Consumption of barley β‐glucan ameliorates fatty liver and insulin resistance in mice fed a high‐fat diet

Consumption of a diet high in barley β‐glucan (BG) has been shown to prevent insulin resistance. To investigate the mechanism for the effects of barley BG, three groups of male 7‐wk‐old C57BL/6J mice were fed high‐fat diets containing 0, 2, or 4% of barley BG for 12 wk. The 2% BG and 4% BG groups had significantly lower body weights compared with the 0% BG group. The 4% BG group demonstrated improved glucose tolerance and lower levels of insulin‐resistance index and glucose‐dependent insulinotropic polypeptide. Consumption of the BG diet decreased hepatic lipid content. Mice on the BG diet also demonstrated decreased fatty acid synthase and increased cholesterol 7α‐hydroxylase gene expression levels. The BG diet promoted hepatic insulin signaling by decreasing serine phosphorylation of insulin receptor substrate 1 and activating Akt, and it decreased mRNA levels of glucose‐6‐phosphatase and phosphoenolpyruvate carboxykinase. In summary, consumption of BG reduced weight gain, decreased hepatic lipid accumulation, and improved insulin sensitivity in mice fed a high‐fat diet. Insulin signaling enhanced due to the expression changes of glucose and lipid metabolism genes by BG consumption. Consumption of barley BG could be an effective strategy for preventing obesity, insulin resistance, and the metabolic syndrome.     

Auraptene regulates gene expression involved in lipid metabolism through PPARα activation in diabetic obese mice

Scope: Peroxisome proliferator‐activated receptor‐α (PPARα) is a key regulator of circulating lipid level. Thus, various food‐derived compounds that activate PPARα as agonists have been screened and characterized. Methods and results: We investigated the effects of auraptene, a citrus‐derived compound serving as a PPARα agonist in vitro, on abnormalities in lipid and glucose metabolisms. In high‐fat‐diet (HFD)‐fed KK‐Ay diabetic obese mice, auraptene treatment suppressed hyperlipidemia and triglyceride accumulation in the liver and skeletal muscle, and increased the mRNA expression levels of the PPARα target genes involved in fatty acid oxidation in the liver and skeletal muscle. Moreover, the adipocyte size in the auraptene‐treated mice was significantly smaller than that in the control HFD‐fed mice resulting in the improvement of HFD‐induced hyperglycemia and abnormalities in glucose tolerance. Conclusions: These findings indicate that auraptene activates PPARα also in vivo and its treatment may improve abnormalities in lipid and glucose metabolisms, suggesting that auraptene is a valuable food‐derived compound for managing metabolic disorders.     

Beneficial effects of mangiferin on hyperlipidemia in high-fat-fed hamsters

Scope : Mangiferin, a natural polyphenol, has been shown to have hypolipidemic effect in rat and mouse. However, the mechanism of action is not well understood. This study was conducted to determine the effect and mechanism of action of mangiferin on hyperlipidemia induced in hamsters by a high‐fat diet. Methods and results: Forty male hamsters were randomly assigned to normal control, high‐fat control, and high fat with mangiferin (50 and 150 mg/kg BW) groups. Mangiferin treatment significantly decreased final body weight, liver weight and visceral fat‐pad weight, serum triglyceride (TG) and total free fatty acid (FFA) concentrations, hepatic TG levels and hepatic and muscle total FFA contents. Mangiferin upregulated mRNA expression of peroxisome proliferator‐activated receptor‐α (PPAR‐α), fatty acid translocase (CD36) and carnitine palmitoyltransferase 1 (CPT‐1), but downregulated mRNA expression of sterol regulatory element‐binding protein 1c (SREBP‐1c), acetyl CoA carboxylase (ACC), acyl‐CoA:diacylglycerol acyltransferase 2 (DGAT‐2) and microsomal triglyceride transfer protein (MTP) in liver. Mangiferin also stimulated mRNA expression of PPAR‐α, CD36, CPT‐1 and lipoprotein lipase (LPL) in muscle. Conclusions : The results suggest that mangiferin may ameliorate hypertriglyceridemia partly by modulating the expression levels of genes involved in lipid oxidation and lipogenesis.     

Chronic dietary intake of quercetin alleviates hepatic fat accumulation associated with consumption of a Western-style diet in C57/BL6J mice

Scope: To determine the effect of consumption of a quercetin‐rich diet on obesity and dysregulated hepatic gene expression. Methods and results: C56BL/6J mice were fed for 20 wk on AIN93G (control) or a Western diet high in fat, cholesterol and sucrose, both with or without 0.05% quercetin. Triglyceride levels in plasma, thiobarbituric acid‐reactive substances (oxidative stress marker) and glutathione levels and peroxisome proliferator‐activated receptor α expression in livers of mice fed with the Western diet were all improved after 8 wk feeding with quercetin. After 20 wk, further reductions of visceral and liver fat accumulation and improved hyperglycemia, hyperinsulinemia, dyslipidemia and plasma adiponectin and TNFα levels in these mice fed with quercetin were observed. The expression of hepatic genes related to steatosis, such as peroxisome proliferator‐activated receptor γ and sterol regulatory element‐binding protein‐1c was also normalized by quercetin. In mice fed with the control diet, quercetin did not affect body weight but reduces the plasma TNFα and hepatic thiobarbituric acid‐reactive substance levels. Conclusion: In mice fed with a Western diet, chronic dietary intake of quercetin reduces liver fat accumulation and improves systemic parameters related to metabolic syndrome, probably mainly through decreasing oxidative stress and reducing PPARα expression, and the subsequent reduced expression in the liver of genes related to steatosis.     

The Hypolipidemic Effect of Total Saponins from Kuding Tea in High‐Fat Diet‐Induced Hyperlipidemic Mice and Its Composition Characterized by UPLC‐QTOF‐MS/MS

Kuding tea are used as a traditional tea material and widely consumed in China. In this study, total saponins (TS) from water extract of Kuding tea was prepared by D101 macroporous resins and analyzed by UPLC‐QTOF‐MS/MS. Then the hypolipidemic effect of TS extract was investigated in high‐fat diet‐induced hyperlipidemic mice. For comprehensive identification or characterization of saponins in TS extract, 3 major saponins of Kudinoside A, Kudinoside F, and Kudinoside D were isolated and used as standards to investigate the MS/MS fragmentation pattern. As a result, 52 saponins were identified or characterized in TS extract from Kuding tea. In addition, the increased levels of mice serum TC, LDL‐C, HDL‐C, and atherogenic index (AI) were significantly reduced after the treatment of TS extract. Also, the liver protective effect of TS extract was obviously judged from the photographs stained with oil red‐O staining. Meanwhile, TS extract significantly upregulated the expression of hepatic scavenger receptors including SR‐AI, SR‐BI, and CD36. Therefore, it is reasonable to assume that the overexpression of hepatic scavenger receptors was involved in the hypolipidemic effect of Kuding tea on the high‐fat diet‐induced hyperlipidemic mice. The TS extract could influence these scavenger receptors, and this could be the potential mechanism of TS extract from Kuding tea in the treatment of lipid disorders. These results give the evidence that the saponins in Kuding tea could provide benefits in managing hypercholesterolemia and may be a good candidate for development as a functional food and nutraceutical.     

Cinnamomum camphora Seed Kernel Oil Ameliorates Oxidative Stress and Inflammation in Diet‐Induced Obese Rats

Cinnamomum camphora seed kernel oil (CCSKO) was found to reduce body fat deposition and improve blood lipid in both healthy and obese rats. The study was aimed to investigate the antioxidative stress and anti‐inflammatory effects of CCSKO in high‐fat‐diet‐induced obese rats. The obese rats were treated with CCSKO, lard, and soybean oil, respectively, for 12 wk. The level of total antioxidant capacity (T‐AOC), activities of superoxide dismutase (SOD), glutathione peroxidase, and catalase, and levels of malondialdehyde (MDA), tumor necrosis factor (TNF)‐α, peroxisome proliferator‐activated receptor (PPAR)‐γ, interleukin (IL)‐6, and P65 were compared among CCSKO, lard, and soybean oil groups. Our results showed that the level of T‐AOC and activities of SOD and catalase were significantly increased and the level of MDA was significantly decreased in CCSKO group. In addition, CCSKO treatment reduced the activities of serum glutamic oxaloacetic transaminase and glutamate‐pyruvate transaminase, and levels of serum TNF‐α, IL‐6, and P65 through raising the level of PPAR‐γ. In conclusion, CCSKO has, for the first time, been found to ameliorate oxidative stress and inflammation in high‐fat‐diet‐induced obese rats.     

Anti‐obesity effect of Liupao tea extract by modulating lipid metabolism and oxidative stress in high‐fat‐diet‐induced obese mice

Liupao tea (LPT) is traditional dark Chinese tea. The effect of LPT extract on high‐fat‐diet‐induced obese mice was investigated systematically. The results showed that LPT extract could reduce body weight and significantly alleviate liver damage and fat accumulation. LPT could also decrease the levels of alanine aminotransferase (ALT), aspartate transaminase (AST), alkaline phosphatase (AKP), total cholesterol (TC), triglycerides (TG), and low‐density lipoprotein cholesterol (LDL‐C) and increase the level of high‐density lipoprotein cholesterol (HDL‐C) in the liver. It also decreased the serum levels of inflammatory cytokines, including tumor necrosis factor alpha (TNF‐α), interferon gamma (IFN‐γ), interleukin (IL)‐1β, and IL‐6 and increased the serum levels of anti‐inflammatory cytokines, including IL‐10 and IL‐4. Moreover, LPT improved the levels of total superoxide dismutase (T‐SOD), glutathione peroxidase (GSH‐Px), and catalase (CAT) and reduced the level of malondialdehyde (MDA) in the liver. Moreover, LPT could upregulate the mRNA and protein expressions of peroxisome proliferator‐activated receptor alpha (PPAR‐α), lipoprotein lipase (LPL), carnitine palmitoyltransferase 1(CPT1), and cholesterol 7 alpha‐hydroxylase (CYP7A1) and downregulate those of PPAR‐γ and CCAAT/enhancer‐binding protein alpha (C/EBP‐α) in the liver. It also increased the mRNA expression of copper/zinc superoxide dismutase (SOD1), manganese superoxide dismutase (SOD2), CAT, gamma‐glutamylcysteine synthetase 1 (GSH1), and GSH‐Px. The components of LPT extract include catechin, rutin, taxifolin, and astragalin, which possibly have a wide range of biological activities. In conclusion, our work verified that LPT extract possessed an anti‐obesity effect and alleviated obesity‐related symptoms, including lipid metabolism disorder, chronic low‐grade inflammation, and liver damage, by modulating lipid metabolism and oxidative stress.     

Okra polysaccharide improves metabolic disorders in high‐fat diet‐induced obese C57BL/6 mice

Okra is a tropical vegetable that is rich in polysaccharides. Here, we investigated the effects of okra polysaccharide (OP) on metabolic disorders in mice. We found that OP lowered body weight and glucose levels, improved glucose tolerance, and decreased serum total cholesterol levels in high‐fat diet‐fed C57BL/6 mice. OP regulated the gene expression of liver X receptors (LXRs) and peroxisome proliferator‐activated receptors (PPARs) and their target genes in the liver and the adipose tissue of the mice. These results suggest that OP may have therapeutic effects on metabolic diseases via the inhibition of LXR and PPAR signaling.     

Rosemary Extract‐Mediated Lifespan Extension and Attenuated Oxidative Damage in Drosophila melanogaster Fed on High‐Fat Diet

Rosemary extract has a potent antioxidant activity and is widely used in the food industry. In this study, the lifespan prolonging and antioxidant activity of rosemary extract was evaluated by high‐fat‐induced oxidative damage in Drosophila melanogaster. The results revealed that the lifespan and climbing ability of fruit flies was enhanced significantly by feeding rosemary extract. Furthermore, feeding with rosemary extract significantly increased the enzyme activity of superoxide dismutase (SOD) and catalase (CAT), and significantly decreased the level of malonaldehyde. The gene expression of SOD, CAT, and nuclear factor erythroid‐2 related factor 2 was enhanced and that for methuselah was significantly reduced. The comet assay showed that high‐fat diet‐induced DNA lesion was significantly reduced in larvae treated with the rosemary extract. Our results suggest that feeding with rosemary extract is effective to the extended lifespan in fruit flies by strengthening of the resistance to high‐fat‐induced oxidative stress and by stimulating, at least in part, the endogenous antioxidant response.     

Dietary Tuna Dark Muscle Protein Attenuates Hepatic Steatosis and Increases Serum High‐Density Lipoprotein Cholesterol in Obese Type‐2 Diabetic/Obese KK‐Ay Mice

Tuna muscle consists of light and dark muscle in approximately equal proportions. However, besides for the light muscle of tuna, cod, sardine, and salmon, few researches have assessed the health‐promoting functions of fish protein. Therefore, we evaluated the mechanisms underlying the alteration of lipid storage and cholesterol metabolism following the intake of tuna dark muscle protein (TDMP) by obese type‐2 diabetic/obese mice. Four‐week‐old male KK‐A^y mice were separated into 2 dietary groups, with one group receiving a casein‐based diet and the other receiving a diet with the substitution of part of the protein (50%, w/w) by TDMP (TDMP diet) for 4 wk. The TDMP diet significantly increased the content of serum high‐density lipoprotein cholesterol, partly due to the reduction of the expression of scavenger receptor class B member 1 in epididymal white adipose tissue. In addition, dietary TDMP decreased the content of hepatic triacylglycerol, which could be due to the enhancement of carnitine palmitoyltransferase‐2 activity through the activation of the expression of the peroxisome proliferative activated receptor‐α in the liver. These results suggest that TDMP could have the potential to prevent the development of obesity‐related diseases by suppressing the storage of hepatic triacylglycerol and cholesterol.     

Hypolipidemic Activity of Peony Seed Oil Rich in α‐Linolenic,is Mediated Through Inhibition of Lipogenesis and Upregulation of Fatty Acid β‐Oxidation

Peony seed oil (PSO) is a new resource food rich in α‐Linolenic Acid(ALA) (38.66%). The objective of this study was to assess the modulatory effect of PSO on lipid metabolism. Lard oil, safflower oil (SFO), and PSO were fed to wistar rats with 1% cholesterol in the diet for 60 d. Serum and liver lipids showed significant decrease in total cholesterol (TC), triglyceride (TG), and low density lipoprotein‐cholesterol (LDL‐C) levels in PSO fed rats compared to lard oil and SFO fed rats. ALA, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), contents were significantly increased, whereas linoleic acid (LA), arachidonic acid (AA) levels decreased in serum and liver of PSO fed rats. Feeding PSO increased ALA level and decreased n‐6 to n‐3 polyunsaturated fatty acid (PUFA) ratio. The hypolipidemic result of PSO indicated that PSO participated in the regulation of plasma lipid concentration and cholesterol metabolism in liver. The decreased expression of sterol regulatory element‐binding proteins 1C (SREBP‐1c), acetyl‐CoA carboxylase (ACC), and fatty acid synthase (FAS)‐reduced lipid synthesis; Activation of peroxisome proliferator–activator receptor (PPARα) accompanied by increase of uncoupling protein2 (UP2) and acyl‐CoA oxidase (AOX) stimulated lipid metabolism and exerted an antiobesity effect via increasing energy expenditure for prevention of obesity.     

Voluntary exercise and green tea enhance the expression of genes related to energy utilization and attenuate metabolic syndrome in high fat fed mice

Obesity and metabolic syndrome are growing public health problems. We investigated the effects of decaffeinated green tea extract (GTE) and voluntary running exercise (Ex) alone or in combination against obesity and metabolic syndrome in high fat (HF) fed C57BL/6J mice. After 16 wk, GTE + Ex treatment reduced final body mass (27.1% decrease) and total visceral fat mass (36.6% decrease) compared to HF‐fed mice. GTE + Ex reduced fasting blood glucose (17% decrease), plasma insulin (65% decrease), and insulin resistance (65% decrease) compared to HF‐fed mice. GTE or Ex alone had less significant effects. In the skeletal muscle, the combination of Ex and GTE increased the expression of peroxisome proliferator‐activated receptor‐γ coactivator‐1α (Ppargc1a), mitochondrial NADH dehydrogenase 5 (mt‐Nd5), mitochondrial cytochrome b (mt‐Cytb), and mitochondrial cytochrome c oxidase III (mt‐Co3). An increase in hepatic expression of peroxisome proliferator‐activated receptor‐α (Ppara) and liver carnitine palmitoyl transferase‐1α (Cpt1a) and a decrease in hepatic expression of stearoyl‐CoA desaturase 1 (Scd1) mRNA was observed in GTE + Ex mice. GTE + Ex was more effective than either treatment alone in reducing diet‐induced obesity. These effects are due in part to modulation of genes related to energy metabolism and de novo lipogenesis.     

Modulation of lipid metabolism by polyphenol‐rich grape skin extract improves liver steatosis and adiposity in high fat fed mice

This study investigated the influence of polyphenol‐rich grape skin extract (GSE) on adiposity and hepatic steatosis in mice fed a high fat diet (HFD) and its underlying mechanisms based on adipose and hepatic lipid metabolism. C57BL/6J mice were fed a normal diet or a HFD (20% fat, w/w) with or without GSE (0.15%, w/w) for 10 weeks. The supplementation of GSE significantly lowered body weight, fat weight, plasma free fatty acid level, and hepatic lipid accumulation compared to the HFD group. Plasma leptin level was significantly lower, while the plasma adiponectin level was higher in the GSE group than in the HFD group. GSE supplementation significantly suppressed the activities of lipogenic enzymes in both adipose and liver tissues, which was concomitant with β‐oxidation activation. Furthermore, GSE reversed the HFD‐induced changes of the expression of genes involved in lipogenesis and β‐oxidation in the liver. These findings suggest that GSE may protect against diet‐induced adiposity and hepatic steatosis by regulating mRNA expression and/or activities of enzymes that regulate lipogenesis and fatty acid oxidation in the adipose tissue and liver.     

Effect of fermented soybean product (Cheonggukjang) intake on metabolic parameters in mice fed a high‐fat diet

As a nontargeted metabolomics approach, we investigated changes in the plasma metabolite levels in a mouse model of obesity induced by a high‐fat diet and fermented soybean product diet. We analyzed the plasma samples by using ultra‐performance liquid chromatography coupled with quadrupole time‐of‐flight mass spectrometry (UPLC‐Q‐TOF‐MS). In the present study, the animals were divided into four groups according to the diet type; normal fat diet control group (ND), high‐fat diet control group (HD), high‐fat diet plus 30% cooked soybean power (HD + S), and high‐fat diet plus 30% 72‐h fermented Cheonggukjang powder (HD + CGJ). To examine the changes in plasma metabolite levels because of high‐fat diet feeding, total cholesterol and triglyceride levels were measured. Total cholesterol and triglyceride levels were lower in the HD + S and HD + CGJ groups than in the ND group. According to partial least‐squares discriminant analysis (PLS‐DA), major metabolites contributing to the discrimination between each group were assigned as lipid metabolites in plasma, e.g., lyso‐phosphatidylcholines and phosphatidylcholines. Therefore, diets containing soy‐based food products, which are rich sources of isoflavonoids, might be helpful for controlling the lipid metabolism under high‐fat diet conditions.     

Stevia rebaudiana Bertoni extract supplementation improves lipid and carnitine profiles in C57BL/6J mice fed a high‐fat diet

BACKGROUND: Stevia (Stevia rebaudiana Bertoni) is a non‐caloric natural‐source alternative to artificially produced sugar substitutes. This study investigated the effect of stevia extract on lipid profiles in C57BL/6J mice. Forty mice were divided into four groups: N‐C (normal diet and distilled water), H‐C (high‐fat diet and distilled water), H‐SC (high fat diet and sucrose, 1 mL kg^?1 per day), and H‐SV (high‐fat diet and stevia extract, 1 mL kg^?1 per day). RESULTS: Body weight gain was significantly higher in the H‐SC group than in the H‐SV group. Triglyceride concentrations in serum and liver were lower in the H‐SV group than in the H‐SC group. Serum total cholesterol concentrations were lower in the H‐SV and H‐C groups compared to the H‐SC group. The concentrations of acid‐insoluble acylcarnitine (AIAC) in serum were higher in the H‐SV group than in the H‐C and H‐SC groups and the acyl/free carnitine level in liver was significantly higher in the H‐SV group than in the N‐C group. These results were supported by mRNA expression of enzymes related to lipid metabolism (ACO, PPARα, ACS, CPT‐I, ACC) assessed by real‐time polymerase chain reaction. CONCLUSION: These results suggest that the supplementation of stevia extract might have an anti‐obesity effect on high‐fat diet induced obese mice. Copyright © 2010 Society of Chemical Industry     

Vitamin E levels,thiobarbituric acid test and sensory evaluation of breast muscles from broilers fed α‐tocopheryl acetate‐ and β‐carotene‐supplemented diets

The objective of this study was to investigate the effect of dietary α‐tocopheryl acetate and β‐carotene supplementation on lipid oxidation of breast meat from broilers fed lard as the fat source. Supplementation of broilers with 100 mg kg^?1 α‐tocopheryl acetate increased the vitamin E levels in raw breast samples significantly (p < 0.05), whereas the presence of 1.5 mg kg^?1 dietary β‐carotene tended to decrease vitamin E deposition. The presence of vitamin E delayed lipid oxidation significantly, but thiobarbituric acid values of samples from broilers fed the β‐carotene‐supplemented diet did not differ from those of control samples. Vitamin E reduced sensory meat rancidity, whilst vitamin E, β‐carotene and their combination modified meat texture. The results show the effectiveness of dietary α‐tocopheryl acetate supplementation in protecting broiler meat against lipid oxidation. Copyright © 2004 Society of Chemical Industry     

Role of TNF‐α polymorphism ‐308 in neurosensory irritation

Neurosensory cutaneous discomfort in response to topical products is common, yet the relationship between symptoms such as stinging and visible irritation is currently unclear. The presence of a polymorphism at position ‐308 on the TNF‐α gene has been associated with skin irritation, i.e., erythema, dryness. Individuals with a G to A transition (AA/GA genotypes) have a lower threshold to experimentally induced irritation than those with the wild type (G allele, GG genotype). We investigated the effect of this polymorphism on neurosensory irritation (NSI). DNA genotyping was used to determine the allele type amongst a population of health care workers. The neurosensory response to lactic acid and water on the nasolabial folds and hands was assessed using a quantitative lactic acid sting test. Both genotypes had a more intense response to lactic acid compared with water on the face. The AA/GA genotypes had directionally higher scores from lactic acid (P = 0.1) and significantly higher stinging intensities from water (P = 0.001) on the face. For the hands, stinging intensities were higher for lactic acid and water amongst the AA/GA genotypes (P = 0.03 and 0.006 respectively). NSI to lactic acid was significantly higher on the face than on the hands (P < 0.05). Our findings indicate that subjects with the A transition at position ‐308 on the TNF‐α gene experience more intense NSI with common ingredients, i.e., lactic acid and water, than those with the wild type. TNF‐α polymorphism ‐308 may account for some of the inter‐individual variability in response to skin care practices.