Normal Diet-fed Rats Research Articles

Catechin-rich green tea extract increases serum cholesterol levels in normal diet- and high fat diet-fed rats

Background In vivo studies using rodents have shown that green tea extract and catechins isolated from green tea can induce a variety of health effects, including anti-obesity, hypoglycemic and hypolipidemic activities [1]. These beneficial effects of green tea have been observed in experiments using high fat, high cholesterol and high fructose diet-fed animals. In the present study, we examined the effects of catechinrich green tea extract on serum glucose and lipid levels in normal diet-and high fat diet-fed rats.

Lipolytic Effects of Zingerone in Adipocytes Isolated from Normal Diet-Fed Rats and High Fat Diet-Fed Rats

Lipolytic Effects of Zingerone in Adipocytes Isolated from Normal Diet-Fed Rats and High Fat Diet-Fed Rats

Lipolytic Effects of Genistein and Daidzein in Adipocytes Derived from Normal Diet-fed Rats and High Fat Diet-fed Rats

Lipolytic Effects of Genistein and Daidzein in Adipocytes Derived from Normal Diet-fed Rats and High Fat Diet-fed Rats

Obesity is the major contributor to vascular dysfunction and inflammation in high-fat diet hypertensive rats

Obesity and hypertension are the two major risk factors that contribute to the progression of end-stage renal disease. To examine whether hypertension further exacerbates oxidative stress and vascular dysfunction and inflammation in obese rats, four groups of male Sprague-Dawley rats were fed either a normal (7% fat) or high-fat (36% fat) diet for 6 weeks and osmotic pumps were implanted to deliver ANG (angiotensin II) or vehicle for an additional 4 weeks.Treatment with the high-fat diet did not alter ANG-induced hypertension compared with the normal diet (174 +/- 6 compared with 170 +/- 5 mmHg respectively). Treatment with the high-fat diet increased body weight gain and plasma leptin levels and induced insulin resistance in normotensive and ANG-induced hypertensive rats. Plasma TBARS (thiobarbituric acid-reacting substances), a measure of oxidative stress, were elevated in high-fat diet-fed rats compared with controls (11.2 +/-1 compared with 8.4 +/- nmol/ml respectively) and was increased further in ANG-induced hypertensive rats fed a high-fat diet (18.8 +/-2.2 nmol/ml). Urinary nitrite excretion was also decreased in rats fed a high-fat diet without or with ANG infusion compared with controls. Afferent arteriolar relaxation to acetylcholine was impaired in rats fed the high-fat diet without or with ANG infusion. Renal cortical TNF-alpha(tumour necrosis factor-alpha), COX-2(cyclo-oxygenase-2) and phospho-IKK (inhibitor of nuclear factor k B kinase) expression increased in high-fat diet-fed rats compared with normal diet-fed rats. The increases in phospho-IKK and COX-2 expression were elevated further in ANG-induced hypertensive rats fed the high-fat diet.These results suggest that ANG-induced hypertension exacerbates oxidative stress and renal inflammation without further impairment in vascular dysfunction in high-fat diet-induced obesity.

Effect of a High‐fat Diet on 24‐Hour Pattern of Circulating Adipocytokines in Rats

We have shown a significant disruption of 24-h pattern of plasma pituitary, adrenal, and gonadal hormones in high-fat-fed rats. Our objective was to assess the effect of a high-fat diet (35% fat) on mean levels and 24-h pattern of several adipocytokines in rats. A normal diet-fed rats (4% fat) were used as controls. When body weight of high-fat-fed rats attained values about 25% higher than controls (after 66 days of treatment), the animals were killed at six different time intervals throughout a 24-h cycle. Plasma concentrations of insulin, adiponectin, interleukin (IL)-1, leptin, ghrelin, plasminogen activator inhibitor-1 (PAI-1), and monocyte chemoattractant protein-1 (MCP-1) were measured in a multianalyte profiling by using the Luminex-100 system. Tumor necrosis factor alpha (TNFalpha) and IL-6 were measured by enzyme-linked immunosorbent assay. A significant hyperglycemia developed in high-fat-fed rats, together with a significant increase in plasma insulin. Mean levels of plasma adiponectin, IL-1, IL-6, TNFalpha, and leptin augmented, and ghrelin decreased, in high-fat-fed rats. The normal daily pattern of plasma insulin, adiponectin, IL-1, IL-6, TNFalpha, leptin, ghrelin, and MCP-1 became disrupted in high-fat-fed rats. The results indicate that a high-fat diet may bring about signs of insulin resistance and mild inflammation in rats, together with the disruption in daily variations of circulating insulin and ghrelin, and of several adipocytokines including leptin, adiponectin, IL-1, IL-6, TNFalpha, and MCP-1.

Increased Plasma Dipeptidyl Peptidase IV (DPP IV) Activity and Decreased DPP IV Activity of Visceral But Not Subcutaneous Adipose Tissue in Impaired Glucose Tolerance Rats Induced by High-Fat or High-Sucrose Diet

Several studies have investigated whether dipeptidyl peptidase IV (DPP IV) activity is correlated to the severity of diabetes; however, it remains unclear. To investigate the roles of DPP IV activity in metabolic abnormalities, impaired glucose tolerance rats were produced using a high-fat (HF) or high-sucrose (HS) diet. HF diet-fed rats obviously exhibited impaired glucose tolerance, with increases in subcutaneous and epididymal fat mass, insulin resistance and dyslipidaemia. In rats fed a HS diet rather than a normal diet, lower body weight and fasting blood glucose were observed temporarily in the early period after HS diet feeding; however, impaired glucose tolerance was evoked to some extent with an increase in epididymal fat mass. Both HF and HS diet-fed rats showed significantly higher plasma DPP IV activity than normal diet-fed rats, in the order of HF diet>HS diet>normal diet. HF and HS diets did not significantly affect DPP IV activity and mRNA expression in the kidney. On the other hand, HF, but not HS, diet caused a significant decrease in DPP IV activity in the liver as compared to the control. Of note, both HF and HS diets caused a significant decrease in DPP IV activity in epididymal fat, even though they did not change DPP IV activity in subcutaneous fat. In conclusion, HF or HS diet-induced impaired glucose tolerance with visceral fat accumulation may be interrelated with increased plasma DPP IV activity and decreased DPP IV activity of visceral but not subcutaneous adipose tissue.

Effects of yeast hydrolysate on neuropeptide Y (NPY) and tryptophan hydroxylase (TPH) immunoreactivity in rats

To investigate the appetite regulation mechanism of low and high molecular weight yeast hydrolysate, neuropeptide Y (NPY) and tryptophan hydroxylase (TPH) expressions were analyzed in the brains on rats using immunohistochemical method; normal diet (control), 0.1 g/kg (BY-1) or 1.0 g/kg (BY-2) of yeast hydrolysate below 10 kDa, 0.1 g/kg (AY-1) or 1.0 g/kg (AY-2) of yeast hydrolysate of 10-30 kDa. Body weight gain was lower in the BY-2 (133.0 g) than in the control (150.1 g) (p < 0.05). Triacylglyceride, total cholesterol, and LDL-cholesterol levels were lower in the BY-2 as compared to control, BY-1 and AY-2 (p < 0.05). NPY staining intensities at paraventricular nucleus (PVN) were lower in the BY groups (BY-1: 96.1, BY-2: 88.6) as compared to the control (105.6) and AY groups (AY-1: 110.5, AY-2: 114.1) (p < 0.05). NPY expression at lateral hypothalamic area (LHA) was lower in the BY-2 (92.3) than in the control (98.9) (p < 0.05). The BY groups (BY-1: 143.9, BY-2: 154.6) had higher TPH staining intensities at dorsal raphe (DR) than the AY-2 (115.9) (p < 0.05). In conclusion, the results indicate that administering yeast hydrolysate of below 10 kDa to normal diet-fed rats reduced body weight gain and serum lipids by altering NPY and TPH expressions.

Appetite suppressive effects of yeast hydrolysate on nitric oxide synthase (NOS) expression and vasoactive intestinal peptide (VIP) immunoreactivity in hypothalamus

To investigate the effects of yeast hydrolysate on appetite regulation mechanisms in the central nervous system, nitric oxide synthase (NOS) expression and vasoactive intestinal peptide (VIP) immunoreactivity in the paraventricular nucleus (PVN) and ventromedial hypothalamic nucleus (VMH) of the hypothalamus were examined. Male Sprague-Dawley (SD) rats were assigned to five groups: control (normal diet), BY-1 and BY-2 (normal diet with oral administration of 0.1 g and 1.0 g of yeast hydrolysate <10 kDa/kg body weight, respectively), AY-1 and AY-2 (normal diet with oral administration of 0.1 g and 1.0 g of yeast hydrolysate 10-30 kDa/kg body weight, respectively). The body weight gain in the BY groups was less than that in the control. In particular, the weight gain of the BY-2 group (133.0 +/- 5.1 g) was significantly lower (p < 0.05) than that of the control group (150.1 +/- 3.7 g). Among the test groups, the BY-2 group was shown to have significantly lower triacylglycerol (TG) levels (p < 0.05) than the other groups. The staining intensities and optical densities of NOS neurons in the PVN of the AY group were significantly higher (p < 0.05) than in the control and BY groups. The staining intensities and optical densities of VIP immunoreactivity in the PVN and VMH of the BY groups were higher than those of the AY groups and the control. In conclusion, these results indicated that yeast hydrolysate of <10 kDa reduced the body weight gain and body fat in normal diet-fed rats and increased the lipid energy metabolism by altering the expression of NOS and VIP in neurons.

Chronic Administration of Satsuma Mandarin Fruit (Citrus unshiu MARC.) Improves Oxidative Stress in Streptozotocin-Induced Diabetic Rat Liver

Fruits and vegetables contain numerous antioxidants such as carotenoids, vitamins, and phenolic phytochemicals. Recent studies have demonstrated that antioxidants may reduce the risk for diabetes or its complications. In this study, we investigated the effects of the chronic administration of Satsuma mandarin fruit on an antioxidant defense system in streptozotocin (STZ)-induced diabetic rat liver. After a ten-week administration of Satsuma mandarin, antioxidant enzymes and glutathione levels in the liver were evaluated. The superoxide dismutase (SOD), catalase, and glutathione-peroxidase (GPx) activities, and glutathione level in the STZ-induced diabetic rats liver decreased significantly compared with those in the age-matched normal rats. The glutathione-reductase (GR) activities did not differ significantly between these two groups. In contrast, the SOD, GR, and glutathione levels in the Satsuma mandarin (1% or 3%) diet-fed STZ-diabetic rat livers were significantly higher than those in the normal diet-fed STZ-diabetic rat livers. In addition, although the serum alanine aminotransferase and gamma-glutamyl-aminotransferase concentrations of normal diet-fed STZ-diabetic rats were significantly higher than those of the age-matched normal rats, these increments of serum liver enzymes were diminished by the chronic administration of Satsuma mandarin. These results suggest that Satsuma mandarin may act as a suppressor against liver cell damage and inhibit the progression of liver dysfunction induced by chronic hyperglycemia.

Increased functional Na(+)-K+ pump activity in the vasculature of fructose-fed hyperinsulinemic and hypertensive rats.

We hypothesized that hyperinsulinemia may alter insulin's ability to stimulate vascular Na+/K(+)-ATPase pump activity and modulate changes in vascular responsiveness associated with hypertension. We measured potassium-induced relaxation as an indicator of Na+/K(+)-ATPase pump activity in isolated femoral arteries from fructose-fed (FF) hyperinsulinemic, Sprague-Dawley rats. FF rats had higher mean arterial blood pressures than did normal diet-fed (NF) rats (FF, 125 +/- 2.2, n = 20, vs. NF, 113.5 +/- 2.5 mmHg, n = 20, p < 0.05) and were hyperinsulinemic (FF, 64 +/- 4 vs. NF, 37 +/- 2, microU/ml insulin, p < 0.01). FF rats were more sensitive to KCl in the Na+/K+ pump bioassay (FF, 0.86 +/- 0.07, n = 21 vs. NF, 1.18 +/- 0.08, n = 17, p < 0.05, expressed as ED50 in mmol/l KCl). Exogenous insulin (100 mU/ml) increased Na+/K+ pump sensitivity in FF rats as compared with a boiled insulin control (insulin 45 +/- 6%, n = 11, vs. control, 11 +/- 7%, n = 13, p < 0.01, expressed as percent increase in sensitivity, i.e., ED50). There were no significant differences in Na+/K+ pump sensitivity between insulin and control responses in the NF animals (insulin 29 +/- 6%, n = 11, vs. control 46 +/- 5%, n = 10, NS). Dose-response curves were obtained in tail and femoral arteries from the same animals to norepinephrine and acetylcholine, basally and after exogenous insulin. FF vessels had reduced sensitivity to norepinephrine as compared with the NF group. Insulin increased sensitivity to acetylcholine-induced relaxations and increased AII-induced contractions in FF-rat vessels. These data suggest that in the FF rat insulin's influence on the vascular Na+/K+ pump is enhanced and may modulate the changes in vascular responsiveness seen in this model.

Modifications of Antioxidant Capacity and Heart Electrical Activity Induced by Hydroperoxide in Normal and Vitamin E-Fed Rats

Wistar rats, fed control or vitamin E-supplemented diet, were subjected to oxidative stress by a ten day treatment with daily intraperitoneal dose of tert-butyl hydroperoxide (TBHP) (0.1µmol/100 g body weight). The effectiveness of both diet and hydroperoxide treatment was established by determining the antioxidant capacity of blood, liver, and heart with an enhanced luminescence method. While the diet addition of vitamin E increased the antioxidant capacity of all the tissues in treated and untreated animals, the hydroperoxide treatment failed to decrease liver antioxidant capacity in control diet fed animals. The effect of the reiterated production of free radicals on electrophysiological properties of myocardium was determined by studying the heart rate in vivo and the time course of the surface electrical activity in papillary muscle fibers in vitro. In vivo, a significant tachycardia was found only in TBHP-treated, normal diet fed rats. The duration of action potential, recorded in Krebs' solution at 26°C, was not affected by diet in untreated animals but was modified by hydroperoxide treatment in a diet-dependent way: shortened in normal diet-fed rats and lengthened in vitamin E-supplemented diet-fed rats. On the basis of analogies with the results of electrophysiological recordings on dif ferent preparations subjected to oxidative stress in vitro, we suggest that the changes of action potential duration might depend on relative levels of added pro-oxidant and cell antioxidants.

Aging impairs pancreatic response to refeeding following a protein-free diet.

Changes in content and recovery of pancreatic enzymes after a protein-free diet were examined in young (8-month) and old (26-month) Fischer-344 female rats. In control rats fed a normal diet for 15 days, no significant difference between young and old rats was observed in pancreatic weight or in pancreatic content of protein, enzymes, and DNA. A 7-day protein-free diet significantly decreased pancreatic wet weight as well as content of protein, chymotrypsin, amylase, and DNA in both age groups, whereas body weight and amount of daily food intake did not differ from respective control values (in normal diet-fed rats) in either age group. In young rats, chymotrypsin and protein contents were significantly greater than control values during the recovery period in which rats were fed a normal diet following the 7-day protein-free treatment. In contrast, these values in old rats remained lower than corresponding control values throughout the entire recovery period. These results agree with our previous study suggesting that aging probably attenuates the reserve capacity of the pancreas for enzyme secretion, but not its basal functions.