Abstract
Non-alcoholic fatty liver disease (NAFLD) was defined in 1980 and has the same histological characteristics as alcoholic liver disease except for alcohol consumption. After 40 years, the understanding of this disease is still imperfect. Without specific drugs available for treatment, the number of patients with NAFLD is increasing rapidly, and NAFLD currently affects more than one-quarter of the global population. NAFLD is mostly caused by a sedentary lifestyle and excessive energy intake of fat and sugar. To ameliorate or avoid NAFLD, people commonly replace high-fat foods with high-carbohydrate foods (especially starchy carbohydrates) as a way to reduce caloric intake and reach satiety. However, there are few studies that concentrate on the effect of carbohydrate intake on liver metabolism in patients with NAFLD, much fewer than the studies on fat intake. Besides, most of these studies are not systematic, which has made identification of the mechanism difficult. In this review, we collected and analysed data from studies on human and animal models and, surprisingly, found that carbohydrates and liver steatosis could be linked by inflammation. This review not only describes the effects of carbohydrates on NAFLD and body lipid metabolism but also analyses and predicts possible molecular pathways of carbohydrates in liver lipid synthesis that involve inflammation. Furthermore, the limitations of recent research and possible targets for regulating inflammation and lipogenesis are discussed. This review describes the effects of starchy carbohydrates, a nutrient signal, on NAFLD from the perspective of inflammation.
Highlights
Carbohydrate consumption has a long history and can be divided into three stages: [1] From the hunting era to the agricultural era, the consumption of meat and plant fruits obtained from primitive hunting and gathering gradually transitioned to the consumption of self-cultivated rice, making rice a staple food. [2] The extensive cultivation of sugar cane made sugar an accessible consumer product
A large number of studies have shown that free sugars can promote de novo lipogenesis (DNL) in the liver, resulting in the accumulation of a large number of lipids and leading to Non-alcoholic fatty liver disease (NAFLD)[4,5]
Regardless of age and sex differences, we found that there was no correlation between total carbohydrate intake or starchy carbohydrate intake and blood lipids, but there was a correlation between free sugar and TG, which indicates that the intake of starchy carbohydrates did not affect the lipid content directly in the body
Summary
Carbohydrate consumption has a long history and can be divided into three stages: [1] From the hunting era to the agricultural era, the consumption of meat and plant fruits obtained from primitive hunting and gathering gradually transitioned to the consumption of self-cultivated rice, making rice a staple food. [2] The extensive cultivation of sugar cane made sugar an accessible consumer product. Plasma uric acid levels are correlated with the glycaemic index of food[25], and starchy carbohydrates and free sugars are substances with a high glycaemic index; it is possible that starchy carbohydrates and free sugars can activate inflammasomes through uric acid, leading to further increases in oxidative stress and inflammation in the liver Both immune cells and macrophages in the liver have a vital role in mediating the immune response and regulating inflammation levels in the body. Excessive intake of AGEs from a high-fat and high-sugar diet obviously caused liver lipid accumulation and fibrosis, pathological changes in hepatocyte balloon-like vacuoles, and increased content of 4-hydroxynonenal, a marker of chronic oxidative stress[50]. Studies have shown that RAPTOR (a key component of mTORC1) regulates prostaglandins synthesised by cyclooxygenase-2 (COX-2), thereby promoting beige fat production, while RAPTOR-deficient mice are resistant to diet-induced obesity, indicating that the mTORC1 pathway functions in hepatic inflammation. The classic inflammatory mTORCR1 pathway or various inflammation-related factors may lead to the regulation of inflammation levels that can interfere with lipid production, further indicating that inflammation mediates lipid synthesis
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