The Effect of Dietary Energy Restriction on Body Weight Gain and the Development of Noninsulin‐Dependent Diabetes Mellitus (NIDDM) in Psammomys obesus

Abstract

Food intake was restricted to 75% of ad libitum levels in 37 male Psammomys obesus (Israeli Sand Rats) from the ages of 4 (weaning) to 10 weeks. Energy restriction reduced the mean bodyweight at 10 weeks by 29% compared with 44 ad libitum fed controls. Hyperglycemia was prevented completely in the food-restricted group, and mean blood glucose concentrations were significantly reduced (3.8 * 0.2 vs. 5.5 * 0.4 pmoVL; pe0.05) compared with control animals. Plasma insulin concentrations were also decreased significantly compared with ad libitum fed controls (105 * 13 vs. 241 f 29 mU/L; pe0.05). Although energy restriction prevented hyperglycemia from developing in 10-week-old P. obesus, 19% of the food restricted animals still developed hyperinsulinemia. We concluded that hyperphagia between the ages of 4 to 10 weeks may be essential for the development of noninsulin-dependent diabetes mellitus in P. obesus, but that hyperinsulinemia may still occur in the absence of hyperphagia and hyperglycemia, suggesting a Submitted for publication December 18, 1995. Accepted for publication October 17, 1996. From the 'School of Nutrition and Public Health, Deakin University, Geelong, Victoria, Australia, and the 'International Diabetes Institute, Caulfield, Australia. Reprint requests to G.R. Collier, School of Nutrition and Public Health, Deakin University, Geelong, Victoria, Australia, 3217. Copyright 0 1997 NAASO. significant genetic influence on the development of hyperinsulinemia in this animal model.

Synthetic protease inhibitor camostat prevents and reverses dyslipidemia, insulin secretory defects, and histological abnormalities of the pancreas in genetically obese and diabetic rats

“…Adipose tissue produces and secretes a large number of hormones, cytokines, and proteins that affect glucose homeostasis and insulin sensitivity, including leptin, TNF-a, peroxisome proliferator-activated receptor (PPAR) c, resistin, and adiponectin [28,29]. Previous studies have shown that reduction of body weight by caloric restriction [30][31][32], surgical removal of intra-abdominal fat pads [33,34], or oral administration of a-glucosidase inhibitor acarbose [35,36] results in improvement of insulin actions in obese rodent models including OLETF rats. Therefore, it is possible that the effects of camostat in OLETF rats observed in the present study are based on weight loss or failure of weight gain.…”

The Metabolic Syndrome X

“…84 In the gerbil, Psammomys obesus, dietary energy restriction to slow weight gain has also had powerful effects to prevent hyperglycemia, although some hyperinsulinemia still developed under calorie restraint. 85…”

Leptin resistance in a polygenic, hyperleptinemic animal model of obesity and NIDDM: Psammomys obesus

“…In a laboratory setting, on a diet of normal laboratory chow, a signi®cant proportion of these animals develop hyperinsulinaemia, hypertriglyceridaemia, hypercholesterolaemia and elevated leptin levels, making it a unique model of obesity and NIDDM. 11,12,14 The phenotypic range of body weight and plasma leptin concentrations in Psammomys obesus make it more analogous to human obesity than the single-gene mutant models such as obaob mice. Therefore the ®ndings of these studies may be particularly relevant to the use of leptin as a therapeutic agent for human obesity.…”

“…Previous studies have shown that these animals had signi®cantly greater body fat content than those classi®ed as lean (body weight`190 g at 12 weeks of age). 11,12,14 Experimental protocol A group of Psammomys obesus were housed individually and followed for at least a 7 d period, with free access to food and water, to establish baseline data for food intake (measured by the rate of disappearance), body weight, blood glucose and plasma insulin concentrations. The animals were characterised (as described above) into lean or obese groups (n 24 in each group).…”