Antrodia camphorata ameliorates high-fat-diet induced hepatic steatosis via improving lipid metabolism and antioxidative status

Nonalcoholic fatty liver disease (NAFLD) commonly results from excessive dietary fat intake which characterized by obesity and insulin resistance. Wild fruiting body of Antrodia camphorata (AC) was assayed for alleviative effects on NAFLD. An NAFLD animal model was successfully established in male 7-week-old C57BL/6 mice fed with high-fat diet (HFD) for 36 weeks. The HFD mice exhibited obese and impaired glucose metabolism. After an induction of NAFLD syndrome, AC was given for one week via gavage. Mice with AC treatment showed lowered (p < 0.05) serum TG and TC, lowered (p < 0.05) liver TG content, improved (p < 0.05) oxidative status (TBARS values and GSH levels), and ameliorated (p < 0.05) liver damage (AST, ALT, and LDH values). In addition, AC activated (p < 0.05) gene expressions of PPAR-α with its downstream genes in the liver and caused higher (p < 0.05) rectal temperature, which showed AC attenuates hepatic lipid accumulation by promoting lipid oxidation and further suggests the role of AC in energy expenditure. Overall, our findings revealed that AC possesses alleviative effect on NAFLD.     

Salicornia Extract Ameliorates Salt‐Induced Aggravation of Nonalcoholic Fatty Liver Disease in Obese Mice Fed a High‐Fat Diet

High‐fat and high‐salt intakes are among the major risks of chronic diseases including obesity, nonalcoholic fatty liver disease (NAFLD), and nonalcoholic steatohepatitis (NASH). Salicornia is a halophytic plant known to exert antioxidant, antidiabetic, and hypolipidemic effects, and Salicornia‐extracted salt (SS) has been used as a salt substitute. In this study, the effects of SS and purified salt (PS) on the aggravation of NAFLD/NASH were compared. C57BL/6J male mice (8‐wk‐old) were fed a high‐fat diet (HFD) for 6 mo and divided into 3 dietary groups, which were additionally fed HFD, HFD + SS, and HFD + PS for 13 wk. PS induced aggravation of NAFLD/NASH in HFD‐fed mice. Although the actual salt intake was same between the PS and SS groups as 1% of the diet (extrapolated from the World Health Organization [WHO] guideline), SS induced less liver injury and hepatic steatosis compared to PS. The hepatic mRNA expressions of inflammatory cytokines and fibrosis marker were significantly lower in the SS group than the PS group. Oxidative stress is one of the major causes of inflammation in NAFLD/NASH. Results of the component analysis showed that the major polyphenols that exhibited antioxidant activity in the Salicornia water extract were ferulic acid, caffeic acid, and isorhamnetin. These results suggest that even the level of salt intake recommended by WHO can accelerate the progression of liver disease in obese individuals consuming HFD. It is proposed that SS can be a salt substitute for obese individuals who consume HFD.     

氧化苦参碱改善非酒精性脂肪肝病的作用及转录组学研究

目的 研究氧化苦参碱(oxymatrine, Oxy)的抗非酒精性脂肪性肝病(non-alcoholic fatty liver disease, NAFLD)作用及机制。方法 将大鼠随机分为正常组、模型组、白藜芦醇组(50 mg/kg)和Oxy低、高剂量组(50 mg/kg和100 mg/kg); 采用高脂饮食(high-fat diet, HFD)饲喂16周诱导NAFLD大鼠模型, 从第8周开始按分组对应灌胃给药; 测定各组大鼠体重、肝脏重量和肝脏指数; 采用试剂盒检测大鼠血清天门冬氨酸氨基转移酶(aspartate transaminase, AST)、丙氨酸氨基转移酶(alanine transaminase, ALT)、低密度脂蛋白胆固醇(low density lipoprotein cholesterol, LDL-c)、高密度脂蛋白胆固醇(high density lipoprotein cholesterol, HDL-c)、总胆固醇(total cholesterol, TC)和甘油三酯(triglyceride, TG)水平; 采用苏木素-伊红(hematoxylin-eosin, HE)、油红O和Masson染色检查大鼠肝脏病理变化; 采用高通量测序技术分析大鼠肝脏基因表达。结果 与正常组比较, 模型组大鼠体重、肝脏重量及肝脏指数显著增加(P<0.01); 血清中AST、ALT、LDL-c、TC和TG水平显著升高, HDL-c水平显著降低(P<0.01); 肝脏肝小叶结构出现损伤, 呈现弥漫性小泡、大泡脂肪变性及气球样变; 肝脏中脂滴和蓝色胶原纤维显著增多(P<0.01)。与模型组比较, Oxy组大鼠体重、肝脏重量及肝脏指数显著降低(P<0.05, P<0.01); 血清中肝损伤及脂代谢相关指标水平显著恢复(P<0.01); 肝脏结构趋于正常, 肝脏仅有轻微的小泡脂肪变性; 肝脏中脂滴和蓝色胶原纤维显著减少(P<0.01)。转录组结果显示, 正常组、模型组和Oxy组样本各自聚集在一起; 正常组与模型组间有499个差异基因, 模型组与Oxy组间有434个差异基因, 共有差异基因218个, 集中于环磷酸鸟苷(cyclic guanosine monophosphate, cGMP)/蛋白激酶G (protein kinase G, PKG)、磷脂酰肌醇3-激酶(phosphatidylinositol3-kinase, PI3K)/蛋白激酶B (protein kinase B, Akt)、环磷酸腺苷(cyclic adenosine monophosphate, cAMP)、松弛素、胰岛素抵抗、Rap1和Hippo信号通路。结论 Oxy具有明确的抗NAFLD作用, 具体表现为对HFD诱导的NAFLD大鼠的肥胖的缓解以及肝功能、脂代谢紊乱、肝脂肪变性和肝纤维化的改善, 机制可能与调控cGMP/PKG、PI3K/Akt、cAMP、松弛素、胰岛素抵抗、Rap1和Hippo信号通路有关。     

荞麦粉对高脂膳食大鼠脂代谢的影响

本文研究了荞麦粉(buckwheat,BW)对高脂膳食大鼠脂代谢的影响。将50只成年Wistar雄性大鼠随机分为基础对照组、高脂模型组、荞麦粉低、中、高剂量组(1、5、10 g/kg·d),每天喂食一次,饲喂30 d后腹主动脉取血,取出肝脏、肾周及睾丸附近脂肪,分别测定血清和肝脏中的总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)和低密度脂蛋白胆固醇(LDL-C)的水平,并观察肝脏病理切片。结果表明,与高脂膳食组相比,荞麦剂量组大鼠体重和食物摄入量都明显减少,肝重和脂肪重及其指数也明显降低,血清和肝脏中TC、TG、LDL-C的浓度降低,HDL-C的浓度升高。肝脏光镜结构表明,荞麦剂量组的肝脏脂肪变性均减轻,其中荞麦粉高剂量作用最为明显。说明荞麦粉干预高脂膳食,可起到降血脂、改善肝脏脂代谢、保护肝脏的作用,同时能够减少相关疾病的发生。     

虾青素对肝脂代谢与昼夜节律的调节作用

研究虾青素对非酒精性脂肪性肝病（non-alcoholic fatty liver disease,NAFLD）的干预作用及与代谢相关的昼夜节律紊乱的缓解作用。采用高脂/高胆固醇饲喂建立NAFLD小鼠模型和添加虾青素的干预模型。动物实验选用SPF级C57BL/6小鼠,随机分成正常组、高脂模型组和高脂添加虾青素组。采用常规酶联免疫吸附测定法测定血清中甘油三酯、总胆固醇（total cholesterol,TC）、高密度脂蛋白胆固醇（high density lipoprotein cholesterol,HDL-C）、低密度脂蛋白胆固醇（low density lipoprotein cholesterol,LDL-C）浓度及谷丙转氨酶（alanine aminotransferase,ALT）、谷草转氨酶（aspartate transaminase,AST）活力等肝损伤指标,苏木精-伊红染色法观察肝组织形态学变化,荧光定量聚合酶链式反应（real-time quantitative polymerase chain reaction,qPCR）检测与肝脂代谢、胆固醇代谢、昼夜节律相关的基因表达及昼夜节律变化。结果显示：与正常组相比,高脂模型组小鼠体质量、肝脏指数、肥胖指数均高度显著增加（P＜0.001）,虾青素干预后肝脏指数、肥胖指数均极显著降低（P＜0.01）。高脂饲喂导致小鼠血脂水平升高（HDL-C除外）,尤其是LDL-C浓度升高明显,而虾青素干预可以有效降低TC和LDL-C浓度,并升高HDL-C浓度,改善脂质的代谢。高脂/高胆固醇饲喂会高度显著升高小鼠血清ALT、AST活力（P＜0.001）,造成肝损伤。与高脂模型组相比,虾青素干预可极显著降低小鼠ALT、AST活力（P＜0.01）,缓解肝脏损伤,并明显改善肝脏脂质代谢关键酶的基因表达,包括脂肪酸合成酶和胆固醇合成关键酶羟甲基戊二酸单酰辅酶A还原酶。同时,虾青素干预也增加了胆固醇7α-羟化酶的表达量,促进胆固醇氧化。虾青素调节上述基因的表达具有昼夜节律性,能够缓解或修正由高脂导致的生物钟节律相关因子时钟昼夜节律调节器及脑和肌肉芳香烃受体核转运体样蛋白1以及肝脏脂质代谢关键基因昼夜节律表达的紊乱。本研究表明虾青素具有改善高脂所致肝代谢紊乱的节律性调节作用。     

Taurine ameliorates alcoholic steatohepatitis via enhancing self-antioxidant capacity and alcohol metabolism

Chronic alcohol consumption or alcohol abuse is the main cause of alcoholic steatohepatitis or further cirrhosis. This study was to exam if the antioxidant capacity and alcohol metabolism in livers of chronic alcohol-fed rats were improved by supplementing taurine (Tau). Rats were randomly divided into four groups with five times per week of treatment: 1) isocaloric solution; 2) 3 g alcohol/kg BW/day; 3) 3 g alcohol/kg BW/day + 1 g taurine (Tau)/kg BW/day; and 4) 3 g alcohol/kg BW/day + 2 g Tau/kg BW/day. A 6-week alcohol consumption resulted in lower (p < 0.05) body weight gain and self-antioxidant capacities, as well as increased (p < 0.05) liver size, serum/hepatic lipids, and AST and ALT values. However, alcohol-fed rats co-treated with Tau have decreased (p < 0.05) liver lipid levels via increasing fecal lipid output and cholesterol metabolism. Besides, co-treatment of Tau also enhanced (p < 0.05) self-antioxidant capacities and alcohol metabolism in livers via enhancing GSH contents, CAT, GSH-Px, ADH, and ALDH activities, but decreasing MDA contents. In a histological examination of rat liver, microvesicular steatosis and necrotic cells were observed in alcohol-fed rats without Tau while largely suppressed microvesicular steatosis and no necrotic cells were observed in alcohol-fed rat supplemented with Tau. Therefore, Tau could be an effective hepatoprotective agent against alcohol-induced damage via enhancing self-antioxidant capacity and alcohol metabolism.     

Acid-treated high-amylose corn starch suppresses high-fat diet-induced steatosis

Resistant starch (RS) has been reported to improve steatosis as well as obesity. Type 4 resistant starch (RS4), a chemically modified starch, is particularly hard to digest and suggesting higher efficacy. However, because the effects of RS4 on steatosis are not yet fully understood, the effects of RS4 on steatosis were examined using a murine high-fat diet model. Seven-week-old male mice were divided into three groups and fed a normal diet, a high-fat diet (HFD), or a high-fat diet with added RS (HFD + RS). Amylofiber SH^® produced from acid-treated corn starch was used as the dietary RS. At 22 weeks old, hepatic steatosis and short chain fatty acid (SCFA) content and gut microbiota in cecum stool samples were analyzed. The ratio of body weight to 7 weeks was significantly suppressed in the HFD + RS group compared to the HFD group (132.2 ± 1.4% vs. 167.2 ± 3.9%, p = 0.0076). Macroscopic and microscopic steatosis was also suppressed in the HFD + RS group. Analysis of cecum stool samples revealed elevated SCFA levels in the HFD + RS group compared with the HFD group. Metagenome analysis revealed that Bifidobacterium (17.9 ± 1.9% vs. 3.6 ± 0.7%, p = 0.0019) and Lactobacillus (14.8 ± 3.4% vs. 0.72 ± 0.23%, p = 0.0045), which degrade RS to SCFA, were more prevalent in the HFD + RS group than the HFD group. In conclusion, RS4 suppressed steatosis, and increased Bifidobacterium and Lactobacillus, and SCFAs. RS4 may prevent steatosis by modulating the intestinal environment.     

Dietary Intake of Structured Lipids with Different Contents of Medium‐Chain Fatty Acids on Obesity Prevention in C57BL/6J Mice

Three medium‐ and long‐chain triacylglycerols (MLCT) with different contents of medium‐chain fatty acids (MCFA) (10% to 30%, w/w) were prepared and evaluated for their anti‐obesity potential in C57BL/6J mice. The group fed with a high fat diet of MLCT containing 30% (w/w) MCFA showed significantly decreased body weight and fat mass (P < 0.05) relative to the control mice fed an obesity‐inducing high fat rapeseed oil diet. In addition, serum parameters including triacylglycerols, total cholesterol, glucose, high‐density lipoprotein cholesterol, low‐density lipoprotein cholesterol, apolipoprotein A1 and apolipoprotein B in the treatment group fed with 30% (w/w) MCFA were close to those of mice fed with a low fat rapeseed oil diet, but significantly different (P < 0.05) from those of the obesity control group. Moreover, the intake of MLCT with high content of MCFA reduced the size of adipocytes. In addition, the visceral fat and liver weights, as well as the liver triacylglycerol for 3 treatment groups were lower than those of the obesity control group. These results demonstrate the great potential of MLCT with high content of MCFA in weight loss.     

High‐fat Diet‐induced Intestinal Hyperpermeability is Associated with Increased Bile Acids in the Large Intestine of Mice

Metabolic syndrome is characterized by low‐grade chronic systemic inflammation, which is associated with intestinal hyperpermeability. This study examined the effects of 3 high‐fat diets (HFDs) composed of different fat sources (soybean oil and lard) on the intestinal permeability, tight junction (TJ) protein expression, and cecal bile acid (BA) concentrations in mice, and then analyzed their interrelations. C57/BL6 mice were fed the control diet, HFD (soybean oil), HFD (lard), and HFD (mix; containing equal concentrations of soybean oil and lard) for 8 wk. Glucose tolerance, intestinal permeability, TJ protein expression, and cecal BA concentration were evaluated. Feeding with the 3 HDFs similarly increased body weight, liver weight, and fat pad weight, and induced glucose intolerance and intestinal hyperpermeability. The expression of TJ proteins, zonula occludens‐2 and junctional adhesion molecule‐A, were lower in the colons of the 3 HFD groups than in the control group (P < 0.05), and these changes appeared to be related to intestinal hyperpermeability. Feeding with HFDs increased total secondary BA (SBA) and total BA concentrations along with increases in some individual BAs in the cecum. Significant positive correlations between intestinal permeability and the concentrations of most SBAs, such as deoxycholic acid and ω‐muricholic acids, were detected (P < 0.05). These results suggest that the HFD‐induced intestinal hyperpermeability is associated with increased BA secretion. The abundance of SBAs in the large intestine may be responsible for the hyperpermeability.     

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.     

High-protein compound yogurt with quinoa improved clinical features and metabolism of high-fat diet–induced nonalcoholic fatty liver disease in mice

Gut microbiota dysbiosis plays a crucial role in the occurrence and progression of nonalcoholic fatty liver disease (NAFLD), which may be influenced by nutritional supplementation. Quinoa, a type of pseudocereal, has gained prominence due to its high nutritional value and diverse applications. This study aimed to determine whether yogurt containing quinoa can ameliorate NAFLD and alleviate metabolic disorders by protecting against the divergence of gut microbiota. Our findings suggested that quinoa yogurt could significantly reduce the body weight gain and fat tissue weight of high-fat diet (HFD)–fed obese mice. In addition, quinoa yogurt significantly reduced liver steatosis and enhanced glucose homeostasis and insulin sensitivity. Additional research indicates that quinoa yogurt can reduce the levels of proinflammatory cytokines (i.e., tumor necrosis factor α, IL-1β, and IL-6) and inhibit endotoxemia and systemic inflammation. The characteristics of the gut microbiota were then determined by analyzing 16S rRNA. In addition, we discovered that the gut microbiota was disturbed by HFD consumption. Particularly, intestinal probiotics and beneficial intestinal secretions were increased, leading to the expression of glucagon-like peptide-1 in the colon, contributing to NAFLD. Furthermore, endotoxemia and systemic inflammation in HFD-fed mice were restored to the level of control mice when they were fed yogurt and quinoa. Therefore, yogurt containing quinoa can effectively alleviate NAFLD symptoms and may exert its effects via microbiome-gut-liver axis mechanisms. According to some research, the role of the enteric-liver axis may also influence metabolic disorders to reduce the development of NAFLD.     

Chestnut (Castanea crenata) inner shell extract inhibits development of hepatic steatosis in C57BL/6 mice fed a high-fat diet

The effects of chestnut inner shell extract (CISE) on hepatic steatosis and lipid metabolism in mice fed high-fat diet (HFD) were evaluated. Hepatic triacylglycerol and plasma lipid levels decreased significantly in CISE-administered mice compared to control group. Relative mRNA expression levels for lipogenic genes SREBP-1c, FAS, ACCs, ACAT, and HMG-CoA were significantly decreased in CISE-administered mice (P < 0.05). CISE suppressed FAS and HMG-CoA reductase activity and increased CPT activity. To determine the active compound of CISE, the fractionation of CISE have conducted and resulted in the isolation of scoparone and scopoletin, as main compounds contained in CISE. Based on these results, we speculate that the inhibitory effect on hepatic steatosis of CISE containing scoparone and scopoletin may be the result of suppression of lipid synthesis and the acceleration of fatty acid oxidation in mice fed HFD, suggesting that CISE may be beneficial in preventing hepatic steatosis.     

Micronutrients in High-Fat Diet Modify Insulin Resistance and Its Regulatory Genes in Adult Male Mice

Scope

Obesity and insulin resistance (IR) are associated with epigenetic changes of gene expression. However, the relationship between micronutrients, epigenetic regulation of gene expression, and IR during development of diet-induced obesity has yet to be defined. Our objective is to describe the effect of micronutrient addition to diets on IR and its related genes during obesity development.

Methods and results

Male C57BL/6J mice are fed a high-fat (HFD) or low-fat (LFD) diets with or without a multi-vitamin mineral mix (MVM) addition containing vitamins A, B1, B6, B12, and Zn, and Se for 9 weeks. Compared to LFD mice, HFD mice have higher body weight, IR, fasting glucose, insulin, C-peptide, leptin, and hepatic triglyceride concentrations, and dysregulated gene expression in liver, muscle, pancreas, and fat tissues (p < 0.05). The addition of MVM reduces these HFD-induced effects. HFD downregulates 27 genes associated with insulin regulation and adipose tissue function across all tissues by an average of 47% and upregulates five genes by 230% (p < 0.001). Adding MVM downregulates five genes and upregulates one in HFD-fed mice. Both HFD and MVM alter one-carbon metabolites.

Conclusion

Addition of micronutrients to the HFD decreases IR and modifies associated gene expression in obese and lean mice.     

Antiobesity and lipid lowering effects of theaflavins on high-fat diet induced obese rats

Theaflavins are major polyphenols in black tea. This study investigated antiobesity and lipid lowering effects of black tea extract (BTE), a highly purified theaflavins mixture (TFs, 83.84%) and theaflavin (TF1, 93.25%) on high-fat diet (HFD) induced obese rats. The body weight was slightly reduced by BTE and TFs (p > 0.05), and was significantly decreased by TF1 (p < 0.05) relative to the HFD control group. All samples remarkably decreased the food intake, adiposity index and the serum levels of total cholesterol (TC), triacylglycerol (TG) and low-density lipoprotein cholesterol (LDL-C) (p < 0.05), except that BTE and TF1 insignificantly decreased the TC concentration (p > 0.05). Moreover, administration of BTE, TFs and TF1 all significantly decreased atherogenic index (AI), enhanced insulin sensitive index (ISI), inhibited the hepatic lipase (HL) activity (p < 0.05), and slightly reduced leptin level in liver, decreased serum alanine transaminase (ALT) activity and increased serum superoxide dismutase (SOD) activity (p > 0.05) as compared to that of the HFD controls. These results indicated that theaflavins were one of the functional components which contributed to the antiobesity and lipid lowering effects of black tea, and might reduce the risk of type 2 diabetes and cardiovascular disease (CVD) in obese patients.     

Hypolipidaemic and hypoglycaemic effects of total flavonoids from seed residues of Hippophae rhamnoides L. in mice fed a high-fat diet

BACKGROUND: The present study was designed to investigate the hypolipidaemic and hypoglycaemic effects of total flavonoids from seed residues of Hippophae rhamnoides L. (FSH) in a high‐fat diet fed mouse model. Consumption of a high‐fat diet (HFD) for 4 weeks caused a significant rise of serum total cholesterol in mice. These hypercholesterolaemic mice then were orally administrated with different doses of FSH (50, 100 and 150 mg kg^?1 body weight) and simvastatin (20 mg kg^?1 body weight) for another 12 weeks under continuous HFD feeding. RESULTS: FSH administration markedly reduced total mouse body, liver, and epididymal fat pad weights. Serum total cholesterol and low density of lipoprotein‐cholesterol levels were also significantly decreased by FSH treatment. Additionally, FSH significantly lowered total cholesterol and triglyceride concentrations in liver, and the results were corroborated by transmission electron microscope findings. The rise in serum glucose was significantly suppressed by FSH treatment while improving impaired glucose tolerance. CONCLUSION: These results suggest that FSH possesses hypolipidaemic and hypoglycaemic properties in mice fed a high‐fat diet and could be developed as a supplement in healthcare foods and drugs. Copyright © 2011 Society of Chemical Industry     

Protective effect of whey protein hydrolysates against oxidative stress in d-galactose-induced ageing rats

The protective effect of whey protein hydrolysate (WPH) against oxidation was studied in d-galactose-induced ageing rats. The rats were divided into a normal group, a d-galactose model group, low-, middle-, and high-dose WPH groups, and an ascorbic acid group. The three WPH groups and the ascorbic acid group also received d-galactose treatment. Administration of WPH significantly increased body weight gain, spleen index and high-density lipoprotein content (P < 0.05) and decreased the triglyceride and low-density lipoprotein contents (P < 0.05) compared with the ageing model group. WPH had a protective effect against d-galactose-induced ageing in rats as shown by the increased activities of superoxide dismutase, catalase and glutathione peroxidase and decrease in the malonaldehyde contents (P < 0.05) in the serum, spleen, liver, and lungs. The protective effect of WPH on d-galactose-induced ageing in rats can be attributed to enhanced antioxidant defences and the elevation of antioxidase activity.     

Piperine reverses high fat diet-induced hepatic steatosis and insulin resistance in mice

This study examined the effect of piperine on hepatic steatosis and insulin resistance induced in mice by feeding a high-fat diet (HFD) for 13 weeks and elucidated potential underlying molecular mechanisms. Administration of piperine (50 mg/kg body weight) to mice with HFD-induced hepatic steatosis resulted in a significant increase in plasma adiponectin levels. Also, elevated plasma concentrations of insulin and glucose and hepatic lipid levels induced by feeding a HFD were reversed in mice when they were administered piperine. However, piperine did not reduce body weight and other biochemical markers to an extent where they became equal to the levels found in the CD-fed mice. Piperine reversed HFD-induced down-regulation of adiponecitn-AMP-activated protein kinase (AMPK) signalling molecules which play an important role in mediating lipogenesis, fatty acid oxidation and insulin signalling in the livers of mice. The expressions of lipogenic target genes were decreased, whereas the expression of carnitine palmitoyltransferase 1 (CPT1) gene involved in fatty acid oxidation was increased in the livers of the Pin50 group. Piperine significantly decreased the phosphorylation of insulin receptor substrate-1 (IRS-1) compared with the HFD-fed mice. Administration of piperine appeared to reverse preexisting HFD-induced hepatic steatosis and insulin resistance, probably by activation of adiponectin-AMPK signalling in mice.     

Protective effect of selenium-polysaccharides from the mycelia of Coprinus comatus on alloxan-induced oxidative stress in mice

We investigated the effect of selenium-polysaccharide (SPS) isolated from selenium-enriched mycelia of Coprinus comatus on hypoglycaemic, hypolipidemic and antioxidant activities in diabetic mice. Compared with untreated diabetic mice, the administration of SPS for 20 days caused a significant decrease (p < 0.05) in blood glucose levels. Simultaneously, the alteration in lipid metabolism was partially attenuated as evidenced by decreased serum total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL) levels and by increased high-density lipoprotein cholesterol (HDL) concentration in diabetic mice (p < 0.05). In addition, the SPS caused a significant decrease (p < 0.05) in the level of malondialdehyde (MDA) and a significant increase (p < 0.05) in the activities of enzymic antioxidants and the levels of non-enzymic antioxidants in liver and kidney of diabetic mice. Furthermore, the effects of SPS was more potent than that of polysaccharide (PS) from mycelia of C. comatus at the same dose.     

Hypoglycemic effects of black glutinous corn polysaccharides on alloxan-induced diabetic mice

To investigate substances from corn with the potential to affect blood sugar levels, black glutinous corn polysaccharides (BGCP) were isolated and evaluated for hypoglycemic activity in alloxan-induced diabetic mice. Mice were administered daily doses of 800, 500 or 200 mg/kg BGCP for 4 weeks. Blood glucose, serum insulin levels, body weight and the organ weight of liver, kidney, spleen and thymus were measured. All three BGCP-treated groups showed reduced blood glucose levels, and treatment with 800 mg/kg resulted in greater hypoglycemic effects than treatment with lower doses. At week 4 of the trial, mice receiving 800 or 500 mg/kg BGCP showed blood glucose levels that were significantly lower (P < 0.05) than untreated diabetic control mice. Administration of alloxan led to significant loss of body weight after 2, 3 and 4 weeks. BGCP treatment did not affect the weight of the thymus and spleen compared to untreated diabetic control mice. The weight of the liver decreased and the weight of kidney increased in alloxan-treated diabetic mice, but kidney weight did not increase in diabetic mice treated with 800 mg/kg BGCP.     

粉葛多糖改善金黄地鼠非酒精性脂肪肝及对肠道菌群的调节作用

目的 研究粉葛多糖对高脂饮食诱导的金黄地鼠非酒精性脂肪肝(nonalcoholic fatty liver disease, NAFLD)的改善作用及与肠道菌群的关系。方法 金黄地鼠随机分为空白组、高脂模型组、粉葛多糖高剂量组(100 mg/kg)、粉葛多糖低剂量组(50 mg/kg)。15周后,测定肝脏重量、肝指数、血脂及脂多糖(lipopolysaccharide, LPS)水平,肝脏及结肠切片H E染色,结肠内容物16S rRNA测序。结果 与高脂模型组相比,粉葛多糖显著降低了肝脏重量及肝指数,改善了总胆固醇(total cholesterol, TC)、低密度脂蛋白胆固醇(low-density lipoprotein cholesterol, LDL-C)水平,甘油三酯(triglyceride, TG)及LPS水平显著降低,可改善肠道屏障损伤及肝脏脂肪变性;在肠道菌群门水平上,粉葛多糖能降低肠源性LPS主要来源菌门Proteobacteria的相对丰度至0.05%,在属水平上,粉葛多糖能促进与肥胖呈负相关的Parabacteroides及与肠道黏膜修复相关的Lachnospiraceae NK4A136 group富集。结论 粉葛多糖可能通过调节肠道菌群改善高脂饮食诱导的金黄地鼠NAFLD。