Cadmium: An Emerging Role in Adipose Tissue Dysfunction

Abstract

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.