Article
Biochemistry & Molecular Biology
S. Gomez-Zorita, I. Milton-Laskibar, M. T. Macarulla, L. Biasutto, A. Fernandez-Quintela, J. Miranda, A. Lasa, N. Segues, L. Bujanda, M. P. Portillo
Summary: In this study, pterostilbene was found to partially prevent high-fat high-fructose feeding induced liver steatosis in rats, showing a dose-response pattern. It mainly acts by reducing de novo lipogenesis and increasing triglyceride assembly and release, with an improvement in mitochondrial functionality observed. At the same dose, the effects induced by pterostilbene and resveratrol, as well as the mechanisms involved, were similar.
Article
Biology
Hwa Lee, Seona Cho, Anna Kang, Dong-Ha Shin, Ho-Yong Park, Tae-Sook Jeong
Summary: The combined use of Arazyme and ESLs can reduce HFD-induced body weight gain, hyperglycemia, and hepatic steatosis by regulating liver-gut bile acid circulation, significantly reducing treatment doses and enhancing therapeutic effects, thereby reducing therapeutic healthcare costs.
Article
Endocrinology & Metabolism
Francois Marchildon, Jingyi Chi, Sean O'Connor, Hilary Bediako, Paul Cohen
Summary: This study found that PRDM16 is required for the activation of beige fat in myostatin null mice, but the activation of beige fat is not necessary for the protection from obesity, glucose intolerance, insulin resistance, and hepatic steatosis in these mice. Increasing muscle mass can compensate for the inactivation of beige fat, suggesting that targeting muscle mass may be a therapeutic approach to mitigate the effects of adipose tissue dysfunction in obesity and metabolic syndrome.
MOLECULAR METABOLISM
(2021)
Review
Endocrinology & Metabolism
Muenevver Demir, Stefan R. Bornstein, Christos S. Mantzoros, Nikolaos Perakakis
Summary: Non-alcoholic fatty liver disease (NAFLD) is a condition characterized by excessive fat accumulation in the liver, which can lead to liver inflammation, fibrosis, and cirrhosis. Studies suggest that the amount of liver fat may independently contribute to the development and progression of NAFLD and metabolic diseases. This review discusses the tools for quantifying liver fat, the relationship between liver fat and NAFLD progression, and potential approaches to reducing liver fat.
Article
Gastroenterology & Hepatology
Akihiro Kawahara, Keishi Kanno, Sayaka Yonezawa, Yuichiro Otani, Tomoki Kobayashi, Susumu Tazuma, Masanori Ito
Summary: This study investigates the effects of hepatic stellate cell (HSC) depletion on the development of hepatic steatosis and fibrosis in a murine non-alcoholic steatohepatitis (NASH) model. The results suggest that depletion of HSCs may improve hepatic lipid metabolism and fibrogenesis, making them potential therapeutic targets for NASH treatment.
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
(2022)
Article
Immunology
Zhen Tian, Xinyue Wang, Tianshu Han, Changhao Sun
Summary: This study demonstrates that the selective MAO-B inhibitor, selegiline, can reduce body weight gain, hepatic steatosis, and dyslipidemia induced by a high-fat diet. These protective effects may be attributed to improved inflammatory response, oxidative stress, and hepatic lipid metabolism.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2023)
Article
Multidisciplinary Sciences
Yanli Jiang, Jie Zou, Fengxian Fan, Pin Yang, Laiyang Ma, Tiejun Gan, Shaoyu Wang, Jing Zhang
Summary: This study investigated the association between liver proton density fat fraction (PDFF) and serum biomarkers and liver fibrosis stages using multi-echo Dixon (ME-Dixon) and breath-hold single-voxel high-speed T2-corrected multi-echo H-1 magnetic resonance spectroscopy (HISTO) at 1.5 T. The study included 75 patients suspected of liver fibrosis and 23 healthy participants. PDFF was compared among liver fibrosis stages and correlated with serum fat biomarkers. Both ME-Dixon and HISTO sequences measured liver fat content noninvasively, which was not directly associated with liver fibrosis stages.
SCIENTIFIC REPORTS
(2023)
Article
Toxicology
Miao Li, Yu Cai, Xi Chen, Luyong Zhang, Zhenzhou Jiang, Qinwei Yu
Summary: This study found that TAM may induce hepatic steatosis by upregulating the expression of lipid synthetase and downregulating the expression of SIRT1. The SIRT1 agonist was found to relieve TAM-induced hepatic steatosis and may serve as a potential therapeutic drug.
TOXICOLOGY RESEARCH
(2022)
Article
Nutrition & Dietetics
Wenya Zheng, Ziyu Song, Sha Li, Minmin Hu, Horia Shaukat, Hong Qin
Summary: The study demonstrated that sesamol (SEM) has inhibitory effects on oxidative stress induced by chronic high-fat diet (HFD) in the liver, reversing inflammation and enhancing antioxidant defenses through the Nrf2 pathway, ultimately protecting liver health.
Article
Chemistry, Medicinal
Mingjie Sun, Yu Li, Songtao Su, Jiayi Gao, Lin Yu, Xinyi Qi, Huanjie Liang, Xiangling Li, Xinyu Qi, Yunxiao Liang, Lei Zhou, Guo Zhang, Yixing Li
Summary: Non-alcoholic fatty liver disease (NAFLD) is a significant health concern with limited effective treatment options. This study explored the potential of Tussilagone (TUS), a natural sesquiterpene, to treat NAFLD. In vitro and in vivo experiments demonstrated that TUS reduced lipid synthesis, improved glucose metabolism, increased energy metabolism, and decreased oxidative stress levels. TUS also showed promising results in reducing fat accumulation and improving liver injury in mice. These findings suggest that TUS may be a promising compound for the treatment of NAFLD by regulating lipid metabolism.
PHYTOTHERAPY RESEARCH
(2023)
Article
Nutrition & Dietetics
Atsushi Nakamura, Tsubasa Yoshimura, Hitoshi Asakura
Summary: This study investigated the relationship between hepatic fat loss and malnutrition in chronic liver disease using magnetic resonance imaging. The results showed that decreased body fat mass and triglycerides, as well as increased nutritional assessment score, were associated with hepatic fat loss. Furthermore, hepatic fat loss and Child-Pugh score were identified as independent prognostic factors for patients with cirrhosis. These findings emphasize the importance of preserving liver fat content in nutritional therapy for cirrhotic patients.
EUROPEAN JOURNAL OF CLINICAL NUTRITION
(2023)
Article
Endocrinology & Metabolism
Olga Horakova, Gabriella Sistilli, Veronika Kalendova, Kristina Bardova, Marko Mitrovic, Tomas Cajka, Ilaria Irodenko, Petra Janovska, Karoline Lackner, Jan Kopecky, Martin Rossmeisl
Summary: This study examined the effect of thermoneutral environment on the progression of non-alcoholic fatty liver disease (NAFLD) in C57BL/6N mice. The results showed that thermoneutrality did not have a significant effect on NAFLD progression in mice fed a high-fat diet. However, in mice fed a standard diet, thermoneutrality increased weight gain, hepatic steatosis, and other NAFLD-associated phenotypes.
FRONTIERS IN ENDOCRINOLOGY
(2023)
Article
Endocrinology & Metabolism
Qiongyu Lu, Ziting Liu, Luyao Zhao, Linru Xu, Chu Liu, Ling Li, Yiren Cao, Fengchan Li, Lili Wu, Lei Wang, Ting Chen, Tao You, Lijie Ren, Guixue Wang, Chaojun Tang, Li Zhu
Summary: The study found that Sema7A plays an inhibitory role in obesity and hepatic steatosis, suggesting it as a potential new therapeutic target for obesity and metabolic diseases.
MOLECULAR METABOLISM
(2023)
Article
Biochemistry & Molecular Biology
Byeong Moo Kim, Dae Hyun Kim, Yeo Jin Park, Sugyeong Ha, Yeon Ja Choi, Hak Sun Yu, Ki Wung Chung, Hae Young Chung
Summary: PAR2 plays a regulatory role in autophagy during HFD-induced hepatic steatosis, and its deficiency protects male mice from the effects of HFD-induced hepatic steatosis, which is associated with AMPK activation and autophagy levels.
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
(2021)
Article
Medicine, Research & Experimental
Lingyan Ma, Yinhua Ni, Luting Hu, Yufeng Zhao, Liujie Zheng, Song Yang, Liyang Ni, Zhengwei Fu
Summary: Spermidine administration can reduce fat mass and plasma lipid profile in HFD-induced obese mice, improve hepatic steatosis, reduce adipose tissue inflammation, and enhance gut barrier function. Additionally, spermidine treatment also enhances thermogenic gene expression in brown adipose tissue.