METABOLIC SYNDROME INDUCED BY FRUCTOSE IN ADOLESCENCE: A REVIEW
DOI:
https://doi.org/10.31692/2764-3433.v1i2.69Schlagwörter:
Fructose; Adolescence; Metabolic syndromeAbstract
Metabolic Syndrome (MetS) is characterized as a set of metabolic disorders such as abdominal obesity, glucose intolerance, hyperinsulinemia, dyslipidemia and hypertension. The factors that contribute to development of metabolic syndrome are the sedentary lifestyle, high consumption of diets high in fats and carbohydrates, such as fructose. The literature has shown the fructose consumption by adolescents is increasing. The main cause is the consumption of sucrose and High Fructose Corn Syrup (HFCS) that produce glucose and fructose at high doses (55% fructose and 42% glucose). The liver is the main organ of fructose metabolism. In this organ, fructose induces lipogenic precursor production, such as acetyl-coA, leading to a high triglycerides and fat synthesis. This process causes fat deposition in the liver, developing hepatic steatosis and also central and peripheral insulin resistance both in adults and adolescents. On intestine, fructose is not immediately absorbed, interacting with the intestinal microbiota and changing it. In high levels of glucose conditions, non-insulin-dependent tissues such as nerve tissue, lense and erythrocytes can activate the polyol pathway and induce endogenous fructose production. That observation was obtained during adolescence and adult life. On adipose tissue, the metabolism of fructose in adipocyte results in generation of precursors of fatty acid synthesis, expression of GLUT-5 transporters in adipocyte plasma membrane and greater expression of enzyme responsible that contribute to glucocorticoids production, 11-hydroxysteroid dehydrogenase type 1 (11-HSD1). On pancreas, high fructose diet showed an increase in markers of stress in endoplasmic reticulum both in pancreas and in liver at the level of mRNAs and enzymes. On brain, fructose alters some functions related to hippocampal plasticity. This review focus on the effect of diet enriched by fructose in adolescence, that causes metabolic dysfunction in different tissues, characterizing the early metabolic syndrome.
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