Effect of feeding sucrose or starch diets on parameters of glucose tolerance in the LA/N-corpulent rat

Michaelis, Otho E.; Ellwood, Kathleen C.; Tulp, Orien L.; Greenwood, M. R. C.

doi:10.1016/s0271-5317(86)80203-2

Cited by 46 publications

(67 citation statements)

References 15 publications

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“…Furthermore, the very high levels of circulating b-hydroxybutyrate, one of the main ketone bodies produced by the liver, determined in the plasma of STDfed WKY rats supported this non-predominant oxidative glucose utilisation (McGarry & Foster 1980, Laffel 1999. Moreover, the disparity observed between the circulating levels of ketone bodies in STD-and CAF-fed WKY rats may be an indication that the source of the dietary carbohydrates plays a key role in carbohydrate metabolism, as has been previously described for other rat strains (Michaelis et al 1986). Therefore, although no effect of diet on the amount of carbohydrate intake was observed, the complexity of the major carbohydrate form found in each type of diet was different.…”

Section: Discussionsupporting

confidence: 77%

Leptin signal transduction underlies the differential metabolic response of LEW and WKY rats to cafeteria diet

Martínez-Micaelo

González-Abuín

Ardévol

et al. 2015

Journal of Molecular Endocrinology

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Although the effect of genetic background on obesity-related phenotypes is well established, the main objective of this study is to determine the phenotypic responses to cafeteria diet (CAF) of two genetically distinct inbred rat strains and give insight into the molecular mechanisms that might be underlying. Lewis (LEW) and Wistar-Kyoto (WKY) rats were fed with either a standard or a CAF diet. The effects of the diet and the strain in the body weight gain, food intake, respiratory quotient, biochemical parameters in plasma as well as in the expression of genes that regulate leptin signalling were determined. Whereas CAF diet promoted weight gain in LEW and WKY rats, as consequence of increased energy intake, metabolic management of this energy surplus was significantly affected by genetic background. LEW and WKY showed a different metabolic profile, LEW rats showed hyperglycaemia, hypertriglyceridemia and high FFA levels, ketogenesis, high adiposity index and inflammation, but WKY did not. Leptin signalling, and specifically the LepRb-mediated regulation of STAT3 activation and Socs3 gene expression in the hypothalamus were inversely modulated by the CAF diet in LEW (upregulated) and WKY rats (downregulated). In the present study, we show evidence of gene-environment interactions in obesity exerted by differential phenotypic responses to CAF diet between LEW and WKY rats. Specifically, we found the leptin-signalling pathway as a divergent point between the strain-specific adaptations to diet.

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Section: Discussionsupporting

confidence: 77%

Leptin signal transduction underlies the differential metabolic response of LEW and WKY rats to cafeteria diet

Martínez-Micaelo

González-Abuín

Ardévol

et al. 2015

Journal of Molecular Endocrinology

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“…At the age of 4-5 wk, all animals were placed on diets containing 54% carbohydrate as sucrose and 10% casein, 10% lactalbumin, 5.99% cellulose, 4% lard, 4% corn oil, 4% beef tallow, 4% coconut oil, 3.1% AIN salt mix (American Institute of Nutrition, Rockville, MD), and 1% vitamin mix (8). Animals were studied after 8 days to 10 wk on the diet.…”

Section: Methodsmentioning

confidence: 99%

“…The availability of the obese LA/N-cp rat (8,9), a genetically inbred strain of an obese hyperinsulinemic but nondiabetic model with the same cp allele as the SHR/N-cp rat, provided an additional basis for evaluation of the effect of hyperglycemia on pancreatic islet function. This nonhyperglycemic animal could be compared with the diabetic rat.…”

mentioning

confidence: 99%

Comparison of Insulin Secretory Patterns in Obese Nondiabetic LA/N-cp and Obese Diabetic SHR/N-cp Rats: Role of Hyperglycemia

Recant

Voyles²,

Timmers³

et al. 1989

Diabetes

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Obese diabetic SHR/N-(cp/cp) rats are a genetic model for non-insulin-dependent diabetes mellitus. When SHR/N-cp rats are overtly diabetic, they are hyperinsulinemic and hyperglycemic in the fed state when consuming commercial chow or semipurified high-carbohydrate diets. Obese SHR/N-cp rats were hyperinsulinemic by 4 wk of age, although hyperglycemia did not appear until 3-4 wk later and was exacerbated by a high-sucrose diet (mean +/- SE 1488 +/- 238 microU/ml insulin and 425 +/- 51 mg/dl glucose). The control SHR/N-cp rats (+/?) on the sucrose diet remained lean and normoglycemic. The obese diabetic SHR/N-cp rats showed three alterations in pancreas perfusion data (not present in control rats): 1) paradoxically high insulin secretion at low glucose levels (2.5 mM), 2) secretion of insulin in response to arginine (10 mM) in the absence of glucose, and 3) impaired response of insulin secretion to high glucose (16.7 mM). To determine whether hyperglycemia was responsible for the abnormalities of insulin secretion, perfusion studies were conducted in obese nondiabetic LA/N-cp rats and compared with the SHR/N-cp rats. The obese LA/N-cp rats resembled the corpulent SHR/N-cp rats in every way, except that they were normoglycemic on the sucrose diet. The obese LA/N-cp rats had two of the three alterations in insulin secretion shown by obese SHR/N-cp rats, lacking only the impaired response to high glucose, suggesting that hyperglycemia was required for that defect to occur.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Glucose intolerance is associated with the expression of obesity and is characterized by insulin and glucagon resistance with decreased hormone binding to liver plasma membranes , decreased insulin binding and insulin-stimulated glucose uptake by adipocytes (Baly et al, 1989), and increased gluconeogenic activity in the liver and kidney (Yamini et al, 1988). However, it is unlikely that these metabolic alterations can entirely explain the glucose intolerance, because other genetically obese rats (e.g., Zucker fatty and obese LA/N-cp) exhibit similar metabolic characteristics but are euglycemic or show only mildly impaired glucose tolerance (Michaelis et al, 1986b;Zucker and Antoniades, 1972).…”

Section: Cause(s) Of Diabetesmentioning

confidence: 99%

The Spontaneous Hypertensive/NIH-corpulent Rat: A New Rodent Model for the Study of Non-insulin-dependent Diabetes Mellitus and Its Complications

Michaelis¹,

Hansen²

1990

ILAR Journal

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Effect of feeding sucrose or starch diets on parameters of glucose tolerance in the LA/N-corpulent rat

Cited by 46 publications

References 15 publications

Leptin signal transduction underlies the differential metabolic response of LEW and WKY rats to cafeteria diet

Leptin signal transduction underlies the differential metabolic response of LEW and WKY rats to cafeteria diet

Comparison of Insulin Secretory Patterns in Obese Nondiabetic LA/N-cp and Obese Diabetic SHR/N-cp Rats: Role of Hyperglycemia

The Spontaneous Hypertensive/NIH-corpulent Rat: A New Rodent Model for the Study of Non-insulin-dependent Diabetes Mellitus and Its Complications

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