Peroxisome proliferator-activated receptor alpha (PPAR) plays a crucial role in the transcriptional regulation of myocardial lipid metabolism. In vitro studies on isolated cardiomyocytes showed that PPAR activation induces expression of numerous genes involved in virtually all steps of fatty acid catabolism. However, there is very few data on the effect of PPAR activation on the content and composition of myocardial lipids in vivo. Therefore, our main aim was to examine effects of selective PPAR agonist WY-14643 on the content and fatty acid composition of major lipid classes in the heart of rats fed a standard chow (STD) or a high-fat diet (HFD). In STD rats WY-14643 paradoxically decreased palmitate oxidation rate in the heart, however, in HFD animals such effect was not observed. WY-14643 markedly reduced myocardial free fatty acid and diacylglycerol content in STD rats, whereas in HFD group the opposite effect was observed. These changes reflected alterations in plasma lipid concentration which suggests that effects of WY-14643 on the heart were indirect and secondary to changes in plasma lipid availability induced by the drug. Basal myocardial glucose uptake was not affected by PPAR agonist in either group, however, glycogen content in the heart was markedly increased. WY-14643 exerted profound influence on the fatty acid composition of myocardial phospholipids in both diet groups. These changes included increased percentage of monounsaturated fatty acids and replacement of n-3 polyunsaturated fatty acids (PUFA) by those from the n-6 family. This action of WY-14643 might be detrimental to the heart since n-3 PUFA possess cardioprotective and antiarrhythmic properties.
In 142 Wistar rats fed high (30% kcal) or low (7% kcal) fat diet the effect of various amounts of magnesium and calcium on blood pressure was studied. The animals were divided into 19 groups consisting of 6—8 rats, which consumed experimental or control diet for 6 weeks. Two experiments were performed on the high fat diet. In experiment I six groups of animals received a diet with 0.04% magnesium, 0.15% magnesium, 0.3% magnesium, 2.0% calcium, 4.0% calcium, or 0.3% magnesium + 0.9% calcium respectively. In experiment II the other six groups of animals were kept on the same diets. In the first experiment the rats drank water, in the second water with 1.5% NaCl. In experiment III, on the low fat diet, three groups of animals were fed a diet with 0.3% magnesium, 2.0% calcium or 4.0% calcium respectively. The rats drank water. A reducing blood pressure effect of magnesium, calcium and both minerals together in rats fed the high fat diet in both models of experiment was found. However, it should be mentioned that the effect was more pronounced in NaCl induced arterial hypertension. The addition of these minerals to the low fat diet did not influence blood pressure. Diet supplementation with calcium and/or magnesium influenced ascorbic acid metabolism by decreaseing urine output and increasing its content in some tissues. Rats with experimental hypertension excreated greater amounts of PGF2 in urine in relation to the control group.
Background. Resistant starch (RS) is part of potato starch that is not digested in the gastrointestinal tract. RS4 is a chemically modified starch (for example by oxidation and esterification) and physically (by heating). Objective. The study was aimed at determining the effect of resistant starch on lipid metabolism and activity of hepatic enzymes in Wistar strain rats fed high-fat diets containing 15% of lard or 15% of soybean oil. Material and methods. Four types of diets were administered to the animals (4 groups of males, n=32): control diet (K1) containing 15% of soybean oil; control diet (K2) containing 15% of lard as well as two groups receiving the same diets with 10% addition of resistant starch RS4 (K1S and K2S). Results. The mean concentration of total cholesterol was lower in the group of animals fed a diet with vegetable oil (39.9 mg/dl) as compared to that reported in the group of rats fed the lard-supplemented diet (55.2 mg/dl). Compared to the control groups in both groups of animals receiving the diet supplemented with resistant starch RS4 the total cholesterol concentration in serum decreased by ca. 25% (differences were statistically significant). In groups of rats receiving oil- or lard-containing diets with the addition of the resistant starch preparation the concentration of triglycerides in serum decreased by ca. 47% and 10%, respectively. Conclusions. A beneficial effect of the resistant starch RS4 added to Wistar rats diets on the lipid metabolism has been shown. The concentrations of total cholesterol and triglycerides in the serum were lower and concentration of HDL-cholesterol was higher in the rats fed with the diets containing the addition of the RS4 preparation as compared to the control groups. Based on the activity of hepatic enzymes the degree of liver damage was lower in groups of rats fed with diets containing resistant starch RS4 as compared to the control groups.
The present study evaluated the protective effect of bergenin on high fat diet (HFD) induced diabetic mice. C57BL/6J mice were segregated in two groups, one fed standard diet (NC) and the other fed HFD for 16 weeks. Mice were fed continuously with high fat diet for 16 weeks and subjected to intragastric administration of bergenin (10, 20 and 40 mg/kg body weight (BW)), metformin (25 mg/kg BW) 9 to 16 weeks. At the end of the treatment nephritic markers, lipid peroxidation product, antioxidant and histopathological examination were carried out to assess the efficacy of the treatment. HFD fed mice showed increased plasma glucose, insulin, altered nephritic markers, antioxidant and histopathological abnormalities. Oral Treatment with bergenin (40 mg/kg BW) showed near normalized levels of plasma glucose, lipid peroxidation product, antioxidants, improved insulin and reduced kidney damage. The effects of bergenin were comparable with standard drug, metformin. These data suggest that bergenin protect kidney from deleterious effect of glucose.
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It was shown that high-fat feeding of mice with cardiac-specific overexpression of peroxisome proliferator-activated receptor (PPAR) alpha but not wild type animals leads to the accumulation of ceramide (an important mediator of lipotoxicity) in the heart [Finck et al. 2003 Proc Natl Acad Sci USA]. To investigate the mechanism of this phenomenon we examined the effects of PPARalpha activation on ceramide metabolism in the myocardium. Male Wistar rats were fed either a standard chow or a high-fat diet. Each group was divided into two subgroups: control and treated with selective PPARalpha activator – WY-14643. In the rats fed on the standard diet WY-14643 did not affect the myocardial content of sphingomyelin and ceramide but reduced the content of sphinganine and sphingosine. It also inhibited the activity of neutral sphingomyelinase and increased the activity of acid sphingomyelinase, whereas the activity of ceramidases and serine palmitoyltransferase (SPT) remained stable. High-fat diet itself did not affect the content of the examined sphingolipids. However, it reduced the activity of sphingomyelinases and ceramidases having no effect on the activity of SPT. Administration of WY-14643 to this group significantly increased the content of myocardial free palmitate, ceramide, sphingomyelin and the activity of SPT. Our results demonstrated that PPARalpha activation modulates myocardial ceramide metabolism and leads to the accumulation of ceramide in the heart of the high-fat fed rats due to its increased synthesis de novo.
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High-density microarrays were recently used to identify the genomic profiles of vascular cells during atherogenesis. This strategy succeeded in identifying both biomarkers and underlying biological processes of the pathological development. However, data documenting the early stages of disease are sparse. To identify the mechanisms involved in atherogenesis, we examined differential gene expression in the aorta of C57BL/6J mice fed a high-fat diet (HFD) or a low-fat diet (LFD), for a short period of time of three weeks. The cDNA microarray analysis revealed that the expression of 448 genes was significantly different between the two groups. As expected, key genes involved in lipid synthesis or catabolism were down- and upregulated, respectively, representing a normal gene expression response to increased cellular lipid levels. Overrepresented biological processes were identified by Gene Ontology (GO) analysis, which revealed that aortic cells differentiate into a new phenotype in mice fed the HFD. This phenotype was represented by changes in the expression of 81 genes associated with extracellular matrix and cytoskeletal modifications. Some of these genes were previously shown to be involved in the cardiovascular diseases process. In conclusion, short-term HFD consumption results in metabolic disturbances leading to a broad induction of genes involved in vessel architecture remodelling.
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Environmental factors such as high fat content in a diet affect pro- and antioxidative balances in tissues. Our study was designed to determine whether a four-week diet enriched to a total of 15% fat content with either a polyunsaturated (linoleic) or saturated (palmitic) fatty acid predisposes or protects the liver tissue against oxidative stress in both non-diabetic and diabetic rats. In the rat liver the activity of catalase, superoxide dismutase, glutathione peroxidase, and the level of thiobarbituric acid reactive substances were determined. Our study suggests that both diets induce oxidative stress in livers of non-diabetic rats. However, in diabetic rats a diet enriched in linoleic acid appears to attenuate oxidative stress.
This study focuses on anti-glycemic and anti-hepatotoxic effects of mangosteen vinegar rind (MVR) on fi ve weeks high-fat diet (HFD) / single dose streptozotocin (STZ) 30 mg/kg BW induced male ICR diabetic mice. Mice were randomly divided into fi ve groups (n=6), normal control, diabetic control, and diabetic groups treated with MVR 100, 200 mg/kg BW and glibenclamide 60 mg/kg BW for one week. After the treatment, lipid profi le, glycogen and bilirubin contents, oxidative damage (malondialdehyde, MDA), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT) were measured in plasma and/or liver tissues. MVR and glibenclamide treatment to HFD/STZ-induced diabetic mice signifi cantly reduced their plasma glucose, plasma lipid profi le, and hepatic lipid profi le (P<0.05). Increased hepatic glycogen content indicates improvement of insulin sensitivity. Moreover, oxidative damage markers were ameliorated in MVR- and glibenclamide-treated groups compared to the diabetic control group. MVR with phenolic compounds content of 75 mg GAE/g dry weight and antioxidant potential of 303 mmol/L Trolox/g dry weight acted as a hepatoprotective agent against oxidative damage.
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Ceramide is involved in the pathogenesis of insulin resistance in skeletal muscles of humans and rodents. However, there are conflicting reports in the literature on the effect of thiazolidinediones (a new class of insulin sensitizing drugs) on skeletal muscle ceramide content. Therefore, the aim of our study was to examine the effect of pioglitazone on the level of ceramide and its metabolites and on the activity of the key enzymes of ceramide metabolism in different skeletal muscle types of the rat. The experiments were carried out on rats fed either a standard chow or a high-fat diet for 21 days. Each group was divided into two subgroups: control and treated with pioglitazone for 14 days. High-fat diet increased the content of ceramide in the soleus and in the red section of the gastrocnemius, but not in the white section of the latter. The activity of neutral Mg2+-dependent sphingomyelinase and acid sphingomyelinase was simultaneously reduced in all examined muscles. Administration of pioglitazone decreased ceramide level in the soleus and in the red section of the gastrocnemius in rats fed either diet. This effect could not be attributed to decreased rate of ceramide formation from sphingomyelin or to its augmented deacylation to sphingosine. Pioglitazone treatment reduced the concentration of plasma free fatty acids in rats fed on either diet. Therefore, we conclude that the drug decreased the muscle content of ceramide by reducing its de novo synthesis. The results of our study indicate that reduction in ceramide level may be one of the mechanisms by which pioglitazone improves skeletal muscle insulin sensitivity.
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