Plasma Of Obese Rats Research Articles

Dietary supplementation with L-leucine reduces nitric oxide synthesis by endothelial cells of rats.

This study tested the hypothesis that elevated L-leucine concentrations in plasma reduce nitric oxide (NO) synthesis by endothelial cells (ECs) and affect adiposity in obese rats. Beginning at four weeks of age, male Sprague-Dawley rats were fed a casein-based low-fat (LF) or high-fat (HF) diet for 15 weeks. Thereafter, rats in the LF and HF groups were assigned randomly into one of two subgroups (n = 8/subgroup) and received drinking water containing either 1.02% L-alanine (isonitrogenous control) or 1.5% L-leucine for 12 weeks. The energy expenditure of the rats was determined at weeks 0, 6, and 11 of the supplementation period. At the end of the study, an oral glucose tolerance test was performed on all the rats immediately before being euthanized for the collection of tissues. HF feeding reduced (P < 0.001) NO synthesis in ECs by 21% and whole-body insulin sensitivity by 19% but increased (P < 0.001) glutamine:fructose-6-phosphate transaminase (GFAT) activity in ECs by 42%. Oral administration of L-leucine decreased (P < 0.05) NO synthesis in ECs by 14%, increased (P < 0.05) GFAT activity in ECs by 35%, and reduced (P < 0.05) whole-body insulin sensitivity by 14% in rats fed the LF diet but had no effect (P > 0.05) on these variables in rats fed the HF diet. L-Leucine supplementation did not affect (P > 0.05) weight gain, tissue masses (including white adipose tissue, brown adipose tissue, and skeletal muscle), or antioxidative capacity (indicated by ratios of glutathione/glutathione disulfide) in LF- or HF-fed rats and did not worsen (P > 0.05) adiposity, whole-body insulin sensitivity, or metabolic profiles in the plasma of obese rats. These results indicate that high concentrations of L-leucine promote glucosamine synthesis and impair NO production by ECs, possibly contributing to an increased risk of cardiovascular disease in diet-induced obese rats.

Irradiation of carotid baroreceptor with low-intensity pulsed ultrasound exerts different metabolic protection in perirenal, epididymal white adipose tissue and interscapular brown adipose tissue of obese rats.

This study was designed to clarify whether the irradiation of carotid baroreceptor (CB) with low-intensity pulsed ultrasound (LIPUS) protects against obesity by rebalancing the autonomic nervous system (ANS). Obesity was induced using a high-fat diet (HFD) for 8weeks in Sprague-Dawley rats. Irradiation with LIPUS was daily (20minutes a day) applied to the right CB. In our study, LIPUS significantly ameliorated metabolic disorders in obese rats. LIPUS partly restored norepinephrine (NE) and acetylcholine (ACH) levels in the perirenal white adipose tissue (PWAT), epididymal white adipose tissue (EWAT), interscapular brown adipose tissue (IBAT), and plasma of obese rats. LIPUS partially rectified the dysregulated AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor (PPAR) α/ɣ pathway in the PWAT, EWAT, and IBAT of obese rats. PPARγ and PPARγ target genes respond more sensitively to HFD and LIPUS in PWAT and EWAT than in IBAT. NE, ACH, uncoupling protein-1, phosphorylated AMPK, PPARα, and PPARα target genes respond more sensitively to HFD and LIPUS in IBAT than in PWAT and EWAT. Conclusion: LIPUS irradiation of CB exerts different metabolic protection in PWAT, EWAT, and IBAT by rebalancing the ANS and rectifying the AMPK/PPARα/ɣ pathway in obese rats.

Swimming exercise increases serum irisin level and reduces body fat mass in high-fat-diet fed Wistar rats.

BackgroundIt has been shown that irisin levels are reduced in skeletal muscle and plasma of obese rats; however, the effect of exercise training on irisin level remains controversial. We aim to evaluate the association of swimming exercise with serum irisin level and other obesity-associated parameters.MethodsForty healthy male Wistar rats were randomly assigned to 4 groups: a normal diet and sedentary group (ND group), normal diet and exercise group (NDE group), high-fat diet and sedentary group (HFD group), and high-fat diet and exercise group (HFDE group. After 8 consecutive weeks of swimming exercise, fat mass and serum irisin level was determined.ResultsHigher serum irisin levels were detected in the HFDE group (1.15 ± 0.28 μg/L) and NDE group (1.76 ± 0.17 μg/L) than in the HFD group (0.84 ± 0.23 μg/L) or the ND group (1.24 ± 0.29 μg/L), respectively (HFDE group vs. HFD group, P < 0.05; NDE group vs. ND group, P < 0.01). Pearson’s correlation analysis showed that serum irisin level negatively correlated with TG level (r = −0.771, P < 0.05), percentage fat mass (r = −0.68, P < 0.05), fat mass (r = −0.576, P < 0.05), visceral fat mass (r = −0.439, P < 0.05) and TC level (r = −0.389, P < 0.05). The fat mass, visceral fat mass and percentage fat mass were lower in the HFDE group than the HFD group (all P values < 0.01).ConclusionSwimming exercise decreases body fat mass in high-fat-fed Wistar rats, which may be attributable to elevated irisin levels induced by swimming exercise.

Cereal based diets modulate some markers of oxidative stress and inflammation in lean and obese Zucker rats

BackgroundThe potential of cereals with high antioxidant capacity for reducing oxidative stress and inflammation in obesity is unknown. This study investigated the impact of wheat bran, barley or a control diet (α-cellulose) on the development of oxidative stress and inflammation in lean and obese Zucker rats.MethodsSeven wk old, lean and obese male Zucker rats (n = 8/group) were fed diets that contained wheat bran, barley or α-cellulose (control). After 3 months on these diets, systolic blood pressure was measured and plasma was analysed for glucose, insulin, lipids, oxygen radical absorbance capacity (ORAC), malondialdehyde, glutathione peroxidase and adipokine concentration (leptin, adiponectin, interleukin (IL)-1β, IL-6, TNFα, plasminogen activator inhibitor (PAI)-1, monocyte chemotactic protein (MCP)-1). Adipokine secretion rates from visceral and subcutaneous adipose tissue explants were also determined.ResultsObese rats had higher body weight, systolic blood pressure and fasting blood lipids, glucose, insulin, leptin and IL-1β in comparison to lean rats, and these measures were not reduced by consumption of wheat bran or barley based diets. Serum ORAC tended to be higher in obese rats fed wheat bran and barley in comparison to control (p = 0.06). Obese rats had higher plasma malondialdehyde (p < 0.01) and lower plasma glutathione peroxidase concentration (p < 0.01) but these levels were not affected by diet type. PAI-1 was elevated in the plasma of obese rats, and the wheat bran diet in comparison to the control group reduced PAI-1 to levels seen in the lean rats (p < 0.05). These changes in circulating PAI-1 levels could not be explained by PAI-1 secretion rates from visceral or subcutaneous adipose tissue.ConclusionsA 3-month dietary intervention was sufficient for Zucker obese rats to develop oxidative stress and systemic inflammation. Cereal-based diets with moderate and high antioxidant capacity elicited modest improvements in indices of oxidative stress and inflammation.

Metabolism of high-density lipoprotein in the hyperlipidemic, diabetic [formula omitted] rat

The SHR N -corpulent rat is a new genetically obese strain that is both hyperlipidemic and diabetic. The high density lipoprotein (HDL) fraction from 12-week-old obese males contained significantly greater amounts of protein (+83%), free (+72%) and esterified (+76%) cholesterol, phospholipid (+94%), and triglyceride (+78%). HDL from obese rats were also enriched in C apolipoproteins (apo C-III 0 and apo C-III 3) but had similar relative amounts of both apo A-I and apo E compared to HDL from their lean littermates. HDL protein turnover, measured with 125I-labeled HDL, showed that obese rats had a smaller fractional catabolic rate (FCR) than lean rats, but due to their much larger HDL pool size, they had a significantly higher rate of HDL protein catabolism (obese, 1.98 ± 0.07 mg/whole animal/h v lean, 1.32 ± 0.05 mg/whole animal/h). Therefore, under steady-state conditions, HDL protein production must also have been increased in the obese animals. To determine whether the increased catabolism of HDL protein was associated with increased catabolism of cholesteryl ester (CE), tissue uptake of HDL CE was measured using the nonhydrolyzable ether analogue [ 3H]cholesteryl linoleyl ether. After four hours 41.6 ± 1.6% of the injected dose was cleared from the plasma of lean rats compared with 37.0 ± 1.1% from the plasma of obese rats. In both groups almost one third of the injected dose appeared in the liver ( (lean, 31.01 ± 1.95% v obese, 30.07 ± 1.17%). However, taking into account that the HDL CE pool in the obese rats was more than 80% larger than in the lean rats, total hepatic catabolism of HDL CE was much greater in the obese animals. Adipose tissue and the small intestine also catabolized more HDL CE in the obese v lean rats. We conclude that the increased levels of HDL protein and HDL CE in the obese rats are due predominantly to overproduction rather than to impaired catabolism of HDL, and that the liver remains quantitatively the most important site for HDL CE catabolism in these animals.

Thyroid status in the obese syndrome of rats.

The thyroid function was explored by comparing serum total and free iodothyronine levels in young male genetically obese Zucker rats and in their lean littermates, aged from 6 to 8 weeks old. Total and free thyroxine (T4) and 3,5,3'triiodothyronine (T3) levels were significantly decreased in obese rat serum while total 3,3',5'-triiodothyronine (rT3) remained constant. Radioactive T4 half life is slower in the plasma of obese rats. Peripheral synthesis of T3 from deiodination of T4 is also decreased in obese rat liver homogenate. These modifications produce changes in liver mitochondria oxidative phosphorylation and in marker enzyme activity, which are usually associated with hypothyroidism and hypothalamic disturbances. Genetic obesity probably involves activation of peripheral deiodination of T4 to rT3 which induces biochemical and metabolic changes.

Brain serotonergic activity and plasma amino acid levels in genetically obese Zucker rats

In order to test the hypothesis that serotonergic activity is abnormal in the brains of genetically obese Zucker rats, levels of serotonin (5-HT), its amino acid precursor, tryptophan (Trp), and its major metabolite, 5-hydroxyindoleacetic acid (5-HIAA) were measured in eight brain regions in groups of obese and non-obese male rats. Plasma albumin levels as well as levels of amino acids and related compounds in plasma and in a cortical sample were also determined in the same animals. While Trp was lower in several brain regions of the obese animals, the only region showing a depressed level of 5-HT in the obese group was the mesencephalon. Obese animals also had a lower amount of 5-HIAA in the diencephalon, but no other differences were significant. Both elevations and depressions were observed in cortical amino acid levels in obese animals. The level of plasma albumin was increased in the obese group. Free Trp was decreased in the plasma of obese rats while levels of other amino acids (methionine, leucine, isoleucine, valine and phenylalanine) which compete with Trp for transport across the blood-brain barrier were elevated. Thus the combination of lower plasma free Trp and increased levels of competitive amino acids appears to contribute to decreased levels of Trp in the brain of genetically obese rats.