Metabolic Syndrome: From Human Organ Disease to Fetal Programming

Metabolic syndrome is defined as a constellation of metabolic disturbances that coexist in a subject. Due to its complex multi factorial etiology, metabolic syndrome causes damage to different organs, representing an increasing and significant global burden. Insulin resistance plays a central role in metabolic syndrome pathogenesis and underpins the majority of metabolic impairments, including the organ diseases that originate from metabolic syndrome. Regarding white adipose tissue, an altered adipokines profile in obesity characterizes a proinflammatory state, which is implicated in the pathogenesis of liver and cardiac disorders. Regarding the liver, nonalcoholic fatty liver disease is a benign disease that can progress towards liver fibrosis in the presence of persistent inflammation and increased oxidative stress. Concerning cardiovascular diseases, adipokines, reactive oxygen species and over activity of the renin angiotensin system play central roles. Another target organ of metabolic syndrome is the ovary, where polycystic ovary syndrome is also related to insulin resistance and can originate from adverse intrauterine conditions. The notion that maternal obesity can trigger metabolic syndrome in the fetus is alarming, given that it can be passed to other generations even if adequate nutrition is provided after birth. This review aimed to assess the main outcomes of metabolic syndrome in white adipose tissue focusing on insulin resistance and adipokines, the cardiovascular system, the liver and ovaries as well as fetal origins; this review also discusses some proposed pharmacological treatments to provide a better understanding of the related pathways in these secondary findings