Cadmium (Cd) is a toxic heavy metal that is widespread in the environment due to the substantial anthropogenic inputs from the agriculture and industrial sectors. The toxic impact of Cd adversely affects human health and is linked with endocrine disruption, carcinogenicity, diabetes-related diseases, and metabolic disorder. One of the main characterizations of Cd is bioaccumulation where its half-life reaches 40 years with an unknown biological role. Several organs were found to be targets for Cd accumulation such as the liver, kidneys, and adipose tissue. Adipose tissue (AT) is a dynamic organ that plays a significant role in the body’s homeostasis through the maintenance of energy storage. Another vital function for AT is the secretion of adipokines which provides a metabolic cross-talk with the whole body’s organs. Cd is found to adversely impact the function of AT. This includes the disruption of adipogenesis, lipogenesis, and lipolysis. As a consequence, dysfunctional AT has disruptive patterns of adipokines secretions. The main adipokines produced from AT are leptin and adiponectin. Both were found to be significantly declined under the Cd exposure. Additionally, adipose tissue macrophages can produce either anti-inflammatory markers or pro-inflammatory markers depending on the local AT condition. Cadmium exposure was reported to upregulate pro-inflammatory markers and downregulate anti-inflammatory markers. However, the exact mechanisms of Cd’s adverse role on AT structure, function, and secretion patterns of adipokines are not totally clarified. Therefore, in this review, we present the current findings related to Cd detrimental effects on adipose tissues.

镉 (Cd) 是一种有毒重金属，由于农业和工业部门的大量人为输入，它在环境中广泛存在。镉的毒性影响对人类健康产生不利影响，并与内分泌紊乱、致癌性、糖尿病相关疾病和代谢紊乱有关。Cd 的主要特征之一是生物蓄积性，其半衰期达到 40 年，具有未知的生物学作用。发现几个器官是 Cd 积累的目标，例如肝脏、肾脏和脂肪组织。脂肪组织 (AT) 是一种动态器官，通过维持能量储存在身体的稳态中发挥重要作用。AT 的另一个重要功能是脂肪因子的分泌，它提供与全身器官的代谢串扰。发现 Cd 对 AT 的功能有不利影响。这包括脂肪生成、脂肪生成和脂肪分解的破坏。因此，功能失调的 AT 具有破坏性的脂肪因子分泌模式。AT产生的主要脂肪因子是瘦素和脂联素。发现两者都在镉暴露下显着下降。此外，脂肪组织巨噬细胞可以根据局部 AT 条件产生抗炎标志物或促炎标志物。据报道，镉暴露会上调促炎标志物并下调抗炎标志物。然而，Cd 对脂肪因子结构、功能和分泌模式的不利作用的确切机制尚未完全阐明。因此，在本次审查中，