand rat Pdx1 has been grossly affected by GC-biased mutation, leading to the highest divergence observed for this gene across the Bilateria. In addition to genomic insights into restricted caloric intake in a desert species, the discovery of a localized chromosomal region subject to elevated mutation suggests that mutational heterogeneity within genomes could influence the course of evolution.

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“…The development of hyperglycaemia in the C. talarum colony is associated with increase in weight, presumably due to inactivity coupled with the ready availability of high calorie food in the form of compound diet pellets. In these respects the tuco-tuco resembles the spiny mouse [4] and the sand rat [3], but the high prevalence of hyperglycaemia in the tuco-tuco colony is of interest.…”

Section: Discussionmentioning

confidence: 99%

“…Spontaneous diabetes mellitus has been demonstrated in a variety of species [1,2], b u t its prevalence in a n y one captive group has been low except for the E g y p t i a n sand rat [3], the spiny mouse [4] a n d the tree shrew [5]. A d e m a n d exists for an animal model of h u m a n diabetes to s t u d y the epidemiology and genetics of the disease a n d the interrelation of vascular lesions to the metabolic defects.…”

mentioning

confidence: 99%

The diabetic syndrome in the tuco-tuco (Ctenomys talarum)

Wise

Weir²,

Hime

et al. 1972

Diabetologia

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Summary. A syndrome of diabetes, which appears to be dependent upon diet, is described in an Argentine rodent, the tuco-tuco. Hyperglycaemia and cataract are shown to be inversely related to age and associated with excess mortality. Pancreatic islet, renal glomerular and lens changes are similar to those of human diabetics. It is suggested that this species forms a useful model of h u m a n maturity onset diabetes. Le syndrome diabdtique chez le Tuco-tuco (Ctenomys talarum)Rdsumd. Les

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Diabetes Mellitus in the Sand Rat Induced by Standard Laboratory Diets

Cited by 132 publications

References 2 publications

Accelerated Triglyceride Secretion A METABOLIC CONSEQUENCE OF OBESITY

Accelerated Triglyceride Secretion A METABOLIC CONSEQUENCE OF OBESITY

Genome sequence of a diabetes-prone rodent reveals a mutation hotspot around the ParaHox gene cluster

The diabetic syndrome in the tuco-tuco (Ctenomys talarum)

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