**2.10 Influences of beverages in non-alcoholic fatty liver disease**

The most popular types of alcoholic drinks include wines, beers, and spirits, whereas non-alcoholic drinks include juices, carbonated and non-carbonated sweetened drinks, and hot beverages like tea and coffee. Even though certain drinks provide fundamental health advantages, beverages are regarded as functional foods because they include well-known macro- or micro-molecules that support optimal health. Independent of the metabolic syndrome, soft drink use can raise the prevalence of NAFLD. Regular soft drink consumption causes the primary effect of fructose, which increases lipogenesis. The additional contribution of aspartame sweetener and caramel colorant, which are rich in advanced glycation end products, may increase insulin resistance and inflammation. Hence, lipids accumulation in the liver can result from regular soft drink consumption [22, 23]. Consuming sugar-sweetened drinks (SSBs) is also linked to increased triglyceride levels, abdominal fat, blood pressure, IR and lower HDL cholesterol levels, which may facilitate the development of NAFLD and obesity. Despite the negative effects of sugar-sweetened beverages and energy drinks, there is some evidence that drinking tea, coffee, and alcoholic beverages may have some positive effects on liver disease. SSBs increase hepatic de novo lipogenesis while reducing fatty acid β-oxidation, which in turn promotes NAFLD. Despite the lifestyle factors, obesity, CVDs and metabolic syndrome, increased deposition of visceral and hepatic fat are the main risk factors linked to daily consumption of sugar-sweetened beverages [24, 25]. Several mechanisms have been investigated to show how fructose might participate in the production of lipids in the liver. Fructose has also been investigated to facilitate hepatic lipid deposition through the dysfunctional mitochondria and mitigate β-oxidation of fatty acids. Another significant component of SSB is glucose, which can either directly or indirectly stimulate hepatic lipid storage by converting into fructose through the polyol pathway in the liver [22]. Moreover, fructose may activate the lipogenic transcription factors sterol receptor element binding protein 1c (SREBP-1c) and carbohydrate response element binding protein (ChREBP). Fructose may limit the breakdown of fatty acids by lowering the activity of β-oxidation in the liver as another mechanism. Numerous studies have

demonstrated that SSB consumption may raise the risk of hyperuricemia by depleting adenosine triphosphate (ATP), which may then increase alanine aminotransferase (ALT) levels [25].
