Yi-g Lin

Preventive Effects of Taurine on Development of Hepatic Steatosis Induced by a High-Fat/Cholesterol Dietary Habit

Nonalcoholic fatty liver (NAFL) is also called hepatic steatosis and has become an emergent liver disease in developed and developing nations. This study was to exam the preventive effects of taurine (Tau) on the development of hepatic steatosis via a hamster model. Although hepatic steatosis of hamsters was induced by feeding a high-fat/cholesterol diet, drinking water containing 0.35 and 0.7% Tau improved (p < 0.05) the serum lipid profile. Meanwhile, the smaller (p < 0.05) liver sizes and lower (p < 0.05) hepatic lipids in high-fat/cholesterol dietary hamsters drinking Tau may be partially due to higher (p < 0.05) fecal cholesterol, triacylglycerol, and bile acid outputs. In the regulation of lipid homeostasis, drinking a Tau solution upregulated (p < 0.05) low-density lipoprotein receptor and CYP7A1 gene expressions in high-fat/cholesterol dietary hamsters, which result in increased fecal cholesterol and bile acid outputs. Drinking a Tau solution also upregulated (p < 0.05) peroxisome proliferator-activated receptor-α (PPAR-α) and uncoupling protein 2 (UPC2) gene expressions in high-fat/cholesterol dietary hamsters, thus increasing energy expenditure. Besides, Tau also enhanced (p < 0.05) liver antioxidant capacities (GSH, TEAC, SOD, and CAT) and decreased (p < 0.05) lipid peroxidation (MDA), which alleviated liver damage in the high-fat/cholesterol dietary hamsters. Therefore, Tau shows preventive effects on the development of hepatic steatosis induced by a high-fat/cholesterol dietary habit.

Antiobesity and Hypolipidemic Effects of Polyphenol-Rich Longan (Dimocarpus longans Lour.) Flower Water Extract in Hypercaloric-Dietary Rats

Plenty of polyphenols, i.e. phenolic acids and flavonoids, were found in longan flower water extract (LFWE) through spectrophotometric and HPLC analyses. Antiobesity and hypolipidemic effects of polyphenol-rich longan flower water extract (LFWE) were investigated in this study. Eight male rats per group were assigned randomly to one of the following dietary groups: (1) normal-caloric diet and pure water (NCD + NDW); (2) hypercaloric diet and pure water (HCD + NDW); (3) HCD and 1.25% (w/v) LFWE (HCD + 1.25% LFWE); (4) HCD and 2.5% (w/v) LFWE (HCD + 2.5% LFWE) for 9 weeks. Body weight, size of epididymal fat, serum triglyceride level and atherogenic index, and hepatic lipids were decreased (p < 0.05) in HCD rats by drinking 2.5% LFWE which may result from downregulated (p < 0.05) pancreatic lipase activity, and sterol regulatory element binding protein-1c (SREBP-1c) and fatty acid synthase (FAS) gene expressions, as well as upregulated (p < 0.05) LDL receptor (LDLR) and peroxisome proliferator-activated-receptor-alpha (PPAR-alpha) gene expressions, and also increased (p < 0.05) fecal triglyceride excretions. Therefore, polyphenol-rich LFWE indeed characterizes antiobesity and hypolipidemic effects in vivo.

Fruiting body of niuchangchih (Antrodia camphorata) protects livers against chronic alcohol consumption damage.

An alcoholic fatty liver disease was induced by drinking water containing 20% (w/w) alcohol. Therapeutic groups were orally administrated dosages of 0.25 g silymarin/kg body weight (BW) and a low dosage of Niuchangchih (Antrodia camphorata) (0.025 g/kg BW) and a high dosage of Niuchangchih (0.1 g/kg BW) per day. Niuchangchih, especially at the high dosage, not only showed a hypercholesterolemic effect (p < 0.05) but also reduced (p < 0.05) hepatic lipids in alcohol-fed rats. Those beneficial effects could be partially attributed to higher (p < 0.05) fecal cholesterol and bile acid outputs, as well as downregulations (p < 0.05) of 3-hydroxy-3-methylglutaryl-CoA reductase, sterol regulatory element-binding protein-1c, acetyl-CoA carboxylase, fatty acid synthase, and malic enzyme gene expressions; meanwhile, there was an upregulation of low-density lipoprotein receptor and peroxisome proliferator-activated alpha gene expression. Besides, Niuchangchih also enhanced (p < 0.05) the liver glutathione, Trolox equivalent antioxidant capacity, and activities of superoxide dismutase, catalase, and glutathione peroxidase and decreased the liver malondialdehyde content, which also partially contributed to the lowered (p < 0.05) serum aspartate aminotransferase levels and no observed lesion in the histological examination of alcohol-fed rats.

Beneficial effects of noni (Morinda citrifolia L.) juice on livers of high-fat dietary hamsters

Polyphenols in noni juice (NJ) are mainly composed of phenolic acids, mainly gentisic, p-hydroxybenoic, and chlorogenic acids. To investigate the beneficial effects of NJ on the liver, hamsters were fed with two diets, normal-fat and high-fat diets. Furthermore, high-fat dietary hamsters were received distilled water, and 3, 6, and 9 mL NJ/kg BW, respectively. After a 6-week feeding period, the increased (p<0.05) sizes of liver and visceral fat in high-fat dietary hamsters compared to the control hamsters were ameliorated (p<0.05) by NJ supplementation. NJ also decreased (p<0.05) serum/liver lipids but enhanced (p<0.05) daily faecal lipid/bile acid outputs in the high-fat dietary hamsters. High-fat dietary hamsters supplemented with NJ had higher (p<0.05) liver antioxidant capacities but lowered (p<0.05) liver iNOS, COX-2, TNF-α, and IL-1β expressions, gelatinolytic levels of MMP9, and serum ALT values compared to those without NJ. Hence, NJ protects liver against a high-fat dietary habit via regulations of antioxidative and anti-inflammatory responses.

Hepatoprotection of noni juice against chronic alcohol consumption: lipid homeostasis, antioxidation, alcohol clearance, and anti-inflammation.

Chronic alcohol consumption leads to steatohepatitis and cirrhosis. Naturally fermented noni juice (NJ) contains polyphenols, polysaccharides, and some trace minerals. This study explored protective effects of NJ against chronic alcohol consumption. Mice were assigned randomly to one of the following groups: (1) control, control liquid diet and distilled water; (2) alcohol, alcohol liquid diet and distilled water; (3) Alc+NJ_1X, alcohol liquid diet and 5 mL NJ/kg BW; (4) Alc+NJ_2X, alcohol liquid diet and 10 mL NJ/kg BW; (5) Alc+NJ_3X, alcohol and 15 mL NJ/kg BW for 4 weeks. NJ decreased (p < 0.05) serum AST, ALT, and alcohol levels and liver lipids, as well as increased (p < 0.05) daily fecal lipid outputs in alcohol-diet fed mice. NJ supplementation not only down-regulated (p < 0.05) lipogenesis but also up-regulated (p < 0.05) fatty acid β-oxidation in livers of alcohol-diet fed mice. NJ also accelerated alcohol clearance via increased (p < 0.05) hepatic ADH and ALDH activities. NJ increased (p < 0.05) hepatic TEAC and GSH levels but decreased (p < 0.05) TBARS value and TLR2/4, P38, ERK 1/2, NFκB P65, iNOS, COX-2, TNF-α, and IL-1β expressions in alcohol-diet fed mice. NJ promotes hepatoprotection against alcohol-induced injury due to regulations of lipid homeostasis, antioxidant status, alcohol metabolism, and anti-inflammatory responses.

Protective Effects of Functional Chicken Liver Hydrolysates against Liver Fibrogenesis: Antioxidation, Anti-inflammation, and Antifibrosis

Via an assay using an Amino Acid Analyzer, pepsin-digested chicken liver hydrolysates (CLHs) contain taurine (365.57 ± 39.04 mg/100 g), carnosine (14.03 ± 1.98 mg/100 g), and anserine (151.58 ± 27.82 mg/100 g). This study aimed to evaluate whether CLHs could alleviate thioacetamide (TAA)-induced fibrosis. A dose of 100 mg TAA/kg BW significantly increased serum liver damage indices and liver cytokine contents. Cell infiltration and monocytes/macrophages in livers of TAA-treated rats were illustrated by the H&E staining and immunohistochemical analysis of cluster of differentiation 68 (CD68, ED1), respectively. A significantly increased hepatic collagen accumulation was also observed and quantified under TAA treatment. A significant up-regulation of transforming growth factor-beta (TGF-β) and SMAD family member 4 (SMAD4) caused by TAA treatment further enhanced alpha smooth muscle actin (αSMA) gene and protein expressions. The liver antioxidant effects under TAA treatment were significantly amended by 200 and 600 mg CLHs/kg BW. Hence, the ameliorative effects of CLHs on liver fibrogenesis could be attributed by antioxidation and anti-inflmmation.