Astilbin lowers the effective caffeine dose for decreasing lipid accumulation via activating AMPK in high‐fat diet‐induced obese mice

2020 ◽  
Vol 101 (2) ◽  
pp. 573-581
Author(s):  
Licong Yang ◽  
Yanping Zhu ◽  
Shusheng Zhong ◽  
Guodong Zheng
2019 ◽  
Vol 23 (3) ◽  
pp. 161
Author(s):  
Wan-Guo Yu ◽  
Yun He ◽  
Yun-Fang Chen ◽  
Xiao-Yao Gao ◽  
Wan-E Ning ◽  
...  

2018 ◽  
Vol 49 (5) ◽  
pp. 1870-1884 ◽  
Author(s):  
Chian-Jiun Liou ◽  
Ciao-Han Wei ◽  
Ya-Ling Chen ◽  
Ching-Yi Cheng ◽  
Chia-Ling Wang ◽  
...  

Background/Aims: Fisetin is a naturally abundant flavonoid isolated from various fruits and vegetables that was recently identified to have potential biological functions in improving allergic airway inflammation, as well as anti-oxidative and anti-tumor properties. Fisetin has also been demonstrated to have anti-obesity properties in mice. However, the effect of fisetin on nonalcoholic fatty liver disease (NAFLD) is still elusive. Thus, the present study evaluated whether fisetin improves hepatic steatosis in high-fat diet (HFD)-induced obese mice and regulates lipid metabolism of FL83B hepatocytes in vitro. Methods: NAFLD was induced by HFD in male C57BL/6 mice. The mice were then injected intraperitoneally with fisetin for 10 weeks. In another experiment, FL83B cells were challenged with oleic acid to induce lipid accumulation and treated with various concentrations of fisetin. Results: NAFLD mice treated with fisetin had decreased body weight and epididymal adipose tissue weight compared to NAFLD mice. Fisetin treatment also reduced liver lipid droplet and hepatocyte steatosis, alleviated serum free fatty acid, and leptin concentrations, significantly decreased fatty acid synthase, and significantly increased phosphorylation of AMPKα and the production of sirt-1 and carnitine palmitoyltransferase I in the liver tissue. In vitro, fisetin decreased lipid accumulation and increased lipolysis and β-oxidation in hepatocytes. Conclusion: This study suggests that fisetin is a potential novel treatment for alleviating hepatic lipid metabolism and improving NAFLD in mice via activation of the sirt1/AMPK and β-oxidation pathway.


2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Jun-Woo Jang ◽  
Dong-Woo Lim ◽  
Ji-Ung Chang ◽  
Jai-Eun Kim

Gambihwan is a herbal prescription used in Korean medicine to treat obesity. The authors evaluated the effects and mechanisms of two types of Gambihwan (GBH1 and 2) administered to high-fat diet– (HFD-) induced obese mice. Four-week-old C57BL/6 mice were fed a HFD for 8 weeks with or without GBH1 or 2 (100-200 mg/kg/day by oral gavage). All mice were subjected to glucose tolerance testing after the 8-week treatment period and then euthanized. Serum insulin, lipids, and inflammatory cytokine levels were analyzed using commercial kits. Hepatic enzyme levels and lipid profiles were also investigated. Liver section slides were stained with Oil Red O (ORO) or hematoxylin and eosin (H&E) to assess lipid accumulation. GBH1 and 2 both significantly decreased body, liver, or adipose tissue weights in HFD-fed mice and significantly improved glucose tolerance (p<0.05 in all groups). Cholesterol levels in both sera and liver homogenates were significantly decreased by GBH1 and 2 (p<0.05 in all groups). In addition, serum inflammatory cytokines (p<0.05 in 200 mg/kg/day groups) and hepatic enzyme levels were significantly diminished by GBH administration at 200mg/kg/day (p<0.05 in all groups). Furthermore, histologic analyses of liver sections revealed GBH suppressed lipid accumulation. Both GBH types suppressed HFD-induced increases in body weight and obesity-related markers in HFD-fed mice despite the difference in constituents between GBH1 and 2. It is strongly assumed that the combination of Ephedrae herba and Coicis semen exerted the antiobesity effect. The results obtained show that the antiobesity effects of GBH warrant further investigation.


2021 ◽  
Vol 22 (23) ◽  
pp. 12665
Author(s):  
Young-Sil Lee ◽  
Eun-Jung Park ◽  
Gun-Seok Park ◽  
Seung-Hyun Ko ◽  
Juyi Park ◽  
...  

Obesity is a major health problem. Compelling evidence supports the beneficial effects of probiotics on obesity. However, the anti-obesity effect of probiotics remains unknown. In this study, we investigated the anti-obesity effects and potential mechanisms of Lactiplantibacillus plantarum ATG-K2 using 3T3-L1 adipocytes and high-fat diet (HFD)-induced obese mice. 3T3-L1 cells were incubated to determine the effect of lipid accumulation with lysate of L. plantarum ATG-K2. Mice were fed a normal fat diet or HFD with L. plantarum ATG-K2 and Orlistat for 8 weeks. L. plantarum ATG-K2 inhibited lipid accumulation in 3T3-L1 adipocytes, and reduced body weight gain, WAT weight, and adipocyte size in HFD-induced obese mice, concurrently with the downregulation of PPARγ, SREBP1c, and FAS and upregulation of PPARα, CTP1, UCP1, Prdm16, and ND5. Moreover, L. plantarum ATG-K2 decreased TG, T-CHO, leptin, and TNF-α levels in the serum, with corresponding gene expression levels in the intestine. L. plantarum ATG-K2 modulated the gut microbiome by increasing the abundance of the Lactobacillaceae family, which increased SCFA levels and branched SCFAs in the feces. L. plantarum ATG-K2 exhibited an anti-obesity effect and anti-hyperlipidemic effect in 3T3-L1 adipocytes and HFD-induced obese mice by alleviating the inflammatory response and regulating lipid metabolism, which may be influenced by modulation of the gut microbiome and its metabolites. Therefore, L. plantarum ATG-K2 can be a preventive and therapeutic agent for obesity.


2020 ◽  
Vol 21 (12) ◽  
pp. 4256
Author(s):  
Dongju Lee ◽  
Yujin Shin ◽  
Jong Seong Roh ◽  
Jiwon Ahn ◽  
Sunhyo Jeoong ◽  
...  

Our previous studies demonstrated that peroxisome proliferator-activated receptor α (PPARα) activation reduces weight gain and improves insulin sensitivity in obese mice. Since excess lipid accumulation in non-adipose tissues is suggested to be responsible for the development of insulin resistance, this study was undertaken to examine whether the lemon balm extract ALS-L1023 regulates hepatic lipid accumulation, obesity, and insulin resistance and to determine whether its mechanism of action involves PPARα. Administration of ALS-L1023 to high-fat-diet-induced obese mice caused reductions in body weight gain, visceral fat mass, and visceral adipocyte size without changes of food consumption profiles. ALS-L1023 improved hyperglycemia, hyperinsulinemia, glucose and insulin tolerance, and normalized insulin-positive β-cell area in obese mice. ALS-L1023 decreased hepatic lipid accumulation and concomitantly increased the expression of PPARα target genes responsible for fatty acid β-oxidation in livers. In accordance with the in vivo data, ALS-L1023 reduced lipid accumulation and stimulated PPARα reporter gene expression in HepG2 cells. These effects of ALS-L1023 were comparable to those of the PPARα ligand fenofibrate, while the PPARα antagonist GW6471 inhibited the actions of ALS-L1023 on lipid accumulation and PPARα luciferase activity in HepG2 cells. Higher phosphorylated protein kinase B (pAkt)/Akt ratios and lower expression of gluconeogenesis genes were observed in the livers of ALS-L1023-treated mice. These results indicate that ALS-L1023 may inhibit obesity and improve insulin sensitivity in part through inhibition of hepatic lipid accumulation via hepatic PPARα activation.


2020 ◽  
Vol 11 (3) ◽  
pp. 2279-2290 ◽  
Author(s):  
Qingquan Ma ◽  
Xinbo Zhou ◽  
Linlin Hu ◽  
Jiayi Chen ◽  
Jialiang Zhu ◽  
...  

Leucine (Leu) and isoleucine (Ile) have similar effects in the management of obesity and related disorders.


Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3338
Author(s):  
Trang Nu Huyen Le ◽  
Ho-Jung Choi ◽  
Hee-Sook Jun

Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disorder that causes excess lipid accumulation in the liver and is the leading cause of end-stage liver disease. Liriope platyphylla is a medicinal herb that has long been used to treat cough, obesity, and diabetes. However, the effect of Liriope platyphylla on NAFLD has not been studied. The aim of this study was to investigate the effect of Liriope platyphylla root ethanolic extract (LPE) on hepatic lipid accumulation in high-fat diet (HFD)-induced obese mice. Six-week-old C57BL/6 male mice were fed a HFD for 8 weeks and then treated with LPE (100 or 250 mg/kg/day) by oral gavage for another 8 weeks. Body weight gain and liver weight were significantly lower in the 250 mg/kg LPE-treated HFD group than in the vehicle-treated HFD group. Histological analysis of liver sections demonstrated that LPE treatment reduced lipid accumulation compared to the vehicle treatment. The serum total cholesterol, AST, and ALT levels significantly decreased in the LPE-treated HFD group compared to those in the vehicle-treated HFD group. The LPE significantly decreases the protein expression levels of SREBP1, ACC, p-ACC, FAS, and SCD1, which are involved in lipogenesis, and PPARγ, CD36/FAT, and FATP5, which are involved in fatty acid uptake, both in vivo and in vitro. Thus, LPE may attenuate HFD-induced NAFLD by decreasing lipid accumulation by inhibiting lipogenesis and fatty acid uptake.


2021 ◽  
Vol 22 (18) ◽  
pp. 9885
Author(s):  
Yun-Mi Kang ◽  
Hyun-Ae Kang ◽  
Divina C. Cominguez ◽  
Su-Hyun Kim ◽  
Hyo-Jin An

Papain is a proteolytic enzyme present in the leaves, fruits, roots, and latex of the Carica papaya (papaya) plant. Although it exhibits a wide range of activities, there are no reports on the anti-obesity effects of papain. This study examined the anti-obesity effect and obesity-involved anti-inflammatory mechanism of papain in in vivo and in vitro models using high-fat diet (HFD)-induced obese mice and 3T3-L1 preadipocytes. Oral administration of papain reduced HFD-induced weight of the body, liver, and adipose tissues of mice. Papain also reduced hepatic lipid accumulation and adipocyte size. Moreover, serum total cholesterol and triglyceride levels were markedly reduced in papain-treated mice. In addition, papain inhibited the differentiation of preadipocytes and oil accumulation in 3T3-L1 preadipocytes and rat primary preadipocytes. Mechanistically, papain significantly downregulated the protein levels of key adipogenesis regulators and reversed the expression of pro-inflammatory cytokines and adipokines in HFD-induced obese mice and 3T3-L1 preadipocytes. Papain also markedly enhanced activation of the AMP-activated protein kinase pathway in both models. Collectively, these results suggest that papain exerts anti-obesity effects in HFD-induced mice and 3T3-L1 preadipocytes by regulating levels of adipogenic factors involved in lipid metabolism and inflammation; thus, it could be useful in the prevention and treatment of obesity.


2017 ◽  
Vol 18 (7) ◽  
pp. 1393 ◽  
Author(s):  
Qiming Yang ◽  
Meng Qi ◽  
Renchao Tong ◽  
Dandan Wang ◽  
Lili Ding ◽  
...  

2017 ◽  
Vol 45 (05) ◽  
pp. 1017-1031 ◽  
Author(s):  
Mi Young Song ◽  
Seok Yong Kang ◽  
Anna Kang ◽  
Ji Hye Hwang ◽  
Yong-Ki Park ◽  
...  

The cortex of Cinnamomum cassia Presl (Cinnamomi Cortex: CC) has commonly been used for weight control in traditional medicines, but without a scientific basis. Therefore, this study was undertaken to investigate the anti-obesity effect of CC extract in a high-fat diet (HFD)-induced obese mouse model and in C2C12 mouse skeletal muscle cells. Male C57BL/6 mice were fed a normal diet or a HFD for 16 consecutive weeks, and orally administered CC extract (100 or 300[Formula: see text]mg/kg) or metformin (250[Formula: see text]mg/kg; positive control) daily for 16 weeks. CC extract administration significantly decreased body weights, food intakes, and serum levels of glucose, insulin, total cholesterol and ALT levels, prevented oral glucose tolerance and insulin resistance, inhibited the protein expressions of MyHC and PGC1[Formula: see text] and the phosphorylation of AMPK, suppressed lipid accumulation in liver, decreased adipocyte size and increased muscle mass in obese mice. For this in vitro study, C2C12 myoblasts were differentiated into the myotubes for five days, and then treated with CC extract (0.1 or 0.2[Formula: see text]mg/ml) for 24[Formula: see text]h. CC extract significantly increased ATP levels by increasing the mRNA expressions of mitochondrial biogenesis-related factors, such as, PGC1[Formula: see text], NRF-1, and Tfam, and the phosphorylations of AMPK and ACC. Our results suggest CC extract controls weight gain in obese mice by inhibiting lipid accumulation and increasing energy expenditure, and that its action mechanism involves the up-regulation of mitochondrial biogenesis in skeletal muscle cells.


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