Literature DB >> 10691995

A metabolic syndrome of hypertension, hyperinsulinaemia and hypercholesterolaemia in the New Zealand obese mouse.

J R Ortlepp1, R Kluge, K Giesen, L Plum, P Radke, P Hanrath, H G Joost.   

Abstract

BACKGROUND: New Zealand obese (NZO) mice exhibit a polygenic obesity associated with hyperinsulinaemia and hyperglycaemia. Here we show that the strain presents additional features of a metabolic syndrome, i.e. elevated blood pressure, serum cholesterol and serum triglyceride levels.
MATERIALS AND METHODS: A back-cross model of NZO mice with the lean Swiss Jackson Laboratory (SJL) strain was established in order to investigate further the correlation between hypertension, obesity, serum insulin and hyperglycaemia.
RESULTS: Systolic blood pressure was significantly elevated at 6 weeks of age and appeared to parallel the weight gain of the animals. Serum insulin levels, presumably reflecting insulin resistance, and systolic blood pressure values were significantly correlated with the body mass index (r2 = 0.707 and 0.486, respectively) in the back-cross mice. In contrast, blood pressure was only weakly correlated with serum insulin (r2 = 0.288) in non-diabetic mice, and was independent of serum insulin levels in diabetic animals.
CONCLUSION: The data are consistent with the concept that hypertension and insulin resistance are a characteristic consequence of the genetic constellation leading to obesity in the NZO strain, and that these traits reflect related mechanisms. It appears unlikely, however, that hypertension is a direct consequence of hyperinsulinaemia.

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Year:  2000        PMID: 10691995     DOI: 10.1046/j.1365-2362.2000.00611.x

Source DB:  PubMed          Journal:  Eur J Clin Invest        ISSN: 0014-2972            Impact factor:   4.686


  18 in total

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9.  Skeletal muscle mitochondrial uncoupling prevents diabetes but not obesity in NZO mice, a model for polygenic diabesity.

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10.  Leptin Receptor Blockade Attenuates Hypertension, but Does Not Affect Ventilatory Response to Hypoxia in a Model of Polygenic Obesity.

Authors:  Lenise J Kim; Mi-Kyung Shin; Huy Pho; Laszlo Otvos; Sergio Tufik; Monica L Andersen; Luu V Pham; Vsevolod Y Polotsky
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