SVKM's Dr. Bhanuben Nanavati College of Pharmacy, Vile Parle (W), Mumbai 400056, India.
Shobhaben Pratapbhai Patel School of Pharmacy & Technology Management, SVKM's NMIMS, V.L. Mehta Road, Vile Parle (W), Mumbai 400056, India.
Pharmacol Res. 2021 Jun;168:105602. doi: 10.1016/j.phrs.2021.105602. Epub 2021 Apr 8.
Diabetes is a chronic metabolic disorder with a high rate of morbidity and mortality. Insufficient insulin secretion and insulin action are two major causes for the development of diabetes, which is characterized by a persistent increase in blood glucose level. Diet and sedentary life style play pivotal role in development of vascular complications in type 2 diabetes. Dietary modification is associated with a reprogramming of nutrient intake, which are proven to be effective for the management of diabetes and associated complications. Dietary modifications modulate various molecular key players linked with the functions of nutrient signalling, regulation of autophagy, and energy metabolism. It activates silent mating type information regulation 2 homolog1 (SIRT1) and AMP-activated protein kinase (AMPK). AMPK mainly acts as an energy sensor and inhibits autophagy repressor Mammalian target of rapamycin (mTOR) under nutritional deprivation. Under calorie restriction (CR), SIRT1 gets activated directly or indirectly and plays a central role in autophagy via the regulation of protein acetylation. Dietary modification is also effective in controlling inflammation and apoptosis by decreasing the level of pro-inflammatory cytokines like nuclear factor kappa- beta (NF-kβ), tissue growth factor-beta (TGF-β), tissue necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). It also improves glucose homeostasis and insulin secretion through beta cell regeneration. This indicates calorie intake plays a crucial role in the pathogenesis of type 2 diabetes-associated complications. The present review, emphasizes the role of dietary modifications in diabetes and associated complications.
糖尿病是一种慢性代谢紊乱疾病，发病率和死亡率都很高。胰岛素分泌不足和胰岛素作用障碍是糖尿病发展的两个主要原因，其特征是血糖水平持续升高。饮食和 sedentary life style 在 2 型糖尿病血管并发症的发生发展中起着关键作用。饮食改变与营养素摄入的重新编程有关，这已被证明对糖尿病及其相关并发症的管理有效。饮食改变调节与营养信号转导、自噬调节和能量代谢功能相关的各种分子关键因素。它激活沉默交配型信息调节 2 同源物 1（SIRT1）和 AMP 激活蛋白激酶（AMPK）。AMPK 主要作为能量传感器，在营养缺乏时抑制自噬抑制剂哺乳动物雷帕霉素靶蛋白（mTOR）。在热量限制（CR）下，SIRT1 直接或间接被激活，并通过调节蛋白质乙酰化在自噬中发挥核心作用。饮食改变还通过降低核因子 kappa-β（NF-kβ）、组织生长因子-β（TGF-β）、肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）等促炎细胞因子的水平，有效控制炎症和细胞凋亡。它还通过β细胞再生改善葡萄糖稳态和胰岛素分泌。这表明热量摄入在 2 型糖尿病相关并发症的发病机制中起着至关重要的作用。本综述强调了饮食改变在糖尿病及其相关并发症中的作用。
