Soft drinks consumption and nonalcoholic fatty liver disease

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a common clinical condition which is associated with metabolic syndrome in 70% of cases. Inappropriate dietary fat intake, excessive intake of soft drinks, insulin resistance and increased oxidative stress combine to increase free fatty acid delivery to the liver, and increased hepatic triglyceride accumulation contributes to fatty liver. Regular soft drinks have high fructose corn syrup which contains basic sugar building blocks, fructose 55% and glucose 45%. Soft drinks are the leading source of added sugar worldwide, and have been linked to obesity, diabetes, and metabolic syndrome. The consumption of soft drinks can increase the prevalence of NAFLD independently of metabolic syndrome. During regular soft drinks consumption, fat accumulates in the liver by the primary effect of fructose which increases lipogenesis, and in the case of diet soft drinks, by the additional contribution of aspartame sweetener and caramel colorant which are rich in advanced glycation end products that potentially increase insulin resistance and inflammation. This review emphasizes some hard facts about soft drinks, reviews fructose metabolism, and explains how fructose contributes to the development of obesity, diabetes, metabolic syndrome, and NAFLD.

Figure 1

Prevalence of fatty liver among metabolic syndrome and prevalence of metabolic syndrome among fatty liver. MS: Metabolic syndrome; FL: Fatty liver. Alberti, Circulation (2009). P < 0.001.

Figure 2

Daily amount of soft drinks consumption in nonalcoholic fatty liver disease (NAFLD) patients with (n = 31) or without metabolic syndrome (n = 29) and in controls (n = 30). ^aP < 0.07; fatty liver without metabolic syndrome vs fatty liver with metabolic syndrome, ^bP < 0.001 between fatty liver subgroups and controls[14,15].

Figure 3

Fructose metabolism in the liver. Hepatic fructose metabolism begins with phosphorylation of fructokinase. Fructose carbon enters the glycolytic pathway at the triose phosphate level. Thus, fructose bypasses the major control point by which glucose carbon enters glycolysis. This allows fructose to serve as an unregulated source of glycerol-3-phosphate and acetyl-CoA for hepatic lipogenesis.

Figure 4

Changes in total abdominal adipose tissue, superficial adipose tissues (SAT), and visceral adipose tissue (VAT) volume after consuming glucose- or fructose-sweetened beverages for 10 wk. ^aP < 0.05, ^bP < 0.01, 10 wk vs 0 wk; paired Student’s t test. Glucose, n = 14; Fructose, n = 17. Data represent mean ± SE (Stanhope, J Clin Invest, 2009).

Figure 5

Mechanisms of detrimental effects of fructose.