A comparison between the impact of two types of dietary protein on brain glucose concentrations and oxidative stress in high fructose-induced metabolic syndrome rats.

The present study explored the potential of fish proteins to counteract high glucose levels and oxidative stress induced by fructose in the brain. A total of 24 male Wistar rats consumed sardine protein or casein with or without high fructose (64%). After 2 months, brain tissue was used for analyses. The fructose rats exhibited an increase in body mass index (BMI), body weight, absolute and relative brain weights and brain glucose; however, there was a decrease in food and water intake. Fructose disrupts membrane homeostasis, as evidenced by an increase in the brain hydroperoxides and a decrease in catalase (CAT) and glutathione peroxidase (GSH-Px) compared to the control. The exposure to the sardine protein reduced BMI, food intake, glucose and hydroperoxides, and increased CAT and GSH-Px in the brain. In conclusion, the metabolic dysfunctions associated with the fructose treatment were ameliorated by the presence of sardine protein in the diet by decreasing BMI, brain glucose and lipid peroxidation, and increasing CAT and GSH-Px activities.

The metabolic syndrome of fructose-fed rats: effects of long-chain polyunsaturated ω3 and ω6 fatty acids. V. Post-mortem findings.

The present study deals with the possible effects of dietary ω3 and ω6 fatty acids upon the metabolic syndrome found in rats exposed for 8 weeks to a diet containing 64% (w/w) D-fructose instead of starch. Fructose-fed rats were found to display a modest increase in plasma albumin and protein concentration and more pronounced increases in plasma urea, creatinine, phospholipids, triglycerides and cholesterol concentrations, glycated hemoglobin concentration and liver contents of cholesterol, triglycerides and phospholipids. The plasma concentrations of HDL-cholesterol, calcium and iron were decreased, however, in the fructose-fed rats. In general, the partial substitution of sunflower oil by either safflower oil or salmon oil opposed the metabolic perturbations otherwise associated with the fructose-induced metabolic syndrome in the fructose-fed rats, with salmon oil demonstrating particular efficacy. Consideration is given to the possible biological determinants of these perturbations and their attenuation in rats exposed to safflower or salmon oil.

The metabolic syndrome of fructose-fed rats: effects of long-chain polyunsaturated ω3 and ω6 fatty acids. VI. Further post-mortem investigations.

The present study documents the increases in systolic arterial blood pressure, plasma leptin concentration and kidney proliferating cell nuclear antigen index, as well as the decreases in glutathione reductase, superoxide dismutase and catalase enzymatic activities in the liver, heart, kidney, soleus muscle and visceral adipose tissue homogenates of female rats exposed for 8 weeks to a diet containing 64% (w/w) D-fructose instead of 64% starch. In the fructose-fed rats, the partial substitution of sunflower oil by either safflower oil or salmon oil often opposed the fructose-induced changes in these variables. The present results, thus, extend to these functional, hormonal and enzymatic parameters the knowledge that the dietary supply of long-chain polyunsaturated ω6 fatty acids, mainly C18:2ω6, and long-chain polyunsaturated ω3 fatty acids opposes the undesirable features of the fructose-induced metabolic syndrome, with salmon oil demonstrating particular efficacy.

The metabolic syndrome of fructose-fed rats: effects of long-chain polyunsaturated ω3 and ω6 fatty acids. VII. Oxidative stress.

In the present study, the plasma concentration, and liver, heart, kidney, soleus muscle and visceral adipose tissue content of thiobarbituric acid reactive substrates (TBARS), carbonyl radicals, hydroperoxides and nitric oxide were measured in control rats exposed for 8 weeks to a diet containing 64% (w/w) starch and 5% sunflower oil and in animals fed a diet containing 64% D-fructose and 5% sunflower oil or 3.4% sunflower oil mixed with 1.6% safflower or salmon oil. Coherent measurements of the plasma concentrations or tissue contents of these metabolites revealed increases in TBARS, carbonyl radical and hydroperoxide levels and a decrease in nitric oxide levels in the 5% sunflower oil-fed rats. In the fructose-fed rats, the partial substitution of sunflower oil by either safflower or salmon oil minimized the changes. These findings provide further evidence in support of the favorable effects of the dietary supply of long-chain polyunsaturated ω6 and ω3 fatty acids upon the metabolic disturbances prevailing in the fructose-induced metabolic syndrome.

The metabolic syndrome of fructose-fed rats: effects of long-chain polyunsaturated ω3 and ω6 fatty acids. III. Secretory behaviour of isolated pancreatic islets.

In the present study, rats were exposed from the 8th week after birth and for the ensuing 8 weeks to diets containing either starch or fructose (64% w/w) and sunflower oil (5%). Two further groups of rats were exposed to the fructose-containing diet with substitution of part (1.6%) of the sunflower diet by an equal amount of either salmon oil rich in long-chain polyunsaturated ω3 fatty acids or safflower oil reach in long-chain polyunsaturated ω6 fatty acids. The insulin content of the islets and their secretory response to D-glucose (5.6, 8.3 and 16.7 mM), to the combination of D-glucose (5.6 mM) and D-fructose (10.0 mM) and to 2-ketoisocaproate (10.0 mM) were then measured. In the sunflower oil-fed rats, the dietary substitution of starch by fructose decreased basal insulin output, lowered the apparent Km for the insulinotropic action of D-glucose and altered the insulinotropic efficiency of the latter hexose relative to that of other nutrients. Some of these secretory perturbations were opposed by the enrichment of the diet in long-chain polyunsaturated fatty acids, especially ω3 fatty acids. It is proposed that these changes in B-cell secretory behaviour may be linked, in part at least, to both the apparent caloric efficiency of each diet, and hence to the regulation of the islet content in endogenous nutrients, and to alteration of insulin sensitivity considered as a major feature of the present animal model of metabolic syndrome.

Dietary sardine protein lowers insulin resistance, leptin and TNF-α and beneficially affects adipose tissue oxidative stress in rats with fructose-induced metabolic syndrome.

The present study aims at exploring the effects of sardine protein on insulin resistance, plasma lipid profile, as well as oxidative and inflammatory status in rats with fructose-induced metabolic syndrome. Rats were fed sardine protein (S) or casein (C) diets supplemented or not with high-fructose (HF) for 2 months. Rats fed the HF diets had greater body weight and adiposity and lower food intake as compared to control rats. Increased plasma glucose, insulin, HbA1C, triacylglycerols, free fatty acids and impaired glucose tolerance and insulin resistance was observed in HF-fed rats. Moreover, a decline in adipose tissues antioxidant status and a rise in lipid peroxidation and plasma TNF-α and fibrinogen were noted. Rats fed sardine protein diets exhibited lower food intake and fat mass than those fed casein diets. Sardine protein diets diminished plasma insulin and insulin resistance. Plasma triacylglycerol and free fatty acids were also lower, while those of α-tocopherol, taurine and calcium were enhanced as compared to casein diets. Moreover, S-HF diet significantly decreased plasma glucose and HbA1C. Sardine protein consumption lowered hydroperoxide levels in perirenal and brown adipose tissues. The S-HF diet, as compared to C-HF diet decreased epididymal hydroperoxides. Feeding sardine protein diets decreased brown adipose tissue carbonyls and increased glutathione peroxidase activity. Perirenal and epididymal superoxide dismutase and catalase activities and brown catalase activity were significantly greater in S-HF group than in C-HF group. Sardine protein diets also prevented hyperleptinemia and reduced inflammatory status in comparison with rats fed casein diets. Taken together, these results support the beneficial effect of sardine protein in fructose-induced metabolic syndrome on such variables as hyperglycemia, insulin resistance, hyperlipidemia and oxidative and inflammatory status, suggesting the possible use of sardine protein as a protective strategy against insulin resistance and related situations.

The metabolic syndrome of fructose-fed rats: effects of long-chain polyunsaturated ω3 and ω6 fatty acids. IV. D-glucose metabolism by isolated pancreatic islets.

The major aim of the present study was to search for changes of D-glucose metabolism in isolated pancreatic islets possibly involved in the alteration of their secretory response to the hexose, as observed when comparing rats exposed for 8 weeks to diets containing either starch and sunflower oil or fructose and sunflower oil, as well as rats exposed to diets containing fructose, sunflower oil and either salmon oil or safflower oil. The substitution of starch by fructose in the diet affected unfavourably D-glucose phosphorylation by the isolated islets. In the fructose-fed rats, there was a close parallelism between D-[5-³H]glucose utilization and the dietary ω3/ω6 fatty acid ratio. There was little to distinguish, however, between the four groups of rats in terms of D-[U-¹4C]glucose oxidation. The paired ratio between D-[U-¹4C]glucose oxidation and D-[5-³H]glucose utilization, which always increased as the concentration of the hexose was raised from 2.8 to 8.3 and 16.7 mM, was tightly related, in the fructose-fed rats, to the HOMA index for insulin resistance.

The metabolic syndrome of fructose-fed rats: effects of long-chain polyunsaturated ω3 and ω6 fatty acids. I. Intraperitoneal glucose tolerance test.

The present series of experiments aim mainly at investigating the possible influence of changes in the com-position of dietary lipids (sunflower oil, salmon oil, safflower oil) upon the metabolic syndrome found in rats exposed to a fructose-rich diet. For purpose of comparison, a control group of rats received the sunflower oil diet with substitution of fructose by starch. An intraperitoneal glucose tolerance test, performed after overnight starvation fifty days after the start of the experiments at the 6th week after birth, indicated, as expected, impaired tolerance to glucose and deterioration of insulin sensitivity (HOMA index), without changes in the insulinogenic index, when comparing the fructose-fed rats to the starch-fed rats both exposed to the sunflower oil diet. In the fructose-fed rats, enrichment of the diet by long-chain polyunsaturated ω3 fatty acids supplied by salmon oil, a modest improvement of insulin sensitivity was opposed, in term of glucose homeostasis, by a decreased secretory response to glucose of insulin-producing cells. Last, in the fructose-fed rats, the partial substitution of sunflower oil by safflower oil rich in long-chain polyunsaturated ω6 fatty acids further deteriorated glucose homeostasis, with a higher mean HOMA index and a severe decrease of the insulinogenic index. These findings justify further investigations on such items as the time course for changes in metabolic and hormonal variables and both the metabolic and secretory responses of isolated pancreatic islets to selected nutrient secretagogues.

Fish protein improves the total antioxidant status of streptozotocin-induced diabetes in spontaneously hypertensive rat.

BACKGROUND: We measured the effects of fish protein (FP) on blood pressure, glycemia and antioxidant status in spontaneously hypertensive (SH) rats with streptozotocin-induced diabetes (STZ). MATERIAL/METHODS: Two groups of 12 rats each were fed 20% casein (C) or FP for 2 months. The total antioxidant status of blood and organs (liver, kidney and heart) was measured by the KRL test. Antioxidant enzyme activities (G-Px, G-Red, and SOD) and antioxidant substances (GSH, NO) were determined in organs, and vitamin C in plasma. RESULTS: FP lowered blood pressure in SH rats, but not in SH-STZ. Blood and plasma antioxidant status increased 35% and 9%, respectively, with FP in SH-STZ compared to SH rats; when compared to C, these values were more enhanced. SOD activity values were elevated with FP in SH-STZ rats, compared to the C diet, regardless of organ. Higher kidney NO and heart GSH values were noted in SH-STZ rats than SH. In SH rats fed FP, the GSH value was 2.26 times higher in liver, and NO was 3 times higher in heart. Higher NO was noted in kidney (1.84 times) and heart (1.91 times), GSH in heart (1.79 times), and vitamin C in plasma (+46%) in SH-STZ rats with FP than with C. CONCLUSIONS: Fish protein has a beneficial effect on blood pressure in SH rats but not in SH-STZ, and plays an important role in antioxidative defense. This protein may be useful in future treatments of such diseases as diabetes and hypertension.

Dietary fish protein lowers blood pressure and alters tissue polyunsaturated fatty acid composition in spontaneously hypertensive rats.

OBJECTIVE: To investigate the effect of two types of dietary protein on blood pressure, liver fatty acid desaturation and composition, and urine 6-keto-prostaglandin-F (PGF(1alpha)) level, the metabolite of prostacyclin. METHODS: 5-wk-old spontaneously hypertensive rats were fed 20% casein or purified fish protein. The fat source was 5% ISIO oil, which contains 47.9% (omega-6) and 1.7% (omega-3) total polyunsaturated fatty acids. After 2 mo on the diet, systolic blood pressure was reduced with fish protein compared with casein (189.8 +/- 10.5 versus 220.7 +/- 8.7). RESULTS: Excretion of 6-keto-PGF(1alpha) in urine was negatively correlated with blood pressure. Liver cholesterol and phospholipid concentrations were 1.71- and 1.27-fold lower with fish protein than with casein, respectively. The fish protein diet lowered the 20:4(omega-6) proportion and the ratio of 20:4(omega-6) to 18:2(omega-6) in liver microsomal lipids and phospholipids, which was due to the reduced microsomal Delta6(omega-6) desaturation activity. Dietary protein source did not affect omega-3 fatty acid composition, and this was associated with a similar activation of Delta6(omega-3) desaturation in liver microsomes. CONCLUSIONS: The present data indicated a significant blood pressure-lowering effect caused by fish protein, rather than by casein, that modified the fatty acid composition of liver phospholipids and liver microsomal total lipids.