Exploring the Interplay between Fatty Acids, Inflammation, and Type 2 Diabetes

Immuno Pub Date : 2024-03-01 DOI:10.3390/immuno4010006

Dequina A. Nicholas, Jacques C. Mbongue, Darysbel Garcia-Pérez, Dane Sorensen, Heather Ferguson Bennit, M. De León, William H. R. Langridge

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Abstract

Around 285 million people worldwide currently have type 2 diabetes and it is projected that this number will be surpassed by 2030. Therefore, it is of the utmost importance to enhance our comprehension of the disease’s development. The regulation of diet, obesity, and inflammation in type 2 diabetes is believed to play a crucial role in enhancing insulin sensitivity and reducing the risk of onset diabetes. Obesity leads to an increase in visceral adipose tissue, which is a prominent site of inflammation in type 2 diabetes. Dyslipidemia, on the other hand, plays a significant role in attracting activated immune cells such as macrophages, dendritic cells, T cells, NK cells, and B cells to visceral adipose tissue. These immune cells are a primary source of pro-inflammatory cytokines that are believed to promote insulin resistance. This review delves into the influence of elevated dietary free saturated fatty acids and examines the cellular and molecular factors associated with insulin resistance in the initiation of inflammation induced by obesity. Furthermore, it explores novel concepts related to diet-induced inflammation and its relationship with type 2 diabetes.

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探索脂肪酸、炎症和 2 型糖尿病之间的相互作用

目前，全球约有 2.85 亿人患有 2 型糖尿病，预计到 2030 年，这一数字将被超过。因此，加强我们对该疾病发展的了解至关重要。在 2 型糖尿病中，饮食、肥胖和炎症的调节被认为在提高胰岛素敏感性和降低糖尿病发病风险方面起着至关重要的作用。肥胖会导致内脏脂肪组织增加，而内脏脂肪组织是 2 型糖尿病的主要炎症部位。另一方面，血脂异常在吸引巨噬细胞、树突状细胞、T 细胞、NK 细胞和 B 细胞等活化免疫细胞进入内脏脂肪组织方面起着重要作用。这些免疫细胞是促炎细胞因子的主要来源，而促炎细胞因子被认为会促进胰岛素抵抗。本综述深入探讨了膳食中游离饱和脂肪酸升高的影响，并研究了在肥胖诱发炎症的过程中与胰岛素抵抗相关的细胞和分子因素。此外，它还探讨了有关饮食诱发炎症及其与 2 型糖尿病关系的新概念。

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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Immuno

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