scholarly journals AFomitopsis pinicola JesengFormulation Has an Antiobesity Effect and Protects against Hepatic Steatosis in Mice with High-Fat Diet-Induced Obesity

2016 ◽  
Vol 2016 ◽  
pp. 1-10
Author(s):  
Hoe-Yune Jung ◽  
Yosep Ji ◽  
Na-Ri Kim ◽  
Do-Young Kim ◽  
Kyong-Tai Kim ◽  
...  
Keyword(s):  
Fatty Liver ◽  
High Fat Diet ◽  
Cholesterol Biosynthesis ◽  
Viscum Album ◽  
Control Group ◽  
High Fat ◽  
Fomitopsis Pinicola ◽  
Acanthopanax Senticosus ◽  
Nonalcoholic Fatty Liver ◽  
Diet Induced Obesity

This study investigated the antiobesity effect of an extract of the Fomitopsis pinicola Jeseng-containing formulation (FAVA), which is a combination of four natural components:Fomitopsis pinicola Jeseng;Acanthopanax senticosus;Viscum album coloratum; andAllium tuberosum. High-fat diet- (HFD-) fed male C57BL/6J mice were treated with FAVA (200 mg/kg/day) for 12 weeks to monitor the antiobesity effect and amelioration of nonalcoholic fatty liver diseases (NAFLD). Body and white adipose tissue (WAT) weights were reduced in FAVA-treated mice, and a histological examination showed an amelioration of fatty liver in FAVA-treated mice without decreasing food consumption. Additionally, FAVA reduced serum lipid profiles, leptin, and insulin levels compared with the HFD control group. The FAVA extract suppressed lipogenic mRNA expression levels from WAT concomitantly with the cholesterol biosynthesis level in the liver. These results demonstrate the inhibitory effects of FAVA on obesity and NAFLD in the diet-induced obese (DIO) mouse model. Therefore, FAVA may be an effective therapeutic candidate for treating obesity and fatty liver caused by a high-fat diet.

scholarly journals Systemic Overexpression of GDF5 in Adipocytes but Not Hepatocytes Alleviates High-Fat Diet-Induced Nonalcoholic Fatty Liver in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Yan Yang ◽  
Wenting Zhang ◽  
Xiaohui Wu ◽  
Jing Wu ◽  
Chengjun Sun ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Lentiviral Vector ◽  
Cell Model ◽  
Control Group ◽  
High Fat ◽  
Fatty Acid Binding ◽  
Nonalcoholic Fatty Liver

Objective. Our recent study demonstrated that growth differentiation factor 5 (GDF5) could promote white adipose tissue thermogenesis and alleviate high-fat diet- (HFD-) induced obesity in fatty acid-binding protein 4- (Fabp4-) GDF5 transgenic mice (TG). Here, we further investigated the effects of systemic overexpression of the GDF5 gene in adipocytes HFD-induced nonalcoholic fatty liver disease (NAFLD). Methods. Fabp4-GDF5 TG mice were administered an HFD feeding. NAFLD-related indicators associated with lipid metabolism and inflammation were measured. A GDF5 lentiviral vector was constructed, and the LO2 NAFLD cell model was induced by FFA solution (oleic acid and palmitic acid). The alterations in liver function, liver lipid metabolism, and related inflammatory indicators were analyzed. Results. The liver weight was significantly reduced in the TG group, which was in accordance with the significantly downregulated expression of TNFα, MCP1, Aim2, and SREBP-1c and significantly upregulated expression of CPT-1α and ACOX2 in TG mouse livers. Compared to that of cells in the FAA-free control group, LO2 cells with in situ overexpression of GDF5 developed lipid droplets after FFA treatment; the levels of triglycerides, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were significantly increased in both the GDF5 lentivirus and control lentivirus groups compared with those of the FAA-free group. Additionally, the levels of FAS, SREBP-1, CPT-1α, and inflammation-associated genes, such as ASC and NLRC4, were unaltered despite GDF5 treatment. Conclusion. Systemic overexpression of GDF5 in adipose tissue in vivo significantly reduced HFD-induced NAFLD liver damage in mice. The overexpression of GDF5 in hepatocytes failed to improve lipid accumulation and inflammation-related reactions induced by mixed fatty acids, suggesting that the protective effect of GDF5 in NAFLD was mainly due to the reduction in adipose tissue and improvements in metabolism. Hence, our study suggests that the management of NAFLD should be targeted to reduce the overall amount of body fat and improve metabolic status before the progression to nonalcoholic steatohepatitis occurs.

scholarly journals Jiangzhi Ligan Decoction Alleviated Nonalcoholic Fatty Liver Disease Induced by High-Fat-Diet in Rats via GSDMD-mediated Canonical/Non-canonical Pyroptosis Pathway

2021 ◽  
Author(s):  
XIAO ZHOU ◽  
Kangkang Yin ◽  
Wei Jiang ◽  
Ziwei Dai ◽  
Biao Tang
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Liver Lipid ◽  
Normal Control Group ◽  
Control Group ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Hepatoprotective Effects

Abstract Background Hepatoprotective effects of Chinese herbal formula Jiangzhi Ligan Decoction (JZLGD) against nonalcoholic fatty liver disease (NAFLD) have been demonstrated, but its mechanism is not clear. The aim of this study was to evaluate the protective effects of against high-fat diet (HFD) induced NAFLD in rat, and to further explore the potential molecular mechanism. Methods SD rats were assigned to five different groups: normal control group, NAFLD model group and JZLGD-treated NAFLD group (3 doses of JZLGD: 2.3, 4.6, 9.2 g/kg of body weight, respectively). All the rats were fed a HFD for 18 weeks except the normal control group(a normal diet). After 12 weeks, rats in JZLGD-treated NAFLD group were administered different doses of JZLGD by oral gavage once daily for another period of 6 weeks, and the rest were given the same dosage of normal saline. After the intervention, blood and liver from each sample were carefully removed and analyzed accordingly. Results We found that JZLGD significantly reduced the liver index, levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum. Furthermore, pathological examinations showed that JZLGD markedly reduced liver lipid droplets and improved liver lipid accumulation, NAFLD activity score and ballooning pathology scoring were also decreased. The detection of cytokines showed that JZLGD could significantly reduced the levels of serum inflammatory factors IL-1β, IL-18, tumor necrosis factor α (TNF-α) and IL-6, protected HFD rats from inflammation. In addition, NAFLD treatment, exhibited significant reduction in serum triglyceride (TG), total cholesterol (TC), low density lipoprotein (LDL) and free fatty acid (FFA) when compared to NAFLD control rats. JZLGD intervention also reduced the level of serum lipopolysaccharide (LPS) and the expression of NOD-like receptor family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), caspase-1, caspase-11, GSDMD, GSDMD N-terminus (GSDMD-N), IL-1β, IL-18 in the liver. Conclusion These results demonstrate the hepatoprotective effects of JZLGD in NAFLD mice, the effects may be mediated via downregulation of NLRP3 /caspase-1/GSDMD mediated canonical pyroptosis pathway and LPS /caspase-11/GSDMD mediated non-canonical pyroptosis pathway.

scholarly journals Effects of Mogrosides on High-Fat-Diet-Induced Obesity and Nonalcoholic Fatty Liver Disease in Mice

Molecules ◽  
2018 ◽  
Vol 23 (8) ◽  
pp. 1894 ◽  
Author(s):  
Xiaobing Zhang ◽  
Yunfei Song ◽  
Yipei Ding ◽  
Wei Wang ◽  
Ling Liao ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
High Purity ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Molecular Mechanisms ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Diet Induced Obesity

Obesity and nonalcoholic fatty liver disease (NAFLD) are highly prevalent and cause numerous metabolic diseases. However, drugs for the prevention and treatment of obesity and NAFLD remain unavailable. In this study, we investigated the effects of mogrosides (luo han guo, LH) in Siraitia grosvenorii saponins on high-fat-diet-induced obesity and NAFLD in mice. We found that compared with the negative control, LH reduced body and liver weight. LH also decreased fat accumulation and increased AMP-activated protein kinase (AMPK) phosphorylation (pAMPK) levels in mouse livers. We also found that high-purity mogroside V upregulated pAMPK expression in HepG2 cells. In addition, high-purity mogroside V inhibited reactive oxygen species production and upregulated sequestosome-1 (SQSTM1, p62) expression in THP-1 cells. These results suggest that LH may affect obesity and NAFLD by enhancing fat metabolism and antioxidative defenses. Mogroside V may be a main component of LH. However, the exact molecular mechanisms and active components responsible for the inhibitory effects of LH on obesity and NAFLD require further investigation.

scholarly journals Maternal tadalafil therapy for fetal growth restriction prevents non-alcoholic fatty liver disease and adipocyte hypertrophy in the offspring

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takuya Kawamura ◽  
Hiroaki Tanaka ◽  
Ryota Tachibana ◽  
Kento Yoshikawa ◽  
Shintaro Maki ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fetal Growth ◽  
Fetal Programming ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Control Group ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

AbstractWe aimed to investigate the effects of maternal tadalafil therapy on fetal programming of metabolic function in a mouse model of fetal growth restriction (FGR). Pregnant C57BL6 mice were divided into the control, L-NG-nitroarginine methyl ester (L-NAME), and tadalafil + L-NAME groups. Six weeks after birth, the male pups in each group were given a high-fat diet. A glucose tolerance test (GTT) was performed at 15 weeks and the pups were euthanized at 20 weeks. We then assessed the histological changes in the liver and adipose tissue, and the adipocytokine production. We found that the non-alcoholic fatty liver disease activity score was higher in the L-NAME group than in the control group (p < 0.05). Although the M1 macrophage numbers were significantly higher in the L-NAME/high-fat diet group (p < 0.001), maternal tadalafil administration prevented this change. Moreover, the epididymal adipocyte size was significantly larger in the L-NAME group than in the control group. This was also improved by maternal tadalafil administration (p < 0.05). Further, we found that resistin levels were significantly lower in the L-NAME group compared to the control group (p < 0.05). The combination of exposure to maternal L-NAME and a high-fat diet induced glucose impairment and non-alcoholic fatty liver disease. However, maternal tadalafil administration prevented these complications. Thus, deleterious fetal programming caused by FGR might be modified by in utero intervention with tadalafil.

scholarly journals Exercise in mice ameliorates high-fat diet-induced nonalcoholic fatty liver disease by lowering HMGCS2

Aging ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 8960-8974
Author(s):  
Xiaoli Qian ◽  
Ting Wang ◽  
Jiahong Gong ◽  
Li Wang ◽  
Xuyan Chen ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
High Fat ◽  
Nonalcoholic Fatty Liver
Sign in / Sign up

Export Citation Format

Share Document