Prepuberty is a window period for curcumin to prevent obesity in postnatal overfed rats.

BACKGROUND: Overnutrition in early life increases the risk of obesity and metabolic diseases. We investigated the effects and the window period of a curcumin (CUR) diet on postnatal overfed rats. METHODS: Male rats aged 3 days were randomly divided into normal litters (NL, 10 pups/litter) and small litters (SL, 3 pups/litter). After weaning (Week 3, W3), NL rats were fed a normal diet (NL) and SL rats were fed a normal diet (SL) or 2% CUR diet from weaning (W3) (SL-CURW13), beginning of puberty (W6) (SL-CURW16), or end of puberty (W8) (SL-CURW18) for 10 weeks. RESULTS: Body weight, glucose intolerance and hyperlipidemia in the SL rats were higher than in the NL rats, especially after puberty. After the CUR intervention, SL-CURW13 and SL-CURW16 rats showed lower body weight gain, adipose tissue weight and mRNA level of C/EBPα in SAT, along with higher mRNA levels of ß-catenin. There was no difference between SL and SL-CURW18 rats. Glucose tolerance, serum lipids and hepatic lipids recovered to normal in the SL-CURW13 rats, but only partially in the SL-CURW16 and SL-CURW18 rats. CONCLUSION: Prepuberty is a window period for CUR intervention to improve programmed outcomes in postnatal overfed rats. IMPACT: Overnutrition during the first 1000 days of life has persistent negative effects on metabolism. Strategies should be taken to prevent overnutrition in early life to reduce the risk of obesity and metabolic disease in later life. A small-litter rat model was utilized to simulate early-life overnutrition in humans. We investigated the different effects and critical period for curcumin intervention on postnatal overfed rats. Dietary curcumin intervention before puberty could effectively transform nutritional programming to reduce obesity and metabolic disorders caused by early-life overnutrition, and an earlier intervention might predict a better outcome.

A single-center experience of non-bioartificial DFAPP support systems among Chinese patients with hyperlipidemic moderate/severe acute pancreatitis.

To assess the clinical efficacy of Double Filtration Plasmapheresis (DFAPP), a novel blood purification method, in treating hyperlipidemic moderate/severe pancreatitis (HL-M/SAP). A total of 68 HL-M/SAP patients were enrolled in this study. The observation group, comprising 34 patients, received DFAPP treatment, while the control group underwent CVVH + PA treatment. We compared the efficacy changes between the two groups post-treatment. Patients treated with DFAPP showed significant improvements in clinical outcomes. After 72 h of DFAPP treatment, HL-M/SAP patients exhibited notably lower multiple organ failure scores and a reduced mortality rate compared to those in the CVVH + PA group. Triglyceride levels in HL-M/SAP patients treated with DFAPP for 48 h averaged 3.75 ± 1.95, significantly lower than the 9.57 ± 3.84 levels in the CVVH + PA group (P < 0.05). Moreover, CRP levels decreased markedly, IL-17 levels diminished, IL-10 levels increased, and the decline in IL-35 levels was significantly less pronounced compared to the CVVH + PA group. The recurrence rate of pancreatitis was also significantly lower after 6 months. The early implementation of DFAPP in HL-M/SAP patients effectively reduces triglyceride levels, suppresses pro-inflammatory factors, enhances anti-inflammatory factors, and mitigates cytokine storm-induced sepsis damage. Consequently, this leads to a decrease in the incidence of multiple organ failure, improved patient survival rates, and a reduce the recurrence rate of lipogenic pancreatitis.Trial registration: Chinese Clinical Trial Registry, ChiCTR2300076066.

Saponins from Chenopodium quinoa Willd. husks alleviated high-fat-diet-induced hyperlipidemia via modulating the gut microbiota and multiple metabolic pathways.

BACKGROUND: Hyperlipidemia is characterized by abnormally elevated blood lipids. Quinoa saponins (QS) have multiple pharmacological activities, including antitumor, bactericidal and immune-enhancing effects. However, the lipid-lowering effect and mechanisms of QS in vivo have been scarcely reported. METHODS: The effect of QS against hyperlipidemia induced by high-fat diet in rats was explored based on gut microbiota and serum non-targeted metabolomics. RESULTS: The study demonstrated that the supplementation of QS could reduce serum lipids, body weight, liver injury and inflammation. 16S rRNA sequencing demonstrated that QS mildly increased alpha-diversity, altered the overall structure of intestinal flora, decreased the relative richness of Firmicutes, the ratio of Firmicutes/Bacteroidetes (P < 0.05) and increased the relative richness of Actinobacteria, Bacteroidetes, Bifidobacterium, Roseburia and Coprococcus (P < 0.05). Simultaneously, metabolomics analysis showed that QS altered serum functional metabolites with respect to bile acid biosynthesis, arachidonic acid metabolism and taurine and hypotaurine metabolism, which were closely related to bile acid metabolism and fatty acid ß-oxidation. Furthermore, QS increased protein levels of farnesoid X receptor, peroxisome proliferator-activated receptor α and carnitine palmitoyltransferase 1, which were related to the screened metabolic pathways. Spearman correlation analysis showed that there was a correlation between gut microbiota and differential metabolites. CONCLUSION: QS could prevent lipid metabolism disorders in hyperlipidemic rats, which may be closely associated with the regulation of the gut microbiota and multiple metabolic pathways. This study may provide new evidence for QS as natural active substances for the prevention of hyperlipidemia. © 2023 Society of Chemical Industry.

Gut Microbiome and Metabolomics Study of Selenium-Enriched Kiwifruit Regulating Hyperlipidemia in Mice Induced by a High-Fat Diet.

Our previous study showed that as a substitute for statins, selenium-enriched kiwifruit (Se-Kiwi) might reduce blood lipids and protect the liver in Kunming mice, but the underlying mechanism remains unclear. Metabolic regulation of mammalian intestinal microflora plays an important role in obesity and related diseases induced by a high-fat diet (HFD). Here, samples of serum, liver, colon, and fresh feces from the Se-Kiwi-treated hyperlipidemia C57BL/6J mouse model were collected. Based on metabolome (UHPLC-Q-TOF MS) and gut microbiome (16S rDNA) analyses as well as the integrative analysis of physiological and biochemical indices and pathological data of mice, we aimed to systematically illustrate the gut microbiome and metabolomics mechanism of Se-Kiwi in HFD-induced hyperlipidemic mice. As a result, Se-Kiwi can significantly increase the abundance of potentially beneficial gut bacteria such as Parabacteroides, Bacteroides, and Allobaculum in the colon and improve hyperlipidemia by regulating the digestion and absorption of vitamins, pyrimidine metabolism, purine metabolism, and other metabolic pathways, which have been confirmed by the following fecal microbiota transplantation experiment. This process was significantly regulated by the Ada, Gda, Pank1, Ppara, Pparg, and Cd36 genes. These findings may provide a theoretical basis for the research and development of selenium-enriched functional foods in the treatment of hyperlipidemia.

Lactobacillus fermentum CKCC1858 alleviates hyperlipidemia in golden hamsters on a high-fat diet via modulating gut microbiota.

To investigate the effect of probiotic Lactobacillus fermentum CKCC1858, LF on the prevention of hyperlipidemia and its correlation with gut microbiota, golden hamsters were fed a high-fat diet alone or in combination with the probiotic for 6 weeks. The results showed that the LF intervention alleviated HFD-induced hyperlipidemia and liver damage, as evidenced by the reduced serum lipid profile levels and liver function markers. More importantly, the LF intervention attenuated HFD-induced microbiota dysbiosis by enhancing the abundance of SCFA-producing bacteria and reshaping the metabolic functions of the gut microbiota, likely contributing to its pronounced preventive effects on hyperlipidemia. This study elucidated the mechanism of the preventive effect of probiotics on hyperlipidemia in terms of regulating gut microbiota, and provided suggestions for regulating gut microbiota through probiotic interventions to improve lipid metabolism.

Liver triacylglycerol accumulation but not postprandial lipemia is reduced by a skim milk powder diet in male rats.

Increases in postprandial lipids are linked to the development of cardiometabolic and fatty liver disease. Prior work has suggested that dairy possesses beneficial cardiometabolic effects and thus the aim of the current investigation was to test the hypotheses that the habitual consumption of dairy, in the form of skim milk powder (SMP), would protect against increases in circulating lipids and liver lipid accumulation following an oral fat challenge in rats. Male rats were fed either a semipurified low-fat control diet with casein or a diet with an equivalent amount of protein (∼13% kcal) provided through skim milk powder (SMP) for 6 weeks (n = 40/group). Rats were then given an oral gavage of palm oil (5 mL/kg body weight) or an equivalent volume of water, and serum and liver were harvested 90 minutes or 4 hours after. Rats fed the SMP diet gained less weight than controls but there were no differences in glucose tolerance between groups. The fat gavage increased serum lipids in both diet groups, whereas there was a main effect of the fat challenge to increase, and the SMP diet, to decrease liver triacylglycerol accumulation. The percentage of saturated and monounsaturated fatty acids and the protein content/activity of lipogenic enzymes were reduced in livers from SMP-fed rats, whereas the percentage of polyunsaturated fatty acids was increased. In summary, we provide evidence that SMP consumption, although not protecting against postprandial lipemia, markedly attenuates triacylglycerol accumulation and the relative amount of saturated and monounsaturated fatty acids in the liver.

Rice Bran Extract Suppresses High-Fat Diet-Induced Hyperlipidemia and Hepatosteatosis through Targeting AMPK and STAT3 Signaling.

Rice bran, a by-product of rice milling, is abundant in bioactive molecules and is highly recognized for its health-promoting properties, particularly in improving metabolic conditions. Building on this knowledge, we aimed to optimize the extraction conditions to maximize the functional efficacy of rice bran extract (RBE) and further validate its impact on lipid metabolism. We found that the optimized RBE (ORBE) significantly suppressed high-fat diet-induced weight gain, hyperlipidemia, and hepatosteatosis in mouse models. ORBE treatment not only suppressed lipid uptake in vivo, but also reduced lipid accumulation in HepG2 cells. Importantly, we discovered that ORBE administration resulted in activation of AMPK and inhibition of STAT3, which are both crucial players in lipid metabolism in the liver. Collectively, ORBE potentially offers promise as a dietary intervention strategy against hyperlipidemia and hepatosteatosis. This study underlines the value of optimized extraction conditions in enhancing the functional efficacy of rice bran.

The anti-hyperlipidemic effect and underlying mechanisms of barley (Hordeum vulgare L.) grass polysaccharides in mice induced by a high-fat diet.

Hyperlipidemia is a pathological disorder of lipid metabolism that can cause fatty liver, atherosclerosis, acute myocardial infarction, and other diseases, seriously endangering people's health. Polysaccharides have been shown to have lipid-lowering potential. In the current study, the anti-hyperlipidemia effect and potential mechanisms of a polysaccharide (BGP-Z31) obtained from barley grass harvested at the stem elongation stage in high-fat diet (HFD)-treated mice were investigated. Results showed that supplementation with BGP-Z31 (200 and 400 mg kg-1) not only suppressed obesity, organ enlargement, and fat accumulation caused by HFD, but also regulated dyslipidemia, relieved liver function injury, and ameliorated the oxidative stress level. Meanwhile, BGP-Z31 increased the concentrations of acetic acid, propionic acid, butyric acid, and isovaleric acid in HFD-induced mice. Gut microbiota analysis demonstrated that BGP-Z31 had no obvious effect on the gut microbiota diversity in mice treated with HFD, but it positively remodeled the intestinal flora structure by elevating the relative abundances of Bacteroides, Muribaculaceae, and Lachnospiraceae and lowering the Firmicutes/Bacteroides value and the relative abundance of Desulfovibrionaceae. Therefore, our data suggested that BGP-Z31 can be used as a promising nutritional supplement for dietary intervention in hyperlipidemia.

Liposomal Phytosterols as LDL-Cholesterol-Lowering Agents in Diet-Induced Hyperlipidemia.

The high blood level of low-density lipoprotein cholesterol (LDL-C) is a primary risk factor for cardiovascular disease. Plant sterols, known as phytosterols (PSs), can reduce LDL-C in a range of 8-14%. The extent of LDL-C reduction depends on its formulation. Encapsulation into liposomes is one formulation strategy to enhance the efficiency of PSs. PSs (campesterol, stigmasterol, and ß-sitosterol) have frequently been assessed alone or in combination for their LDL-C-lowering ability. However, one naturally abundant PS, brassicasterol, has not yet been tested for its efficacy. We have previously developed a novel liposomal formulation containing the PS mixture present naturally in canola that is composed of brassicasterol, campesterol, and ß-sitosterol. In this work, the efficacy of our novel liposomal PS formulation that includes brassicasterol was assessed in a hamster model. Animals were divided into five groups: (i) liposomal PS in orange juice, (ii) liposomal PS in water, (iii) marketed PS in orange juice, (iv) control orange juice, and (v) control water. The animals were fed a high-fat, cholesterol-supplemented (0.5%) diet to induce hypercholesterolemia. The treatment was administered orally once daily for 4 weeks. Fasting blood samples were collected at baseline, week 2, and week 4. The extent of the reduction of total cholesterol, LDL-C, high-density lipoprotein cholesterol (HDL-C), and triglycerides was compared among the groups. Liposomal PSs in both orange juice and water significantly reduced LDL-C compared to their controls. Furthermore, the liposomal PS was as effective as a marketed PS-containing product in reducing LDL-C. Liposomal PSs in both orange juice and water showed similar efficacy in LDL-C reduction, highlighting that these vehicles/food matrices do not affect the efficacy of PSs. The liposomal formulation of a natural PS mixture extracted from canola oil, with brassicasterol as a major component, exhibited a significant LDL-C reduction in a hamster model.

Lysimachia christinae polysaccharide attenuates diet-induced hyperlipidemia via modulating gut microbes-mediated FXR-FGF15 signaling pathway.

Polysaccharides are one of the most abundant and active components of Lysimachia christinae (L. christinae), which is widely adopted for attenuating abnormal cholesterol metabolism; however, its mechanism of action remains unclear. Therefore, we fed a natural polysaccharide (NP) purified from L. christinae to high-fat diet mice. These mice showed an altered gut microbiota and bile acid pool, which was characterized by significantly increased Lactobacillus murinus and unconjugated bile acids in the ileum. Oral administration of the NP reduced cholesterol and triglyceride levels and enhanced bile acid synthesis via cholesterol 7α-hydroxylase. Additionally, the effects of NP are microbiota-dependent, which was reconfirmed by fecal microbiota transplantation (FMT). Altered gut microbiota reshaped bile acid metabolism by modulating bile salt hydrolase (BSH) activity. Therefore, bsh genes were genetically engineered into Brevibacillus choshinensis, which was gavaged into mice to verify BSH function in vivo. Finally, adeno-associated-virus-2-mediated overexpression or inhibition of fibroblast growth factor 15 (FGF15) was used to explore the farnesoid X receptor-fibroblast growth factor 15 pathway in hyperlipidemic mice. We identified that the NP relieves hyperlipidemia by altering the gut microbiota, which is accompanied by the active conversion of cholesterol to bile acids.

The role of exercise in improving hyperlipidemia-renal injuries induced by a high-fat diet: a literature review.

A diet that is high in sugar and fat is a precursor to various chronic diseases, especially hyperlipidemia. Patients with hyperlipidemia have increased levels of plasma free fatty acids and an ectopic accumulation of lipids. The kidney is one of the main organs affected by this disease and, recently, there have been more studies conducted on renal injury caused by hyperlipidemia. The main pathological mechanism is closely related to renal lipotoxicity. However, in different kidney cells, the reaction mechanism varies due to the different affinities of the lipid receptors. At present, it is believed that in addition to lipotoxicity, hyperlipidemia induced-renal injury is also closely related to oxidative stress, endoplasmic reticulum stress, and inflammatory reactions, which are the result of multiple factors. Exercise plays an important role in the prevention of various chronic diseases and recently emerging researches indicated its positive effects to renal injury caused by hyperlipidemia. However, there are few studies summarizing the effects of exercise on this disease and the specific mechanisms need to be further explored. This article summarizes the mechanisms of hyperlipidemia induced-renal injury at the cellular level and discusses the ways in which exercise may regulate it. The results provide theoretical support and novel approaches for identifying the intervention target to treat hyperlipidemia induced-renal injury.

Ingesting retrograded rice (Oryza sativa) starch relieves high-fat diet induced hyperlipidemia in mice by altering intestinal bacteria.

High-fat diet is a risk factor for many chronic diseases, whose symptoms are probably regulated by ingesting food ingredients such as resistant starch. For cooked rice stored in cold-chain, the starch component can retrograde to generate ordered structures (helices and crystallites) and become resistant. However, the role of retrograded starch in managing hyperlipidemia symptoms is insufficiently understood. Here, compared to the normal high-fat diet, ingesting retrograded starch reduced the triglyceride and low-density lipoprotein cholesterol levels of high-fat diet mice by 17.69% and 41.33%, respectively. This relieved hyperlipidemia could be linked to the changes in intestinal bacteria. Retrograded starch intervention increased the relative abundance of Bacteroides (2.30 times higher), which produces propionic acid (increased by 8.26%). Meanwhile, Bacteroides were positively correlated with butyric acid (increased by 98.4%) with strong anti-inflammatory functions. Hence, retrograded starch intervention may regulate the body's health by altering intestinal bacteria.

Averrhoa carambola L. fruit polyphenols ameliorate hyperlipidemia, hepatic steatosis, and hyperglycemia by modulating lipid and glucose metabolism in mice with obesity.

BACKGROUND: Hyperlipidemia, hepatic steatosis, and hyperglycemia are common metabolic complications of obesity. The objective of the present study is to investigate the in vivo protective effect of Averrhoa carambola L. fruit polyphenols (ACFP) on hyperlipidemia, hepatic steatosis, and hyperglycemia in mice with high-fat diet (HFD)-induced obesity and elucidate the mechanisms of action underlying the beneficial effects of ACFP. Thirty-six specific pathogen-free male C57BL/6J mice (4 weeks old, weighing 17.1-19.9 g) were randomly divided into three groups and fed with a low-fat diet (LFD, 10% fat energy), HFD (45% fat energy), or HFD supplemented with ACFP by intragastric administration for 14 weeks. Obesity-related biochemical indexes and hepatic gene expression levels were determined. The statistical analyses were conducted using one-way analysis of variance (ANOVA) followed by Duncan's multiple range test. RESULTS: The results showed that the body weight gain, serum triglycerides, total cholesterol, glucose, insulin resistance index, and steatosis grade in the ACFP group decreased by 29.57%, 26.25%, 27.4%, 19.6%, 40.32%, and 40%, respectively, compared to the HFD group. Gene expression analysis indicated that ACFP treatment improved the gene expression profiles involved in lipid and glucose metabolism compared to the HFD group. CONCLUSION: ACFP protected from HFD-induced obesity and obesity-associated hyperlipidemia, hepatic steatosis, and hyperglycemia by improving lipid and glucose metabolism in mice. © 2023 Society of Chemical Industry.

Multiple time-dependent pathophysiological changes in a rabbit model of high-fat diet-induced hyperlipidemia.

High-fat diets (HFD) adversely affect organ systems. Several studies have examined HFD-related disorders in animals but only in a few organs and time points. Herein, we evaluated disease development with time-dependent HFD-induced pathological, cardiovascular, and morphological changes in rabbits with lipid metabolism similar to that in humans for 9 weeks. The body weights and waist ratio of the HFD group were higher than those in the control group. HFD significantly increased the total cholesterol, low-density lipoprotein, high-density lipoprotein, and phospholipid levels after 3 weeks. Liver enzyme levels increased with hepatomegaly, steatosis, and fibrosis after 3 or 6 weeks. RBCs and hemoglobin decreased, while platelets increased in the HFD group with atherosclerosis and inflammatory cell infiltration in the aorta after 6 weeks. Ejection fraction and fractional shortening values decreased in the HFD group after 9 weeks. Creatinine increased with glomerulosclerosis in the kidneys of the HFD groups after 3 weeks, indicating renal dysfunction. Lipid accumulation was found in the pancreas after 9 weeks. Lipid accumulation and hypertrophy were observed in the adrenal glands after 3 weeks. Overall, our findings provide global reference data on the time-dependent effects of HFD on the body and may serve as a guide for future HFD risk prevention.

Transcriptomics integrated with metabolomics reveals the ameliorating effect of mussel-derived plasmalogens on high-fat diet-induced hyperlipidemia in zebrafish.

Plasmalogens (Pls), a special group of phospholipids, are effective in ameliorating neurodegenerative disease. In the present study, the metabolic effects of seafood-derived Pls on high fat diet (HFD)-induced hyperlipidemia in zebrafish were evaluated, and the underlying mechanisms of dietary Pls against hyperlipidemia were explored through integrated analyses of hepatic transcriptomics and metabolomics. The results demonstrated that Pls supplementation could effectively alleviate HFD-induced obesity symptoms, such as body weight gain, and decrease total hepatic cholesterol and triglyceride levels. Integrated hepatic transcriptome and metabolome data suggested that Pls mainly altered lipid metabolism pathways (FA metabolism, primary bile acid biosynthesis, steroid hormone biosynthesis, and glycerolipid and glycerophospholipid metabolism) and the TCA cycle, induced the overexpression of anti-oxidation enzymes (Cat, Gpx4, Sod3a and Xdh), reduced disease biomarkers (such as glutarylcarnitine, gamma-glutamyltyrosine, and 11-prostaglandin f2) and gut microbiota-derived metabolites, and increased (±)12(13)-diHOME, EPA, lysoPC and PC levels. Moreover, 5 abnormally regulated metabolites were identified as potential biomarkers associated with hyperlipidemia according to the metabolomics results and suggested the involvement of gut microbiota in the anti-hyperlipidemic effects of Pls. Collectively, these findings suggest that the protective role of Pls is mainly associated with the promotion of unsaturated fatty acid biosynthesis and cholesterol efflux, lipid and phospholipid PUFA remodeling, and anti-oxidation and anti-inflammatory capabilities. This study provides valuable information for reasonably explaining the beneficial effects of seafood-derived Pls in alleviating hyperlipidemia and thus may contribute to the development and application of Pls as functional foods or dietary supplements to protect against obesity and hyperlipidemia.

Black rice regulates lipid metabolism, liver injury, oxidative stress and adipose accumulation in high-fat/cholesterol diet mice based on gut microbiota and untargeted metabonomics.

Black rice displays a series of properties including regulating lipid metabolism and attenuating liver injury. Our study aimed to investigate the effect of Zixiangnuo black rice (ZG), peeled rice (ZPG), rice bran (ZBG) on lipid metabolism, liver inflammation, gut microbiota and metabolite profiles in high-fat/cholesterol (HFCD) diet mice. A total of five treatment groups were fed a normal control diet or a HFCD with or without Highland barley (HB) supplementation for 10 weeks. The results showed that ZBG significantly improved lipid parameters, liver function and injury and blood glucose indexes related to hyperlipidemia compared with HFCD group. ZBG recovered the disorder of gut microbiota by increasing Bacteroidetes/Firmicutes ratio and Lactobacillus abundance, and decreasing Proteobacteria abundance. ZBG enhanced the levels of six short chain fatty acids. Fecal metabolomics analysis showed that the important differential metabolites between ZBG and HFCD group were Deoxycholic acid and Myclobutanil, and metabolic pathways were Arachidonic acid metabolism and ABC transporters. Results suggested that BR or bran were effective dietary candidates to ameliorate hyperlipidemia.

Activation of AMPK Entails the Protective Effect of Royal Jelly against High-Fat-Diet-Induced Hyperglycemia, Hyperlipidemia, and Non-Alcoholic Fatty Liver Disease in Rats.

This study examined the mechanism underlying the protective effect of royal jelly (RJ) against high-fat-diet (HFD)-mediated non-alcoholic liver disease (NAFLD) in rats. Adult male rats were divided into five groups (n = 8 each): control fed a standard diet, control + RJ (300 mg/kg), HFD, HFD + RJ (300 mg/kg), and HFD + RJ + CC (0.2 mg/kg). The treatment with RJ reduced weight gain, increased fat pads, and attenuated fasting hyperglycemia, hyperinsulinemia, and glucose tolerance in the HFD-fed rats. It also reduced the serum levels of liver function enzymes, interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), and leptin but significantly increased the serum levels of adiponectin. In addition, and with no effect on lipid excretion in stool, RJ significantly decreased the hepatic mRNA expression of SREBP1, serum, hepatic cholesterol, and triglycerides but increased hepatic mRNA levels of PPARα. Furthermore, RJ reduced the hepatic levels of TNF-α, IL-6, and malondialdehyde (MDA) in the livers of these rats. Of note, with no effect on the mRNA levels of AMPK, RJ stimulated the phosphorylation of AMPK and increased the levels of superoxide dismutase (SOD) and total glutathione (GSH) in the livers of the control and HFD-fed rats. In conclusion, RJ attenuates NAFLD via its antioxidant potential and adiponectin-independent activation of liver AMPK.

Effects of the polypeptide from peanut meal mixed fermentation on lipid metabolism and intestinal flora of hyperlipidemic mice.

BACKGROUND: Hyperlipidemia is one of the metabolic disorders posing great threat to human health. Our previous studies have shown that the nutritional properties of peanut meal after fermentation are markedly improved, and can effectively improve hyperlipidemia caused by high-fat diet in mice. In this study, in order to facilitate the further utilization of peanut meal, the effect of peanut polypeptide (PP) from peanut meal mixed fermentation on lipid metabolism in mice fed with high-fat diet (HFD) and its possible mechanism were investigated. Fifty male C57BL/6J mice were randomly divided into five groups: normal control group (N), high-fat model group (M), PP low-dose group (PL), PP high-dose group (PH), and atorvastatin positive control group (Y). RESULTS: The results show that PP supplementation can effectively reduce the body weight of mice, decrease the serum total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and leptin levels (P < 0.05), increase the high-density lipoprotein cholesterol (HDL-C) levels (P < 0.05), up-regulate the expression levels of ileal tight junction proteins ZO-1 and occludin (P < 0.05), reduce the hepatocyte injury and lipid accumulation caused by high-fat diet and increase the species richness of intestinal flora. CONCLUSION: PP can significantly improve hyperlipidemia and regulate intestinal flora disorders caused by hyperlipidemia. The possible mechanism may be related to the reduction of serum leptin levels and up-regulating the expression levels of the ileal tight junction proteins ZO-1 and occludin. This study provides evidence for its regulatory role in lipid metabolism and intestinal function, and provides a research basis for the potential nutritional benefits of underutilized food by-products. © 2023 Society of Chemical Industry.

Duyun compound green tea extracts regulate bile acid metabolism on mice induced by high-fat diet.

Duyun compound green tea (DCGT) is a healthy beverage with lipid-lowering effect commonly consumed by local people, but its mechanism is not very clear. We evaluated the effect of DCGT treatment on bile acids (BA) metabolism of mice with high-fat diet (HFD) - induced hyperlipidaemia by biochemical indexes and metabolomics and preliminarily determined the potential biomarkers and metabolic pathways of hyperlipidaemia mice treated with DCGT as well as investigated its lipid-lowering mechanism. The results showed that DCGT treatment could reduce HFD - induced gain in weight and improve dyslipidaemia. In addition, a total of ten types of BA were detected, of which seven changed BA metabolites were observed in HFD group mice. After DCGT treatment, glycocholic acid, tauroursodeoxycholic acid and taurochenodeoxycholic acid were significantly down-regulated, while hyodeoxycholic acid, deoxycholic acid and chenodeoxycholic acid were markedly up-regulated. These results demonstrated that DCGT treatment was able to make the BA metabolites in the liver of hyperlipidaemia mice normal and alleviate hyperlipidaemia by regulating the metabolites such as glycocholic acid, tauroursodeoxycholic acid and taurochenodeoxycholic, as well as the BA metabolic pathway and cholesterol metabolic pathway involved.

Comparison of protective effects of hesperetin and pectolinarigenin on high-fat diet-induced hyperlipidemia and hepatic steatosis in Golden Syrian hamsters.

A comparative study was conducted to determine whether hesperetin and pectolinarigenin could lower total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL), and high-density lipoprotein cholesterol (HDL) in a high-fat diet (HFD)-induced high lipid model in Golden Syrian hamsters. 48 Golden Syrian hamsters (8 weeks old) were fed with a HFD for 15 days. HFD induced significant increases in plasma TC, TG, LDL, and HDL. Then, these high lipid hamsters were divided into four groups and were administered with 0.5% sodium carboxymethyl cellulose (CMC-Na), hesperetin (100 mg/kg/day), pectolinarigenin (100 mg/kg/day) or atorvastatin (1.0 mg/kg/day), for 7 weeks. It was found that pectolinarigenin treatment resulted in significant reductions in body weight, adiposity index, serum levels of TC, TG and hepatic TC, TG and free fatty acid compared to those in control hamsters with hyperlipidemia (P<0.05). However, hesperetin treatment only caused reductions in plasma TC and hepatic TG levels. Besides, the hamsters treated with pectolinarigenin showed a relatively normal hepatic architecture compared to the hepatic steatosis shown in the control group. Moreover, the expressions of fatty-acid synthase (Fasn) and solute carrier family 27 member 1 (Slc27a1) involved in lipid biosynthesis, were suppressed in the pectolinarigenin-treated groups, and the expression of carnitine palmitoyltransferase 1A (Cpt1a) involved in fatty acid oxidation was increased in the pectolinarigenin-treated group. Taken together, these results suggest pectolinarigenin exerts stronger protective effects against hyperlipidemia and hepatic steatosis than hesperetin, which may involve the inhibition of lipid uptake and biosynthesis.