Lipid metabolic effect of Korean red ginseng extract in mice fed on a high-fat diet

BACKGROUND: Ginseng saponin and ginsenosides exert anti‐obesity effects via the modulation of physiological lipid metabolism in vivo or intracellular signalling in cell culture systems. However, the complicated relationship between the anti‐obesity effects of ginseng and gene expression has yet to be defined under in vivo conditions. Therefore, we evaluated the relationship between the anti‐obesity effects of Korean red ginseng extract (KRGE) and hepatic gene expression profiles in mice fed long‐term on a high‐fat diet (HFD) in this study. RESULTS: KRGE reduces the levels of cholesterol, low‐density lipoprotein‐cholesterol (LDL‐C), serum triglycerides, and atherogenic indices. Levels of leptin, adiponectin and insulin, which regulate glucose and lipid metabolism, were impaired profoundly by HFD. However, KRGE treatment brought these levels back to normal. KRGE was found to down‐regulate genes associated with lipid metabolism or cholesterol metabolism (Lipa, Cyp7a1, Il1rn, Acot2, Mogat1, Osbpl3, Asah3l, Insig1, Anxa2, Vldlr, Hmgcs1, Sytl4, Plscr4, Pla2g4e, Slc27a3, Enpp6), all of which were up‐regulated by HFD. CONCLUSION: KRGE regulated the expression of genes associated with abnormal physiology via HFD. Leptin, insulin, and adiponectin, which carry out critical functions in energy and lipid metabolism, were shown to be modulated by KRGE. These results show that KRGE is effective in preventing obesity. Copyright © 2011 Society of Chemical Industry     

Lacticaseibacillus paracasei K71 Alleviates UVB-Induced Skin Barrier Dysfunction by Attenuating Inflammation via Increased IL-10 Production in Mice

Scope

Ultraviolet B (UVB) radiation causes skin barrier dysfunction, leading to decreased water-holding capacity, impaired epidermal barrier function, and increased skin thickness. This study investigates the protective effects of oral administration of Lacticaseibacillus paracasei K71 against skin barrier dysfunction in UVB-irradiated mice.

Methods and results

Mice are fed diets with or without K71 and irradiated with UVB three times a week for 12 weeks. Oral administration of K71 suppresses UVB-induced decrease in stratum corneum water content, mitigates the increase of transepidermal water loss, and decreases epidermal thickness of the dorsal skin. Treatment with K71 reverses the upregulation of inflammatory cytokines and the activation of nuclear factor-κB induced by UVB irradiation and upregulates the expression of anti-inflammatory IL-10 in the dorsal skin. Notable upregulation of IL-10 is observed in the spleens of K71-treated mice. K71 treatment enhances IL-10 production in J774.1 macrophages; however, this enhancement is diminished by inhibiting K71 phagocytosis and TLR3. Furthermore, transfection using K71 RNAs significantly increases IL-10 production.

Conclusion

These results indicate that K71 may alleviate UVB-induced skin barrier dysfunction by attenuating inflammation via increasing IL-10 production and that K71 RNAs may induce IL-10 production in macrophages. Therefore, K71 may be beneficial for preventing skin barrier dysfunction.     

(+)-Catechin Attenuates Multiple Atherosclerosis-Associated Processes In Vitro,Modulates Disease-Associated Risk Factors in C57BL/6J Mice and Reduces Atherogenesis in LDL Receptor Deficient Mice by Inhibiting Inflammation and Increasing Markers of Plaque Stability

Scope

A prospective study of 34492 participants shows an inverse association between (+)-catechin intake and coronary heart disease. The effects of (+)-catechin on atherosclerosis and associated risk factors are poorly understood and are investigated.

Methods and results

(+)-Catechin attenuates reactive oxygen species production in human macrophages, endothelial cells and vascular smooth muscle cells, chemokine-driven monocytic migration, and proliferation of human macrophages and their expression of several pro-atherogenic genes. (+)-Catechin also improves oxidized LDL-mediated mitochondrial membrane depolarization in endothelial cells and attenuates growth factor-induced smooth muscle cell migration. In C57BL/6J mice fed high fat diet (HFD) for 3 weeks, (+)-catechin attenuates plasma levels of triacylglycerol and interleukin (IL)-1β and IL-2, produces anti-atherogenic changes in liver gene expression, and reduces levels of white blood cells, myeloid-derived suppressor cells, Lin⁻ Sca⁺ c-Kit⁺ cells, and common lymphoid progenitor cells within the bone marrow. In LDL receptor deficient mice fed HFD for 12 weeks, (+)-catechin attenuates atherosclerotic plaque burden and inflammation with reduced macrophage content and increased markers of plaque stability; smooth muscle cell and collagen content.

Conclusion

This study provides novel, detailed insights into the cardio-protective actions of (+)-catechin together with underlying molecular mechanisms and supports further assessments of its beneficial effects in human trials.     

Modulatory effects of yerba maté (Ilex paraguariensis) on the PI3K‐AKT signaling pathway

The aim of this study was to evaluate the effects of yerba maté (YM) extract on the phosphatidylinositol 3‐kinase (PI3K)‐AKT signaling pathway in vivo. The mice were introduced to either standard‐ or high‐fat diet (HFD). After 8 weeks on an HFD, mice were randomly assigned to one of the two treatment conditions, water or yerba maté extract at 1.0 g/kg. After treatment, glucose blood level and hepatic insulin response were evaluated. Liver tissue was examined to determine the mRNA levels using the PI3K‐AKT PCR array. The nuclear translocation of forkhead box O1 (FOXO1) was determined by an electrophoretic mobility‐shift assay. Our data demonstrated that yerba maté extract significantly decreased the final body weight, glucose blood levels, and insulin resistance of mice. Molecular analysis demonstrated that an HFD downregulated Akt2, Irs1, Irs2, Pi3kca, Pi3kcg, and Pdk1; after yerba maté treatment, the levels of those genes returned to baseline. In addition, an HFD upregulated Pepck and G6pc and increased FOXO1 nuclear translocation. The intervention downregulated these genes by decreasing FOXO1 nuclear translocation. The results obtained demonstrate for the first time the specific action of yerba maté on the PI3K‐AKT pathway, which contributed to the observed improvement in hepatic insulin signaling.     

Photoperiod-Dependent Effects of Grape-Seed Proanthocyanidins on Adipose Tissue Metabolic Markers in Healthy Rats

Scope

Variations in photoperiod patterns drive metabolic adaptations in mammals, involving important changes in body weight and adiposity. Moreover, (poly)phenols can help heterotrophs adopt metabolic adaptations to face the upcoming environmental conditions. Particularly, proanthocyanidins from grape-seeds show photoperiod-dependent effects on different metabolic parameters. The present study aims to explore whether grape-seed proanthocyanidin extract (GSPE) consumption differently affects the expression of metabolic markers in WAT (subcutaneous and visceral depots) and BAT in a photoperiod-dependent manner.

Methods and results

GSPE (25 mg kg⁻¹ day⁻¹) is orally administrated for 4 weeks to healthy rats exposed to three photoperiods (L6, L12, and L18). In WAT, GSPE consumption significantly upregulates the expression of lipolytic genes in all photoperiods, being accompanied by increased serum concentrations of glycerol and corticosterone only under the L6 photoperiod. Moreover, adiponectin mRNA levels are significantly upregulated in response to GSPE regardless of the photoperiod, whereas Tnfα and Il6 expression are only downregulated in L6 and L18 photoperiods but not in L12. In BAT, GSPE upregulates Pgc1α expression in all groups, whereas the expression of Pparα is only increased in L18.

Conclusions

The results indicate that GSPE modulates the expression of important metabolic markers of WAT and BAT in a photoperiod-dependent manner.     

Dietary Supplementation with the Probiotic SF68 Reinforces Intestinal Epithelial Barrier in Obese Mice by Improving Butyrate Bioavailability

Scope

Modifications in intestinal microbiota and its metabolites, the short-chain fatty acids (SCFA) are main factors altering intestinal epithelial barrier integrity and eliciting the onset of a meta-inflammation observed in obesity. The present study is aimed at evaluating the efficacy of Enterococcus faecium (SF68) administration in counteracting the impairment of gut barrier and enteric inflammation in a model of diet-induced obesity, characterizing the molecular mechanisms underlying such beneficial effects.

Methods and Results

Male C57BL/6J mice, fed with standard diet (SD) or high-fat diet (HFD), are treated with SF68 (10⁸ CFU day⁻¹). After 8 weeks, plasma interleukin (IL)-1β and lipopolysaccharide binding protein (LBP) are measured, analysis of fecal microbiota composition and butyrate content as well as intestinal malondialdehyde, myeloperoxidase, mucins, tight junction protein, and butyrate transporter expression are investigated. After 8 weeks, SF68 administration counteracts the body weight gain in HFD mice, reducing plasma IL-1β and LBP. In parallel, SF68 treatment acts against the intestinal inflammation in HFD-fed animals and improves the intestinal barrier integrity and functionality in obese mice via the increase in tight junction protein and intestinal butyrate transporter (sodium-coupled monocarboxylate transporter 1 ) expression.

Conclusions

Supplementation with SF68 reduces intestinal inflammation and reinforces the enteric epithelial barrier in obese mice, improving the transport and utilization of butyrate.     

l‐Citrulline Supplementation‐Increased Skeletal Muscle PGC‐1α Expression Is Associated with Exercise Performance and Increased Skeletal Muscle Weight

Scope

l ‐citrulline has recently been reported as a more effective supplement for promoting intracellular nitric oxide (NO) production compared to l ‐arginine. Here, the effect of l ‐citrulline on skeletal muscle and its influence on exercise performance were investigated. The underlying mechanism of its effect, specifically on the expression of skeletal muscle peroxisome proliferator‐activated receptor‐gamma coactivator‐1α (PGC‐1α), was also elucidated.

Methods and results

Six‐week‐old ICR mice were orally supplemented with l ‐citrulline (250 mg kg^?1) daily, and their performance in weight‐loaded swimming exercise every other day for 15 days, was evaluated. In addition, mice muscles were weighed and evaluated for the expression of PGC‐1α and PGC‐1α‐regulated genes. Mice orally supplemented with l ‐citrulline had significantly higher gastrocnemius and biceps femoris muscle mass. Although not statistically significant, l ‐citrulline prolonged the swimming time to exhaustion. PGC‐1α upregulation was associated with vascular endothelial growth factor α (VEGFα) and insulin‐like growth factor 1 (IGF‐1) upregulation. VEGFα and IGF‐1 are important for angiogenesis and muscle growth, respectively, and are regulated by PGC‐1α. Treatment with NG‐nitro‐l ‐arginine methyl ester hydrochloride (l ‐NAME), a nitric oxide synthesis inhibitor, suppressed the l ‐citrulline‐induced PGC‐1α upregulation in vitro.

Conclusion

Supplementation with l ‐citrulline upregulates skeletal muscle PGC‐1α levels resulting in higher skeletal muscle weight that improves time to exhaustion during exercise.

     

原花青素B2对高脂膳食小鼠钙代谢及股骨基因表达谱的影响

目的：探究原花青素B2对高脂膳食小鼠钙代谢异常与股骨基因表达的影响。方法：将27 只C57BL/6雄性小鼠随机分为3 组：对照组、高脂膳食组和原花青素B2组,原花青素B2添加量为0.2%（以饲料质量计）;持续饲喂8 周后分析小鼠体质量、血浆脂质水平、钙内稳态、钙吸收能力和骨矿物含量的变化,并运用真核有参转录组技术分析小鼠股骨基因表达变化情况。结果：原花青素B2能够显著提高小鼠钙净吸收和贮留能力（P＜0.05）,并显著降低血脂水平和甲状旁腺素质量浓度,改善高脂膳食导致的小鼠骨矿物、股骨钙含量和最大荷载量的降低。高通量测序发现49 个差异共表达基因,原花青素B2可干预其中48 个基因的表达,基因本体论富集分析发现其归属于生物进程和细胞组分两个分支,京都基因与基因组百科全书（Kyoto Encyclopedia of Genes and Genomes,KEGG）富集分析发现共有13 条通路具有显著性富集意义（P＜0.05）,其中涉及钙代谢相关信号转导和代谢通路5 个基因（Cdkn2a、Adrb1、Fcgr4、Aldh1a3和Calml3）的表达量发生显著改变（P＜0.05）。与高脂膳食组相比,原花青素B2下调Cdkn2a、Adrb1、Fcgr4基因表达量分别为9.19、3.68 倍和3.61 倍,上调Aldh1a3和Calml3基因的表达量分别为2.06 倍和3.29 倍。结论：原花青素B2具有干预高脂膳食导致的小鼠钙代谢异常的作用,其可能与下调破骨细胞活性与上调成骨细胞活性相关基因的表达有关。     

Pine needle extract suppresses adiposity via mediating adipogenic gene expressions of white adipose tissue in high fat diet-fed rats

Effect of pine needle extract (PNE) on adiposity was examined through morphologic examination and adipogenic gene expression of white adipose tissue (WAT) in high fat diet (HFD)-fed rats. Four type diets; normal diet (ND), HFD, and diets respectively supplemented with PNE in both ND and HFD, were fed for 8 weeks. The adipose fat mass and the sizes in WAT were significantly lower in PNE-supplemented HFD group than in HFD group. The serum levels of PNE-supplemented HFD group were similar to those of ND group. The supplementation of PNE to HFD markedly increased adiponectin mRNA, but decreased those of leptin and tumor necrosis factor (TNF)-α in WAT, respectively. PNE enhanced glucose uptake of epididymal WAT under insulin stimulation. The results suggest that the beneficial effect of PNE supplementation on adipose fat and serum profiles in HFD-fed rats is partly modulated by adipogenic genes, such as adiponectin, leptin, and TNF-α mRNA in WAT.     

Dietary quercetin alleviates diabetic symptoms and reduces streptozotocin‐induced disturbance of hepatic gene expression in mice

Quercetin is a food component that may ameliorate the diabetic symptoms. We examined hepatic gene expression of BALB/c mice with streptozotocin (STZ)‐induced diabetes to elucidate the mechanism of the protective effect of dietary quercetin on diabetes‐associated liver injury. We fed normal and STZ‐induced diabetic mice with diets containing quercetin for 2 wk and compared the patterns of hepatic gene expression in these groups of mice using a DNA microarray. Diets containing 0.1 or 0.5% quercetin lowered the STZ‐induced increase in blood glucose levels and improved plasma insulin levels. A cluster analysis of the hepatic gene expressions showed that 0.5% quercetin diet suppressed STZ‐induced alteration of gene expression. Gene set enrichment analysis (GSEA) and quantitative RT‐PCR analysis showed that the quercetin diets had greatest suppressive effect on the STZ‐induced elevation of expression of cyclin‐dependent kinase inhibitor p21(WAF1/Cip1) (Cdkn1a). Quercetin also suppressed STZ‐induced expression of Cdkn1a in the pancreas. Dietary quercetin might improve liver and pancreas functions by enabling the recovery of cell proliferation through the inhibition of Cdkn1a expression. Unexpectedly, in healthy control mice the 0.5 and 1% quercetin diets reduced the expression of ubiquitin C (Ubc), which has heat‐shock element (HSE) in the promoter region, in the liver.     

No Adverse Programming by Post‐Weaning Dietary Fructose of Body Weight,Adiposity, Glucose Tolerance,or Metabolic Flexibility

1 Scope

Metabolic programming can occur not only in the perinatal period, but also post‐weaning. This study aims to assess whether fructose, in comparison to glucose, in the post‐weaning diet programs body weight, adiposity, glucose tolerance, metabolic flexibility, and health at adult age.

2 Methods and results

Three‐week‐old male and female C57BL6/JRccHsd mice are given an intervention diet with 32 energy percent (en%) glucose or fructose for only 3 weeks. Next, all animals are switched to the same 40 en% high fat diet for 9 weeks. Neither body weight nor adiposity differs significantly between the animals fed with glucose or fructose diets at any point during the study in both sexes. Glucose tolerance in adulthood is not affected by the post‐weaning diet, nor are activity, energy expenditure, and metabolic flexibility, as measured by indirect calorimetry. At the end of the study, only in females fasting serum insulin levels and HOMA‐IR index are lower in post‐weaning fructose versus glucose diet (p = 0.02), without differences in pancreatic β‐cell mass.

3 Conclusions

Our present findings indicate no adverse programming of body weight, adiposity, glucose tolerance, and metabolic flexibility by dietary (solid) fructose in comparison to glucose in the post‐weaning diet in mice.     

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.     

Intake of Fish Oil Specifically Modulates Colonic Muc2 Expression in Middle‐Aged Rats by Suppressing the Glycosylation Process

1 Scope

Dietary fats have been shown to affect gut microbiota composition and aging gene expression of middle‐aged rats at a normal dose, but little is known about such an effect on gut barrier. In this study, the changes in colonic Muc2 expression are investigated and the underlying mechanism is also proposed.

2 Methods and results

36 middle‐aged Sprague–Dawley rats are assigned to one of the diets containing soybean oil, lard, or fish oil (4%). The rats are fed for 5 weeks and then goblet cells, Muc2 expression, and inflammatory cytokines in the colon are measured. Proteome analysis is performed. Compared with the lard and soybean oil diet groups, intake of fish oil decreases the number of goblet cells, and inhibits Muc2 and TLRs expression in the colon of middle‐aged rats, which would impair mucus barrier. Several key enzymes involved in glycosylation process, including Agr2, Gale, Gne, Pmm2, Pdxdc1, Plch1, Pfkp, Cmpk1, and Rexo2, show the lowest abundance in the fish oil diet group.

3 Conclusion

Intake of fish oil at a normal dose downregulates colonic Muc2 expression. This negative effect of fish oil may involve the suppression of mucin glycosylation process.     

黄大茶水提物改善高脂小鼠脂肪组织的脂肪酸代谢

目的：探究黄大茶水提物对高脂饮食小鼠脂肪组织脂肪酸代谢的调控机制。方法：将5 周龄雄性C57BL/6小鼠随机分为对照组、高脂饮食组、高脂饮食＋2.5%（终质量分数,下同）黄大茶水提取物组、高脂饮食＋0.5%黄大茶水提取物组。饮食干预处理12 周后,测定小鼠体质量、脂肪组织质量,观察脂肪组织形态,并分析脂肪酸代谢关键基因及蛋白表达量等指标。结果：2.5%黄大茶水提物能高度显著降低高脂小鼠体质量及脂肪组织质量（P＜0.001）;减少脂肪组织的脂质沉积;促进SREBP-1C、FAS、ACC、SCD-1等脂肪酸生成相关基因的表达,促进脂肪酸分解相关基因PGC-1α和CPT-1的表达;不同程度激活腺苷酸活化蛋白激酶（adenosine monophosphate activated protein kinase,AMPK）/乙酰辅酶A羧化酶（acetyl CoA-carboxylase,ACC）通路。结论：2.5%黄大茶水提物饮食干预能显著缓解高脂饮食小鼠肥胖和减少脂质沉积,促进脂肪组织脂肪酸合成和氧化分解代谢,此作用与黄大茶水提物激活AMPK/ACC通路相关。     

Salvianolic Acid B Inhibits High‐Fat Diet‐Induced Inflammation by Activating the Nrf2 Pathway

Salvianolic acid B (Sal B) is a major water‐soluble bioactive component of Salvia miltiorrhiza, which is a traditional Chinese medicine. We investigated the ways in which Sal B affects high‐fat diet (HFD)‐induced immunological function disorder remission using a C57BL/6 mouse model. We gave groups of C57BL/6 mice a normal diet (Control), a normal diet supplemented with Sal B (Control + Sal B), a high‐fat diet (HF), and a high‐fat diet supplemented with Sal B (HF + Sal B) for 10 wk. Sal B supplementation decreased the body weight and plasma lipids, increased the fecal excretion of lipids, prevented the accumulation of chronic oxidative stress, and reversed the disproportionality of CD3⁺CD4⁺ and CD3⁺CD8⁺ T lymphocytes compared to HFD. We found an increase in IL‐6 and TNF‐α, while IL‐10 decreased in plasma after the HFD and Sal B reversed the deregulation of the Thl/Th2 ratio. In addition, HFD‐induced inflammation was stopped by Sal B through the downregulation of nuclear factor‐κB (NF‐κB), cyclooxygenase‐2 (COX‐2), and inducible NO synthesis (iNOS), and the upregulation of nuclear factor‐erythroid 2‐related factor 2 (Nrf2)‐regulated genes. These findings demonstrated that Sal B could effectively attenuate inflammation by activating the Nrf2‐mediated antioxidant defense system.     

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.     

Chlorogenic acid promotes osteoblastogenesis in human adipose tissue-derived mesenchymal stem cells

High-fat diet (HFD)-induced obesity is associated with oxidative stress. The purpose of this study was to examine the antioxidant effect of Phaeodactylum tricornutum extract in mice with diet-induced obesity. Four-week-old C57BL/6J mice were fed a normal diet or HFD with and without 0.7% P. tricornutum lipid extract corresponding to 0.2% fucoxanthin for 8 weeks. P. tricornutum significantly decreased body weight and epidydimal white adipose tissue in mice fed the HFD. Serum triglyceride, glucose, insulin, and leptin levels, as well as homeostasis model assessment for insulin resistance (HOMA-IR) values, were significantly lower in the P. tricornutum group than in the HFD group. P. tricornutum significantly decreased thiobarbituric acid reactive substances (TBARS) and increased glutathione and the activities of superoxide dismutase, catalase, and glutathione peroxidase in the liver compared with the HFD group. Thus, P. tricornutum could exert antiobesity and antioxidant effects in mice fed a HFD.     

Oral Administration of Edible Seaweed Undaria Pinnatifida (Wakame) Modifies Glucose and Lipid Metabolism in Rats: A DNA Microarray Analysis

1 Scope

Wakame is an edible seaweed that is a common constituent in the Japanese diet. Previous studies showed that wakame consumption is associated with the prevention of metabolic syndrome, but the molecular mechanisms underlying the protective effects are poorly understood.

2 Methods and results

To determine if the expression of hepatic genes is affected by ingestion of the brown seaweed Undaria pinnatifida (wakame), rats were fed a diet containing 0, 0.1, or 1.0 g per 100 g dried wakame powder for 28 days. Administration of 1% wakame significantly decreased serum total cholesterol levels. Hepatic gene expression was investigated using DNA microarray analysis, and the results showed that wakame suppresses the lipogenic pathway by downregulating SREBF‐1. Moreover, bile acid biosynthesis and gluconeogenesis were promoted by upregulation of the PPAR signaling pathway, which leads to a reduction in the accumulation of cholesterol and promotion of β‐oxidation.

3 Conclusions

These results suggest that wakame ingestion affects glucose and lipid metabolism by altering the expression of SREBF‐1 and PPAR signal‐related genes.     

凝结芽孢杆菌BC2000联合鞣花酸改善高脂饮食诱导的小鼠胰岛素抵抗

目的：探讨凝结芽孢杆菌BC2000提高鞣花酸（ellagic acid,EA）缓解小鼠胰岛素抵抗的效果及与肠道菌群重塑的关系。方法：将50只C57BL/6J小鼠随机分为5组：低脂饮食（low fat diet,LFD）组、高脂饮食（high fat diet,HFD）组、凝结芽孢杆菌BC2000联合EA干预组（HFD+EA+BC2000组）、凝结芽孢杆菌BC30联合EA干预组（HFD+EA+BC30组）和EA干预组（HFD+EA组）,进行10周干预,测定小鼠相关生理生化指标,对炎性细胞因子进行分析,同时对肝脏和睾周脂肪进行组织学分析并对盲肠内容物进行肠道菌群结构分析。结果显示,BC2000和EA联合食用改善了高脂饮食诱导的小鼠肥胖,减轻了脂肪细胞肥大和肝脏脂肪变性,显著降低了高脂饲喂小鼠血浆的胰岛素、总胆固醇、低密度脂蛋白胆固醇水平和胰岛素抵抗指数（P<0.05）,显著降低血浆黏膜屏障生物标志物脂多糖和连蛋白（Zonulin）水平（P<0.05）,以及慢性炎症标志物肿瘤坏死因子α、超敏C反应蛋白和白细胞介素6(P<0.05)水平,提高盲肠放线菌门（Actinobact...