scholarly journals Aqueous Mulberry Leaf Extract Ameliorates Alcoholic Liver Injury Associating with Upregulation of Ethanol Metabolism and Suppression of Hepatic Lipogenesis

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Yi-Ju Lee ◽  
Ming-Chang Tsai ◽  
Hui-Ting Lin ◽  
Chau-Jong Wang ◽  
Shao-Hsuan Kao
Keyword(s):  
Lipid Accumulation ◽  
Leaf Extract ◽  
Regulatory Element ◽  
Liver Lipid ◽  
The Body ◽  
Ethanol Metabolism ◽  
Chronic Liver Damage ◽  
Alcoholic Fatty Liver ◽  
Mulberry Leaf ◽  
Mulberry Leaf Extract

Excessive alcohol intake is a major cause of chronic liver damage and is highly associated with the development of a spectrum of hepatic disorders, including steatohepatitis, liver cirrhosis, and liver cancer. Thus, we aimed to explore the hepatoprotective effects of an aqueous mulberry leaf extract (AME) on alcoholic fatty liver disorder (AFLD) by using a mouse model fed with excessive ethanol. Compared with the normal diet, the ethanol diet significantly increased the body weight of the mice, while the AME supplement reduced the weight gain caused by the ethanol diet. The ethanol diet also attenuated the activity of alcohol dehydrogenase and antioxidant enzymes but increased lipid peroxidation in the liver, which were reversed by AME supplementation. Additionally, AME supplementation diminished the ethanol diet-induced hepatic leukocyte infiltration and expressions of IL-6 and TNFα. Moreover, AME supplementation also reduced the ethanol-diet-induced lipid accumulation and expression of 1-acylglycerol-3-phosphate acyltransferase, acetyl-CoA carboxylase, low-density lipoprotein receptor, and sterol regulatory element-binding protein-1/2 in the liver. Collectively, AME supplementation improved liver lipid accumulation and proinflammatory response in mice induced by the ethanol diet, which was associated with the upregulation of ethanol-metabolizing enzymes and the downregulation of lipogenesis components.

scholarly journals Phloretin ameliorates hepatic steatosis through regulation of lipogenesis and Sirt1/AMPK signaling in obese mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Chian-Jiun Liou ◽  
Shu-Ju Wu ◽  
Szu-Chuan Shen ◽  
Li-Chen Chen ◽  
Ya-Ling Chen ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Fatty Acid ◽  
Hepatic Steatosis ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Fatty Acid Synthase ◽  
Regulatory Element ◽  
Liver Lipid ◽  
Obese Mice ◽  
Alcoholic Fatty Liver

Abstract Background Phloretin is isolated from apple trees and could increase lipolysis in 3T3-L1 adipocytes. Previous studies have found that phloretin could prevent obesity in mice. In this study, we investigated whether phloretin ameliorates non-alcoholic fatty liver disease (NAFLD) in high-fat diet (HFD)-induced obese mice, and evaluated the regulation of lipid metabolism in hepatocytes. Methods HepG2 cells were treated with 0.5 mM oleic acid to induce lipid accumulation, and then treated with phloretin to evaluate the molecular mechanism of lipogenesis. In another experiment, male C57BL/6 mice were fed normal diet or HFD (60% fat, w/w) for 16 weeks. After the fourth week, mice were treated with or without phloretin by intraperitoneal injection for 12 weeks. Results Phloretin significantly reduced excessive lipid accumulation and decreased sterol regulatory element-binding protein 1c, blocking the expression of fatty acid synthase in oleic acid-induced HepG2 cells. Phloretin increased Sirt1, and phosphorylation of AMP activated protein kinase to suppress acetyl-CoA carboxylase expression, reducing fatty acid synthesis in hepatocytes. Phloretin also reduced body weight and fat weight compared to untreated HFD-fed mice. Phloretin also reduced liver weight and liver lipid accumulation and improved hepatocyte steatosis in obese mice. In liver tissue from obese mice, phloretin suppressed transcription factors of lipogenesis and fatty acid synthase, and increased lipolysis and fatty acid β-oxidation. Furthermore, phloretin regulated serum leptin, adiponectin, triglyceride, low-density lipoprotein, and free fatty acid levels in obese mice. Conclusions These findings suggest that phloretin improves hepatic steatosis by regulating lipogenesis and the Sirt-1/AMPK pathway in the liver.

Effects of Mulberry Leaf Extract Feeding on Lipid Status of Rats Fed High Cholesterol Diets

2007 ◽  
Vol 36 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Surk-Hoon Park ◽  
Mi-Jin Jang ◽  
Jung-Hee Hong ◽  
Soon-Jae Rhee ◽  
Kyung-Ho Choi ◽  
...  
Keyword(s):  
Leaf Extract ◽  
High Cholesterol ◽  
Mulberry Leaf ◽  
Lipid Status ◽  
Mulberry Leaf Extract

Effects of dietary mulberry leaf extract on the growth, gastrointestinal, hepatic functions of Chinese giant salamander ( Andrias davidianus )

2020 ◽  
Vol 51 (6) ◽  
pp. 2613-2623
Author(s):  
Zhanfu Li ◽  
Xiaochuan Chen ◽  
Yongjun Chen ◽  
Weilong Li ◽  
Qifeng Feng ◽  
...  
Keyword(s):  
Leaf Extract ◽  
Andrias Davidianus ◽  
Mulberry Leaf ◽  
Mulberry Leaf Extract ◽  
Chinese Giant Salamander

Impact of mulberry leaf extract on type 2 diabetes (Mul-DM): A randomized, placebo-controlled pilot study

2017 ◽  
Vol 32 ◽  
pp. 105-108 ◽  
Author(s):  
Daniel M. Riche ◽  
Krista D. Riche ◽  
Honey E. East ◽  
Elizabeth K. Barrett ◽  
Warren L. May
Keyword(s):  
Type 2 Diabetes ◽  
Pilot Study ◽  
Leaf Extract ◽  
Mulberry Leaf ◽  
Mulberry Leaf Extract

Safety evaluation of mulberry leaf extract: Acute, subacute toxicity and genotoxicity studies

2018 ◽  
Vol 95 ◽  
pp. 220-226 ◽  
Author(s):  
Yuzhe Li ◽  
Xiaopeng Zhang ◽  
Chunlai Liang ◽  
Jing Hu ◽  
Zhou Yu
Keyword(s):  
Leaf Extract ◽  
Safety Evaluation ◽  
Subacute Toxicity ◽  
Mulberry Leaf ◽  
Mulberry Leaf Extract

PENGARUH ISOPROPIL MYRISTAT SEBAGAI BAHAN PENINGKAT PENETRASI TERHADAP LAJU DIFUSI KRIM PEMUTIH EKSTRAK ETANOL DAUN MURBEI (Morus alba L)

2017 ◽  
Vol 3 (1) ◽  
pp. 43
Author(s):  
Nurul Arfiyanti Yusuf ◽  
Aisyah Fatmawaty
Keyword(s):  
Leaf Extract ◽  
Diffusion Rate ◽  
Morus Alba ◽  
Penetration Enhancers ◽  
Mulberry Leaf ◽  
Mulberry Leaf Extract ◽  
Diffusion Studies ◽  
Before And After ◽  
Franz Diffusion Cells

The research has conducted research on the effectiveness of isopropyl myristat as a penetration enhancer on the diffusion rate of whitening cream mulberry leaf extract (Morus alba L) in vitro. This study aims to determine the effect of the use of isopropyl myristat. Mulberry leaf extract cream made with varying concentrations respectively 3%, 4%, 5% Isopropyl myristat as penetration enhancers made into 3 formulas (F1-F4) with the F1 without penetration enhancers. Evaluation of stability before and after accelerated storage includes observation of the organoleptic, emulsion type determination, measurement of pH, and viscosity. The evaluation results indicate four physically stable formula. In vitro diffusion studies conducted by Franz diffusion cells and footage is measured at a wavelength of 367.4 nm. The results of diffusion studies show that formula with the highest diffusion rate of 0.024 µg/minute on F4 (5% isopropyl myristat).

scholarly journals A Slow-Digesting Carbohydrate Diet during Rat Pregnancy Protects Offspring from Non-Alcoholic Fatty Liver Disease Risk through the Modulation of the Carbohydrate-Response Element and Sterol Regulatory Element Binding Proteins

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 844 ◽  
Author(s):  
Rafael Salto ◽  
Manuel Manzano ◽  
María Dolores Girón ◽  
Ainara Cano ◽  
Azucena Castro ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Regulatory Element ◽  
Liver Lipid ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Sterol Regulatory Element ◽  
Carbohydrate Digestion ◽  
Alcoholic Fatty Liver Disease

High-fat (HF) and rapid digestive (RD) carbohydrate diets during pregnancy promote excessive adipogenesis in offspring. This effect can be corrected by diets with similar glycemic loads, but low rates of carbohydrate digestion. However, the effects of these diets on metabolic programming in the livers of offspring, and the liver metabolism contributions to adipogenesis, remain to be addressed. In this study, pregnant insulin-resistant rats were fed high-fat diets with similar glycemic loads but different rates of carbohydrate digestion, High Fat-Rapid Digestive (HF–RD) diet or High Fat-Slow Digestive (HF–SD) diet. Offspring were fed a standard diet for 10 weeks, and the impact of these diets on the metabolic and signaling pathways involved in liver fat synthesis and storage of offspring were analyzed, including liver lipidomics, glycogen and carbohydrate and lipid metabolism key enzymes and signaling pathways. Livers from animals whose mothers were fed an HF–RD diet showed higher saturated triacylglycerol deposits with lower carbon numbers and double bond contents compared with the HF–SD group. Moreover, the HF–RD group exhibited enhanced glucose transporter 2, pyruvate kinase (PK), acetyl coenzyme A carboxylase (ACC) and fatty acid (FA) synthase expression, and a decrease in pyruvate carboxylase (PyC) expression leading to an altered liver lipid profile. These parameters were normalized in the HF–SD group. The changes in lipogenic enzyme expression were parallel to changes in AktPKB phosphorylation status and nuclear expression in carbohydrate-response element and sterol regulatory element binding proteins. In conclusion, an HF–RD diet during pregnancy translates to changes in liver signaling and metabolic pathways in offspring, enhancing liver lipid storage and synthesis, and therefore non-alcoholic fatty liver disease (NAFLD) risk. These changes can be corrected by feeding an HF–SD diet during pregnancy.

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