Suchergebnisse

Green tea and selenium (Se) improve non-alcoholic fatty liver disease (NAFLD). However, studies on the effect of green tea and Se-enriched green tea on NAFLD are limited. C57BL/6 mice were divided into high-fat diet (HFD), HFD+regular green tea (T), and HFD+Se-enriched green tea (SeT) groups after 12 weeks of feeding with HFD. HFD feeding was continued, and the mice in the HFD+T and HFD+SeT groups drank corresponding tea solution for another 12 weeks. The control (CON) group was given normal diet. At the end of the experiment, serum, liver, fat, and intestinal tract were collected. Results showed that both tea interventions decreased body and fat weight. Histological analysis showed that both tea interventions alleviated steatosis, which is supported by the changes in lipid profiles and lipogenic pathways. Tea interventions significantly increased superoxide dismutase, glutathione peroxidase, and catalase levels; and decreased TNF-α, IL-1β, IL-6, and malondialdehyde contents. HFD significantly increased total bile acid in the intestinal contents and liver, duodenal 5-hydroxytryptamine (5-HT) level and tryptophan hydroxylase gene expression, and hepatic 5-HT, 5-HT receptor 2A, monoamine oxidase-A (MAO-A), and H2O2; all of them reversed by the tea interventions. Furthermore, the improved oxidative stress, inflammatory response, duodenal 5-HT, and hepatic MAO-A were more pronounced in the HFD+SeT group than in the HFD+T group. Our findings revealed that green tea ameliorates NAFLD through peripheral 5-HT signals in HFD fed mice.

Non-alcoholic fatty liver disease is a highly prevalent condition without specific pharmacological treatment, characterized in the initial stages by hepatic steatosis. It was suggested that lipid infiltration in the liver might be reduced by caffeine through anti-inflammatory, antioxidative, and fatty acid metabolism-related mechanisms. We investigated the effects of caffeine (CAF) and green coffee extract (GCE) on hepatic lipids in lean female rats with steatosis. For three months, female Sprague-Dawley rats were fed a standard diet or a cocoa butter-based high-fat diet plus 10% liquid fructose. In the last month, the high-fat diet was supplemented or not with CAF or a GCE, providing 5 mg/kg of CAF. Plasma lipid levels and the hepatic expression of molecules involved in lipid metabolism were determined. Lipidomic analysis was performed in liver samples. The diet caused hepatic steatosis without obesity, inflammation, endoplasmic reticulum stress, or hepatic insulin resistance. Neither CAF nor GCE alleviated hepatic steatosis, but GCE-treated rats showed lower hepatic triglyceride levels compared to the CAF group. The GCE effects could be related to reductions of hepatic (i) mTOR phosphorylation, leading to higher nuclear lipin-1 levels and limiting lipogenic gene expression; (ii) diacylglycerol levels; (iii) hexosylceramide/ceramide ratios; and (iv) very-low-density lipoprotein receptor expression. In conclusion, a low dose of CAF did not reduce hepatic steatosis in lean female rats, but the same dose provided as a green coffee extract led to lower liver triglyceride levels. ; This research was funded by the Spanish Ministry of Economy, Industry, and Competitiveness (SAF2017-82369-R), Generalitat de Catalunya (2017 SGR 38), and European Commission FEDER funds. A.M.V. is a predoctoral fellow, BECAL grant program BCAL04-327, from the Government of Paraguay. A.S.-V. is recipient of the Instituto de Salud Carlos III Miguel Servet fellowship (grant CP II 17/00029).

High-fat (HF) and rapid digestive (RD) carbohydrate diets during pregnancy promote excessive adipogenesis in o spring. This e ect can be corrected by diets with similar glycemic loads, but low rates of carbohydrate digestion. However, the e ects of these diets on metabolic programming in the livers of o spring, 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 di erent rates of carbohydrate digestion, High Fat-Rapid Digestive (HF–RD) diet or High Fat-Slow Digestive (HF–SD) diet. O spring 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 o spring 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 o spring, 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. ; This research was funded by the European Union's Seventh Framework Programme (FP7/2007–2013): project EarlyNutrition, under grant agreement no. 289346.