Aging changes tissue-specific glucose metabolism in rats

Higgins, Janine; Proctor, Deborah R.; Denyer, Gareth

doi:10.1016/s0026-0495(99)90157-9

Cited by 9 publications

(8 citation statements)

References 9 publications

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“…The reason for this might be the generally increased levels of basal insulin in 9-month-old mice compared with 4-month-old mice. This age-dependent increase in basal insulin levels has been well documented previously in mice and is probably caused by the age-dependent increase in fat mass resulting in insulin resistance (23,37,38).…”

Section: Young-adult Li-igf-isupporting

confidence: 68%

Liver-Derived IGF-I is of Importance for Normal Carbohydrate and Lipid Metabolism

et al. 2001

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IGF-I is important for postnatal body growth and exhibits insulin-like effects on carbohydrate metabolism. The function of liver-derived IGF-I is still not established, although we previously demonstrated that liver-derived IGF-I is not required for postnatal body growth. Mice whose IGF-I gene in the liver was inactivated at 24 days of age were used to investigate the long-term role of liver-derived IGF-I for carbohydrate and lipid metabolism. Serum levels of leptin in these mice were increased by >100% at 3 months of age, whereas the fat mass of the mice was decreased by 25% at 13 months of age. The mice became markedly hyperinsulinemic and yet normoglycemic, indicating an adequately compensated insulin resistance. Furthermore, they had increased serum levels of cholesterol. We conclude that liver-derived IGF-I is of importance for carbohydrate and lipid metabolism.

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Section: Young-adult Li-igf-isupporting

confidence: 68%

Liver-Derived IGF-I is of Importance for Normal Carbohydrate and Lipid Metabolism

et al. 2001

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“…Intraperitoneal glucose tolerance test (i. p. GTT) was done by injecting glucose (2 g/kg as 20 % solution) intraperitoneally in overnight-fasted mice without anaesthesia at 4,8,12,24,36, 48 and 60 weeks of age. Blood samples were obtained from the tail vein.…”

Section: Methodsmentioning

confidence: 99%

“…Glucose tolerance is reported to be impaired with advancing age [3,4]. Deterioration of glucose tolerance can be due to impaired insulin secretion or impaired insulin action or both.…”

mentioning

confidence: 99%

Age-dependent changes in phenotypes and candidate gene analysis in a polygenic animal model of Type II diabetes mellitus; NSY mouse

et al. 2000

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Type II (non-insulin-dependent) diabetes mellitus is a polygenic disease characterised by insulin resistance in muscle, fat and liver, and the failure of pancreatic beta cells to adequately compensate for this resistance [1,2]. Glucose tolerance is reported to be impaired with advancing age [3,4]. Deterioration of glucose tolerance can be due to impaired insulin secretion or impaired insulin action or both. The relative contribution of insulin deficiency and insulin resistance to the pathogenesis of age-related glucose intolerance is still controversial [5] because of the difficulty in doing longitudinal studies in humans. Longitudinal analysis of glucose tolerance in animal models with different degrees of glucose intolerance is one of the best ways to address this question.The Nagoya-Shibata-Yasuda (NSY) mouse strain was established as an inbred animal model with spontaneous development of Type II diabetes, by selective breeding for glucose intolerance from out- Abstract Aims/hypothesis.The Nagoya-Shibata-Yasuda (NSY) mouse closely mimics human Type II (non-insulin-dependent) diabetes mellitus in that the onset is age-dependent, the animals are not severely obese, and both insulin resistance and impaired insulin response to glucose contribute to disease development. The aim of this study was to clarify the influence of age on the pathogenesis of diabetes and to analyse a candidate gene for Type II diabetes in this strain. Methods. Several phenotypic characteristics related to diabetes mellitus were monitored longitudinally in male NSY and control C3H/He mice. The nucleotide sequence of Glut4, a candidate gene for Nidd1nsy (a susceptibility gene for Type II diabetes) on Chromosome 11, encoding insulin-sensitive glucose transporter, was determined in NSY and C3H mice. Results. Glucose intolerance worsened with age, and fasting blood glucose and fasting plasma insulin concentration increased with age in NSY mice. Pancreatic insulin content increased until 24 weeks of age but then decreased at 48 weeks of age in NSY mice. The hypoglycaemic response to insulin was statistically significantly smaller in NSY than in C3H/He mice. The nucleotide sequence of GLUT4 cDNA was identical in NSY and C3H/He mice, but both were different from the sequence reported previously. Conclusion/interpretation. Insulin secretion and insulin resistance, as well as ageing possibly play an important part in the disease development in NSY mice. A decline of pancreatic insulin content in older age might cause the relative insulin deficiency in this strain. Nucleotide sequencing suggests that Glut4 is unlikely to be a candidate gene for Nidd1nsy. [Diabetologia (2000) 43: 932±938]

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“…Ikegami et al 2) suggested that aging is associated with glucose intolerance and insulin resistance. According to Higgins et al,5) insulin responsiveness in adipose tissue of older animals may underlie the increased adiposity, which was speculated to be the causative factor in the development of age-related insulin resistance. Escriva et al 6) reported that during aging in Wistar rats and before fasting plasma insulin and glucose levels became altered, specific tissues develop insulin resistance, whereas other tissues remain insulin sensitive, and suggested that fat tissue plays a qualitatively important role in eliciting insulin resistance in elderly animals.…”

Section: Discussionmentioning

confidence: 99%

“…[4][5][6] A lowcarbohydrate/high-fat (LC/HF) diet is also a risk factor of DM. Kaneko et al 7) reported that a dietary modification (a LC/HF diet) before a 75 g oral glucose tolerance test deteriorated glucose tolerance in humans.…”

Section: Introductionmentioning

confidence: 99%

Effect of Aging on the Development of Glucose Intolerance Induced by a Low-Carbohydrate Diet in Rats

Kaneko

Wang

et al. 2003

JOURNAL OF HEALTH SCIENCE

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The effect of aging on the development of glucose intolerance between 2 kinds of diets, a low-carbohydrate/ high-fat (LC/HF) diet and a control diet was investigated. A total of 20 eight-week-old S.D. rats were randomly divided into 2 groups of 10 rats each and at 10, 20, 40, 60 and 80 weeks of age, rats were switched to either control or LC/HF diet for 7 days. At 16:00 on the day following the 7th day of feeding, rats underwent an oral glucose tolerance test (OGTT). LC/HF feeding for 7 days impaired the glucose tolerance in rats. Moreover, insulin secretion decreased with age and insulin resistance increased after 60 weeks of age when rats were fed the LC/HF diet, and fasting plasma free fatty acids (FFA) concentrations increased with age. Thus, we speculated that the age-related impairment of insulin action through the glucose fatty-acid cycle might be closely associated with the onset and development of diabetes mellitus.Key words ---aging, carbohydrate, glucose tolerance, insulin resistance, insulinogenic index, rat age and diet on insulin secretion and insulin action in rats. However, the diets that they used were not isocaloric and the concentrations of nutrients were not constant. In this study, we gave test diets for 7 days to rats of various ages up to 80 weeks old, which corresponds to middle-age in humans, and we compared the effect of aging on the development of glucose intolerance between the 2 kinds of diets, a LC/HF diet and a control diet using a pair-feeding method.

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Aging changes tissue-specific glucose metabolism in rats

Cited by 9 publications

References 9 publications

Liver-Derived IGF-I is of Importance for Normal Carbohydrate and Lipid Metabolism

Liver-Derived IGF-I is of Importance for Normal Carbohydrate and Lipid Metabolism

Age-dependent changes in phenotypes and candidate gene analysis in a polygenic animal model of Type II diabetes mellitus; NSY mouse

Effect of Aging on the Development of Glucose Intolerance Induced by a Low-Carbohydrate Diet in Rats

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