The Bitter Side of Sugar Consumption: A Mitochondrial Perspective on Diabetes Development

IF 2.4 Q3 ENDOCRINOLOGY & METABOLISM
Mariana S. Diniz, Carolina Tocantins, L. Grilo, Susana P. Pereira
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引用次数: 4

Abstract

Type 2 diabetes (T2D) has increased worldwide at an alarming rate. Metabolic syndrome (MetS) is a major risk factor for T2D development. One of the main reasons for the abrupt rise in MetS incidence, besides a sedentary lifestyle, is the westernized diet consumption, with high content of industrialized foods, rich in added dietary sugars (DS), mainly sucrose and fructose. It has been suggested that a higher intake of DS could impair metabolic function, inducing MetS, and predisposing to T2D. However, it remains poorly explored how excessive DS intake modulates mitochondrial function, a key player in metabolism. This review explores the relationship between increased consumption of DS and mitochondrial dysfunction associated with T2D development, pointing to a contribution of the diet-induced accumulation of advanced glycation end-products (AGEs), with brief insights on the impact of maternal high-sugar diet and AGEs consumption during gestation on offspring increased risk of developing T2D later in life, contributing to perpetuate T2D propagation.
糖消费的痛苦一面:线粒体对糖尿病发展的看法
2型糖尿病(T2D)在世界范围内以惊人的速度增长。代谢综合征(MetS)是T2D发展的主要危险因素。除了久坐不动的生活方式外,met发病率突然上升的主要原因之一是西方化的饮食消费,工业化食品含量高,富含添加糖(DS),主要是蔗糖和果糖。有研究表明,高DS摄入量会损害代谢功能,诱发MetS,并易患T2D。然而,对于过量DS摄入如何调节线粒体功能(代谢的关键角色)的研究仍然很少。本综述探讨了DS摄入增加与T2D发展相关的线粒体功能障碍之间的关系,指出饮食诱导的晚期糖基化终产物(AGEs)积累的贡献,并简要介绍了妊娠期母亲高糖饮食和AGEs摄入对后代后期患T2D的风险增加的影响,从而促进了T2D的持续传播。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
2.50
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0.00%
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