The aim of the study was to characterize the time course of the development of high-fat diet-induced hepatic steatosis and its relation to body fat accretion and changes in plasma lipid profile. Female Sprague -Dawley rats were high-fat fed (HF; 42 %, kJ) for 1, 2, 4, 6, 12 and 16 weeks and compared to standard fed rats (SD). Data obtained from HF rats were further analysed by classifying the animals into obesity-prone and obesityresistant. In HF rats, liver lipid content increased rapidly by approximately 200 %d uring the first 2w eeks, decreased almost to baseline levels between weeks 2a nd 6, and re-increased by 17 %b etween weeks 6a nd 16 ( P , 0·05). Body weight, body fat accretion, plasma leptin, NEFA and glycerol concentrations were higher in HF than in SD rats ( P , 0·05). These higher values were established in 2w eeks and the differences between the groups did not further enlarge from weeks 2to16. Obesity-prone rats depicted higher body weight and body fat accretion than obesity-resistant and SD rats. Surprisingly, however, liver lipid content was the same in obesity-prone as in obesity-resistant rats as they were both higher than in SD rats (weeks 2a nd 16; P , 0·05). Our data support the hypothesis that the liver acts as as ystemic buffer, largely increasing its lipid content in the early stage of high-fat feeding. Our results also suggest that the development of non-alcoholic hepatic steatosis is more linked to dietary fat ingestion than to body weight gain.

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This study was undertaken to evaluate the effects of regular endurance-type exercise on glucose tolerance and glucose-stimulated insulin response (GSIR) in ovariectomized (OVX) rats with and without estrogen replacement. To do that, OVX Sprague-Dawley rats were compared with an OVX estradiol-treated group (OVXE2) and a sham-operated (Sham) group. Each of these groups was subdivided into a sedentary and a treadmill-trained (8 wk) group. Intravenous glucose tolerance tests (0.5 g/kg) were conducted in all rats 48 h after the last training session. Plasma levels of 17beta-estradiol and the uterus weight were significantly (P < 0.05) lower in OVX compared with results in Sham and significantly (P < 0.01) higher in OVXE2 (hyperestrogenic) compared with results in Sham. Body weights were significantly (P < 0.01) different among groups, in the following decreasing order: OVX, Sham, and OVXE2. The average daily food intake was significantly (P < 0.01) increased in OVX rats compared with Sham, whereas estradiol treatment diminished this effect (P < 0.01). Exercise training was found to alter none of the above-mentioned variables in all three experimental conditions. Although the mean integrated area under the glucose and insulin curves was not affected by OVX, training induced a significant (P < 0.01) reduction in the mean integrated area under the insulin curve in all three experimental conditions. It is concluded that the positive effects of physical training on improving GSIR in OVX and hyperestrogenic animals are similar to what has been found in Sham.

Regular physical activity is beneficial in preventing the risk of cardiovascular complications of diabetes. Recent studies showed a cardioprotective role of oxytocin (OT) to induce natriuretic peptides (NPs) and nitric oxide (NO) release. It is not known if the diabetic state is associated with a reduced OT-NPs-NO system and if exercise training improves this system. To address this, we investigated the effects of treadmill running using the db/db mouse model of type 2 diabetes. Eight-week-old db/db mice were subjected to running 5 days per week for a period of 8 weeks. The lean db/+ littermates were used as controls. Sedentary db/db mice were obese and hyperglycaemic, and exercise training was not effective in reducing body weight and the hyperglycaemic state. Compared to control mice, db/db mice had lower heart weight and heart-to-body weight ratios. In these mice, this was associated with augmented cardiac apoptosis, cardiomyocyte enlargement and collagen deposits. In addition, db/db mice displayed significant downregulation in gene expression of OT (76%), OT receptors (65%), atrial NP (ANP; 43%), brain NP (BNP; 87%) and endothelial nitric oxide synthase (eNOS) (54%) in the heart (P < 0.05). Exercise training had no effect on expression of these genes which were stimulated in control mice. In response to exercise training, the significant increment of anti-apoptotic Bcl-2 gene expression was observed only in control mice (P < 0.05). In conclusion, downregulation of the OT-NPs-NO system occurs in the heart of the young db/db mouse. Exercise training was not effective in reversing the defect, suggesting impairment of this cardiac protective system in diabetes.