Despite the known metabolic effects of fructose, its dietary intake has continued to increase in recent years ( 17-19). Currently, a large body of evidence has defined sugar as a toxic substance that contributes largely to non-communicable diseases, mainly due to the metabolic effects of fructose and its components ( 13, 15, 16). In 1900, sugar had already been shown to be related to various diseases ( 14). Since the past century, as the intake of added sugar has increased, at par, the effect of sugar on health has also been studied ( 12, 13). Diet, a component of lifestyle, plays a significant role in this epidemic specifically diets rich in fats, protein, sodium, and sugar ( 11). Obesity is a risk factor for the development of type 2 diabetes mellitus (T2DM), cardiovascular disease (CVD) ( 3), metabolic syndrome (MetS) ( 4-6), and is related to various chronic conditions including: high blood pressure ( 7), insulin resistance (IR) ( 8), dyslipidemia, atherosclerosis, a low-grade chronic inflammation, non-alcoholic fatty liver disease (NAFLD) and cancer ( 9).īoth obesity and metabolic syndrome are associated with various factors including genetics, physical activity, environment, and diet ( 6, 10). One out of three adults and three out of ten children or adolescents are obese or overweight ( 1, 2). Obesity is a global health problem that is increasing in prevalence around the world, affecting adults as well as children and adolescents. There is an urgent need for more clinical and educational interventions to regulate/reduce fructose consumption in our population, especially in children and adolescents. Directionality for the effect of fructose on metabolic syndrome is becoming clear: fructose drives hepatic fat, which in turn drives insulin resistance. Fructose derived advance glycation end-products may also induce a state of inflammation by engaging its receptor, RAGE. The hormones involved in satiety control are affected by fructose consumption. These effects include 1) increased de novo lipogenesis, 2) increased liver fat, 3) dyslipidemia 4) increased uric acid production which feeds back on increased fructose metabolism and, 5) increased methylglyoxal and Maillard reaction that may affect adenosyl-monophosphate-dependent kinase Fructose increases cortisol activation especially in visceral fat. The specifics effects of fructose on the liver are particularly germane to the development of a vicious cycle that starts with liver steatosis driving insulin resistance. In this review, we highlight the specific metabolic effects of fructose consumption that are involved in the development of metabolic syndrome non-alcoholic fatty liver disease and its association with obesity.
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