Obesity, manifested by increased adiposity, represents a main cause of morbidity in the developed countries, causing increased risk of insulin resistance and type 2 diabetes mellitus. Recruitment of macrophages and activation of innate immunity represent the initial insult, which can be further exacerbated through secretion of chemokines and adipocytokines from activated macrophages and other cells within the adipose tissue. These events can impact adipogenesis, causing dysfunction of the adipose tissue and increased risk of insulin resistance. Various factors mediate adiposity and related insulin resistance including inflammatory and non-inflammatory factors such as pro and anti-inflammatory cytokines, adipokines and growth factors. In this review we will discuss the role of these factors in adipogenesis and development of insulin resistance and type 2 diabetes mellitus in the context of obesity. Understanding the molecular mechanisms that mediate adipogenesis and insulin resistance could help the development of novel therapeutic strategies for individuals at higher risk of insulin resistance and type 2 diabetes mellitus.

肥胖，表现为肥胖增加，是发达国家发病的主要原因，导致胰岛素抵抗和 2 型糖尿病的风险增加。巨噬细胞的募集和先天免疫的激活是最初的损害，可通过激活的巨噬细胞和脂肪组织内的其他细胞分泌趋化因子和脂肪细胞因子进一步加剧这种损害。这些事件会影响脂肪生成，导致脂肪组织功能障碍和胰岛素抵抗风险增加。多种因素介导肥胖和相关的胰岛素抵抗，包括炎症和非炎症因子，例如促炎和抗炎细胞因子、脂肪因子和生长因子。在这篇综述中，我们将讨论这些因素在肥胖背景下脂肪生成和胰岛素抵抗和 2 型糖尿病发展中的作用。了解介导脂肪生成和胰岛素抵抗的分子机制有助于为胰岛素抵抗和 2 型糖尿病风险较高的个体开发新的治疗策略。