scholarly journals Kaempferide improves glycolipid metabolism disorder by activating PPARγ in high-fat-diet-fed mice

Life Sciences ◽  
2021 ◽  
Vol 270 ◽  
pp. 119133
Author(s):  
Heng Tang ◽  
Qingfu Zeng ◽  
Ting Tang ◽  
Yunjie Wei ◽  
Peng Pu
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder

scholarly journals Kaempferide Improves Glycolipid Metabolism Disorder by Activating PPARγ in High-Fat-Diet-Fed Mice

2020 ◽  
Author(s):  
Qingfu Zeng ◽  
Heng Tang ◽  
Ting Tang ◽  
Peng Pu
Keyword(s):  
Signaling Pathway ◽  
High Fat Diet ◽  
Metabolic Diseases ◽  
Serum Insulin ◽  
High Fat ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder ◽  
Pparγ Agonist ◽  
Underlying Mechanisms

Abstract Background: Kaempferide (Ka, 3,5,7-trihydroxy-4′-methoxyflavone), an active ingredient of Tagetes erecta L has been demonstrated to possess many pharmacological effects, including antioxidant, anti-inflammation, anticancer and antihypertension in previous study. However, there is no evidence of Ka on metabolic disorder in former studies. This study investigated the effects of Ka on glycolipid metabolism and explored the underlying mechanisms of action in vivo and vitro. Methods: High-fat diet (HFD) was used to induce the model of glycolipid metabolism disorder in mice.The hypolipidemic and hypoglycemic effect was detected by several indicators, like blood sample analysis blood glucose, serum insulin, HOMA index and intraperitoneal glucose tolerance tests (IPGTT). The signaling pathways of lipid metabolism (PPARγ/LXRα/ABCA1) and glucose metabolism (PPARγ/PI3K/AKT) were evaluated using Real-Time PCR and Western blot. The primary culture of hepatocytes was prepared to confirm the target of Ka by co-culturing with PPARγ agonist or inhibitor.Results: Administration of Ka at a dose of 10mg/kg for 16 weeks effectively attenuated obesity, hyperlipidemia, hyperglycemia and insulin resistance in HFD mice. Further studies revealed the hypolipidemic and hypoglycemic effects of Ka depended on the activation of PPARγ/LXRα/ABCA1 pathway and PPARγ/PI3K/AKT pathway, respectively. The primary hepatocyte test, co-cultured with PPARγ agonists or inhibitors, further confirmed the above signaling pathway and key protein. Conclusion: Ka played an important role in improving glycolipid metabolism disorder, which were causally associated with weight loss. The underlying mechanisms might are associated with the activation of PPARγ and its downstream signaling pathway. Our study helped to understand the pharmacological actions of Ka, and provides theoretical basis for Ka in the effective treatment of obesity, diabetes and other metabolic diseases.

scholarly journals PO-042 Effect of 8 weeks aerobic combined with resistance exercise on hepatic glycolipid metabolism induced by high fat diet in mice

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Jing Xiao
Keyword(s):  
Lipid Metabolism ◽  
High Fat Diet ◽  
Liver Weight ◽  
Exercise Group ◽  
Diet Group ◽  
Normal Diet ◽  
High Fat ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder ◽  
Glucose And Lipid Metabolism

Objective C57 mice were fed with high-fat diet. After the pathological features were detected, a group of C57 high-fat diet mice were randomly selected for eight weeks aerobic and anti-resistance exercise. To observe the effect of exercise on liver glucose and lipid metabolism in mice fed with high fat. To explore the effect of exercise on liver glucose and lipid metabolism disorder caused by high fat feeding, to provide the direction and evidence for the treatment and rehabilitation of fatty liver and other diseases caused by high fat diet. C57 mice were fed with high-fat diet. After the pathological features were detected, a group of C57 high-fat diet mice were randomly selected for eight weeks aerobic and anti-resistance exercise. To observe the effect of exercise on liver glucose and lipid metabolism in mice fed with high fat. To explore the effect of exercise on liver glucose and lipid metabolism disorder caused by high fat feeding, to provide the direction and evidence for the treatment and rehabilitation of fatty liver and other diseases caused by high fat diet. Methods 30 male C57 mice were 8 weeks old, with an average weight of 20.02 ±0.06 g. The purchased mice were randomly divided into C57 diet group (n = 10) and high-fat diet group (n = 20). A pathological model of hepatic glycolipid metabolism disorder was established by high-fat feed feeding. The success of the model was measured by calculating the area under the blood glucose curve. After modeling, the C57 mice were randomly divided into high fat group and high fat exercise group, with 10 mice in each group. The mice in high fat exercise group were trained 6 days a week for 8 weeks. At the end of the exercise, the three groups were uniformly selected. Results 1. Compared with the normal diet quiet group, there was a significant difference in the area under the blood glucose curve in the high-fat diet quiet group (p < 0. 01). Compared with the quiet high-fat diet group, there was a significant difference in the area under the blood glucose curve after intraperitoneal injection of glucose in the high-fat diet exercise group (p < 0. 05). After two weeks of high fat diet feeding, the body weight of the quiet group was significantly higher than that of the quiet group fed with normal diet (p < 0.05). After two weeks exercise training of high-fat mice, the body weight of high-fat exercise group was significantly lower than that of quiet high-fat mice (p < 0.05). Compared with the normal diet group, the liver weight and liver weight of the high-fat quiet group increased (p < 0 01), while the liver weight and liver / body weight of the high-fat exercise group were lower than those of the high-fat quiet group (p < 0 05). The liver AST (aspartate amino transferase) and ALT(Alanine transferase) in the High-fat diet quiet group were significantly higher than those in the normal diet quiet group (p < 0. 01). The ALT (alanine transferase) in high-fat diet exercise group was lower than that in quiet high-fat diet group (p < 0.05). Conclusions 16-week high-fat diet can establish a pathological model of hepatic glycolipid metabolism disorder. Hyper-insulinemia, hyper-lipidemia and other pathological phenomena will occur in mice. 8 weeks aerobic combined with anti-exercise intervention can improve hepatic glycolipid metabolism disorder and liver function.

scholarly journals Partial Deficiency of Zfp217 Resists High-Fat Diet-Induced Obesity by Increasing Energy Metabolism in Mice

2021 ◽  
Vol 22 (10) ◽  
pp. 5390
Author(s):  
Qianhui Zeng ◽  
Nannan Wang ◽  
Yaru Zhang ◽  
Yuxuan Yang ◽  
Shuangshuang Li ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Energy Metabolism ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Chow Diet ◽  
High Fat ◽  
Glycolipid Metabolism ◽  
Partial Deficiency

Obesity-induced adipose tissue dysfunction and disorders of glycolipid metabolism have become a worldwide research priority. Zfp217 plays a crucial role in adipogenesis of 3T3-L1 preadipocytes, but about its functions in animal models are not yet clear. To explore the role of Zfp217 in high-fat diet (HFD)-induced obese mice, global Zfp217 heterozygous knockout (Zfp217+/−) mice were constructed. Zfp217+/− mice and Zfp217+/+ mice fed a normal chow diet (NC) did not differ significantly in weight gain, percent body fat mass, glucose tolerance, or insulin sensitivity. When challenged with HFD, Zfp217+/− mice had less weight gain than Zfp217+/+ mice. Histological observations revealed that Zfp217+/− mice fed a high-fat diet had much smaller white adipocytes in inguinal white adipose tissue (iWAT). Zfp217+/− mice had improved metabolic profiles, including improved glucose tolerance, enhanced insulin sensitivity, and increased energy expenditure compared to the Zfp217+/+ mice under HFD. We found that adipogenesis-related genes were increased and metabolic thermogenesis-related genes were decreased in the iWAT of HFD-fed Zfp217+/+ mice compared to Zfp217+/− mice. In addition, adipogenesis was markedly reduced in mouse embryonic fibroblasts (MEFs) from Zfp217-deleted mice. Together, these data indicate that Zfp217 is a regulator of energy metabolism and it is likely to provide novel insight into treatment for obesity.

Virgin Grape Seed Oil Alleviates Insulin Resistance and Energy Metabolism Disorder in Mice Fed a High‐Fat Diet

2020 ◽  
Vol 122 (4) ◽  
pp. 1900158
Author(s):  
Xiaojing Li ◽  
Yingbin Shen ◽  
Jianhong Zhu ◽  
Junyong Xiao ◽  
Renhuai Cong ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Energy Metabolism ◽  
High Fat Diet ◽  
Seed Oil ◽  
Grape Seed ◽  
High Fat ◽  
Metabolism Disorder ◽  
Grape Seed Oil ◽  
Energy Metabolism Disorder

scholarly journals Curcumin improves glycolipid metabolism through regulating peroxisome proliferator activated receptor γ signalling pathway in high-fat diet-induced obese mice and 3T3-L1 adipocytes

2017 ◽  
Vol 4 (11) ◽  
pp. 170917 ◽  
Author(s):  
Yanyun Pan ◽  
Dandan Zhao ◽  
Na Yu ◽  
Tian An ◽  
Jianan Miao ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Fasting Blood Glucose ◽  
Signalling Pathway ◽  
Peroxisome Proliferator ◽  
Obese Mice ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor ◽  
Glycolipid Metabolism

Curcumin is an active component derived from Curcuma longa L. which is a traditional Chinese medicine that is widely used for treating metabolic diseases through regulating different molecular pathways. Here, in this study, we aimed to comprehensively investigate the effects of curcumin on glycolipid metabolism in vivo and in vitro and then determine the underlying mechanism. Male C57BL/6 J obese mice and 3T3-L1 adipocytes were used for in vivo and in vitro study, respectively. Our results demonstrated that treatment with curcumin for eight weeks decreased body weight, fat mass and serum lipid profiles. Meanwhile, it lowered fasting blood glucose and increased the insulin sensitivity in high-fat diet-induced obese mice. In addition, curcumin stimulated lipolysis and improved glycolipid metabolism through upregulating the expressions of adipose triglyceride lipase and hormone-sensitive lipase, peroxisome proliferator activated receptor γ/α (PPARγ/α) and CCAAT/enhancer binding proteinα (C/EBPα) in adipose tissue of the mice. In differentiated 3T3-L1 cells, curcumin reduced glycerol release and increased glucose uptake via upregulating PPARγ and C/EBPα. We concluded that curcumin has the potential to improve glycolipid metabolism disorders caused by obesity through regulating PPARγ signalling pathway.

scholarly journals Metabolomics of the Protective Effect of Ampelopsis grossedentata and Its Major Active Compound Dihydromyricetin on the Liver of High-Fat Diet Hamster

2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Lanlan Fan ◽  
Xiaosheng Qu ◽  
Tao Yi ◽  
Yong Peng ◽  
Manjing Jiang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Protective Effect ◽  
High Fat Diet ◽  
Southern China ◽  
Tricarboxylic Acid Cycle ◽  
Acid Oxidation ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Ampelopsis Grossedentata

The flavonoid dihydromyricetin (DMY) is the main component of Ampelopsis grossedentata (Hand-Mazz) W. T. Wang (AG), a daily beverage and folk medicine used in Southern China to treat jaundice hepatitis, cold fever, and sore throat. Recently, DMY and AG were shown to have a beneficial effect on lipid metabolism disorder. However, the mechanisms of how DMY and AG protect the liver during lipid metabolism disorder remain unclear. In this study, we first analyzed the chemical compounds of AG by HPLC-DAD-ESI-IT-TOF-MSn. Of the 31 compounds detected, 29 were identified based on previous results. Then, the effects of DMY and AG on high-fat diet hamster livers were studied and the metabolite levels and metabolic pathway activity of the liver were explored by 1H NMR metabolomics. Compared to the high-fat diet group, supplementation of AG and DMY attenuated the high-fat-induced increase in body weight, liver lipid deposition, serum triglycerides and total cholesterol levels, and normalized endogenous metabolite concentrations. PCA and PLS-DA score plots demonstrated that while the metabolic profiles of hamsters fed a high-fat diet supplemented with DMY or AG were both far from those of hamsters fed a normal diet or a high-fat diet alone, they were similar to each other. Our data suggest that the underlying mechanism of the protective effect of DMY and AG might be related to an attenuation of the deleterious effect of high-fat diet-induced hyperlipidemia on multiple metabolic pathways including amino acid metabolism, ketone body metabolism, energy metabolism, tricarboxylic acid cycle, and enhanced fatty acid oxidation.

scholarly journals Electroacupuncture Prevents Osteoarthritis of High-Fat Diet-Induced Obese Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Lin-Lin Xie ◽  
Yu-Li Zhao ◽  
Jian Yang ◽  
Hui Cheng ◽  
Zhen-Dong Zhong ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Joint Inflammation ◽  
Protective Effects ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Obese Rats

The effects of acupuncture on osteoarthritis (OA) pathogenesis have been demonstrated in vitro and in animal models. However, the potential for acupuncture to mediate protective effects on obese-induced OA has not been examined. Here, we investigated the effects of different acupuncture patterns on OA pathogenesis in high-fat diet- (HFD-) induced obese rats. After 12-week diet-induced obesity, obese rats were treated with three acupuncture protocols for 2 weeks, including ST36, GB34, and ST36+GB34. The results showed that the three acupuncture protocols both prevented obesity-induced cartilage matrix degradation and MMP expression and mitigated obesity-induced systemic and local inflammation but had different regulatory effects on lipid metabolism and gut microbiota disorder of obese-induced OA rats. Furthermore, the three acupuncture protocols increased the microbial diversity and altered the structure of community of feces in obese rats. We found that ST36 and GB34 could inhibit proinflammatory shift in the gut microbiome with an increase in the ratio of Bacteroidetes/Firmicutes and promote the recovery of relative abundance of Clostridium, Akkermansia, Butyricimonas, and Lactococcus. Although both ST36 and GB34 had an anti-inflammatory effect on serum inflammatory mediators, only the acupuncture protocol with both ST36 and GB34 could effectively inhibit LPS-mediated joint inflammation in obesity rats. Therefore, relieving obesity-related chronic inflammation, lipid metabolism disorder, and gut microbiota disorder may be an important mechanism for acupuncture with ST36 and GB34 to promote OA recovery.

scholarly journals Rhus chinensis Mill. Fruits Ameliorate Hepatic Glycolipid Metabolism Disorder in Rats Induced by High Fat/High Sugar Diet

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4480
Author(s):  
Zihuan Wu ◽  
Qingqing Ma ◽  
Shengbao Cai ◽  
Yilin Sun ◽  
Yuanyue Zhang ◽  
...  
Keyword(s):  
Chronic Diseases ◽  
Metabolic Disorders ◽  
Ethanol Extract ◽  
Key Factors ◽  
High Fat ◽  
Glycolipid Metabolism ◽  
High Sugar ◽  
Metabolism Disorder ◽  
Rhus Chinensis ◽  
Underlying Mechanisms

Hepatic glycolipid metabolism disorder is considered as one of the key factors in the pathogenesis of many chronic diseases. The objective of this study was to investigate the protective effect and underlying mechanisms of Rhus chinensis Mill. fruits against hepatic glycolipid metabolic disorders in rats induced by a high fat/high sugar diet. Results showed that ethanol extract, especially at a dose of 600 mg/kg b.w., could effectively ameliorate glycolipid metabolic disorders in rats. The biochemical indexes, including CAT, GSH and HOMA-IR, were significantly improved by the administration of ethanol extract. Immunohistochemistry and Western blot analysis revealed that ethanol extract up-regulated the expression levels of PI3K/AKT, PPAR-α, and the phosphorylation of IRS1 and AMPK proteins, and down-regulated the expressions of SREBP-1 and FAS proteins in the liver, which are closely related to hepatic glycolipid metabolism. Those findings suggested that R. chinensis Mill. fruits could be developed as functional foods and/or nutraceuticals for preventing or controlling some chronic diseases related to hepatic glycolipid metabolism disorder.

scholarly journals Glucosamine Ameliorates Symptoms of High-Fat Diet-Fed Mice by Reversing Imbalanced Gut Microbiota

2021 ◽  
Vol 12 ◽  
Author(s):  
Xubing Yuan ◽  
Junping Zheng ◽  
Lishi Ren ◽  
Siming Jiao ◽  
Cui Feng ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
Inflammatory Responses ◽  
Fasting Blood Glucose ◽  
Intestinal Barrier ◽  
Intestinal Bacteria ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Rdna Sequencing

Glucosamine (GlcN) is used as a supplement for arthritis and joint pain and has been proved to have effects on inflammation, cancer, and cardiovascular diseases. However, there are limited studies on the regulatory mechanism of GlcN against glucose and lipid metabolism disorder. In this study, we treated high-fat diet (HFD)-induced diabetic mice with GlcN (1 mg/ml, in drinking water) for five months. The results show that GlcN significantly reduced the fasting blood glucose of HFD-fed mice and improved glucose tolerance. The feces of intestinal contents in mice were analyzed using 16s rDNA sequencing. It was indicated that GlcN reversed the imbalanced gut microbiota in HFD-fed mice. Based on the PICRUSt assay, the signaling pathways of glucolipid metabolism and biosynthesis were changed in mice with HFD feeding. By quantitative real-time PCR (qPCR) and hematoxylin and eosin (H&amp;E) staining, it was demonstrated that GlcN not only inhibited the inflammatory responses of colon and white adipose tissues, but also improved the intestinal barrier damage of HFD-fed mice. Finally, the correlation analysis suggests the most significantly changed intestinal bacteria were positively or negatively related to the occurrence of inflammation in the colon and fat tissues of HFD-fed mice. In summary, our studies provide a theoretical basis for the potential application of GlcN to glucolipid metabolism disorder through the regulation of gut microbiota.

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