The possible mechanisms of high-fructose diet-induced pancreatic disturbances

Abstract

Excess fructose consumption in the regular human diet causes several health problems. The main source of dietary fructose is sugar-sweetened beverages, which are especially consumed by children and teenagers. Highfructose intake is one of the major responsible factors of the increased prevalence of metabolic syndrome and type 2 diabetes worldwide. The dietary high-fructose-induced metabolic syndrome was evidenced by hyperglycemia, hyperinsulinemia, hyperlipidemia, hypertension, fatty liver disease, central adiposity, and inflammation. Molecular findings indicated that there was a suppression of insulin signaling and activation of oxidative stress in different tissues including the liver, blood vessels, adipose tissue, and kidney in the excess intake of fructose. However, there is a limited mechanistic study on the pancreatic disturbances induced by dietary high-fructose. The hyperglycemic condition in the consumption of high-fructose may lead to morphologic and pathological changes to increase the capacity of insulin secretion in the pancreas. High-fructose can activate the mitogenic and apoptotic pathways, thus probably inducing hyperplasia in β-cells. The overactivation of β-cells can trigger oxidative and endoplasmic reticulum stress as well as inflammation in the pancreas. In conclusion, high-fructose consumption may cause pancreatic disturbance possibly through stimulation of cellular oxidative stress, inflammation, mitogenesis, and apoptosis. Pancreas is one of the first organs affected by metabolic abnormalities, therefore, elucidation of potential mechanisms underlying high-fructose diet-induced pancreatic pathologies would be valuable in the prevention and treatment of the metabolic syndrome as well as type 2 diabetes.