Nicholas Dequina A, Mbongue Jacques C, Garcia-Pérez Darysbel, Sorensen Dane, Ferguson Bennit Heather, De Leon Marino, Langridge William H R
School of Biological Sciences, University of California Irvine, Irvine, CA 92697, USA.
Department of Biological Sciences, School of Arts and Sciences, Oakwood University, Huntsville, AL 35896, USA.
Immuno. 2024 Mar;4(1):91-107. doi: 10.3390/immuno4010006. Epub 2024 Mar 1.
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.
目前全球约有2.85亿人患有2型糖尿病，预计到2030年这一数字将被超越。因此，增强我们对该疾病发展的理解至关重要。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关键作用。肥胖会导致内脏脂肪组织增加，而内脏脂肪组织是2型糖尿病炎症的一个突出部位。另一方面，血脂异常在吸引活化的免疫细胞（如巨噬细胞、树突状细胞、T细胞、NK细胞和B细胞）到内脏脂肪组织中起重要作用。这些免疫细胞是促炎细胞因子的主要来源，据信促炎细胞因子会促进胰岛素抵抗。本综述深入探讨了饮食中游离饱和脂肪酸升高的影响，并研究了肥胖诱导炎症起始过程中与胰岛素抵抗相关的细胞和分子因素。此外，还探讨了与饮食诱导炎症及其与2型糖尿病关系相关的新概念。
