Metabolicsyndrome is a worldwide epidemic disorder. MetS is a cluster of risk factorsi.e. abdominal obesity, dyslipidemia, high blood pressure, insulin resistanceand proinflammatory states.
It is a strong, independent contributor to theonset of coronary heart disease and type 2 diabetes (T2D). Metabolic syndrome is defined by the WHO as the presence of insulinresistance (IR) and any two of the following criteria which include (a) increased abdominal girth, (b) hypertension, (c) elevated triglycerides levels, (d) low high-density lipoprotein level, and (e) elevated blood glucose levels (type II DM).It has been estimated that people with MetS are at twice the risk of developingCVD compared with those without the syndrome, and experience a five-foldincreased risk of type 2 diabetes.Adiposetissue acts in an autocrine, paracrine or endocrine fashion to control variousmetabolic functions and may contribute to the development of obesity mediatedMetS. Adipose tissue also participates in the regulation of energy homeostatisas an important endocrine organ that secretes a number of bioactive mediatorswith diverse functions termed as “adipokine” or “adipocytokine”such as IL-6, TNF-?, resistin, resistin binding protein-4, leptin, adiponectin,adipsin.Thereis accumulating evidence that excess visceral fat (often referred to asabdominal or central obesity) is especially predictive of the MetS andincreased risk of metabolic risk factors.
Central obesity is linked withhyperinsulinemia, insulin resistance, diabetes, dyslipidemia, hypertension,albuminuria, and proinflammatory and prothrombotic clinical states. Waistcircumference (WC) and waist-to-hip ratio (WHR) are widely accepted modes ofdefining central obesity. Optimum waist circumferences are lower for Asianscompared with white people. It has been hypothesized that adipokines are apossible link between obesity and the other components of the MetS.Otheridentified adipokines include Adipocyte FattyAcid Binding Protein (A-FABP), visfatin, Lipocalin-2 Chemerin,Omentin, Progranulin, Apelin. These adipokines are postulatedas a potential link between abdominal obesity and the vasculature, and havebeen shown to mediate insulin resistance. The increasing visceral fataccumulation leads to the overproduction of some adipokine such as IL-6, TNF-?or resistin which deteriorates insulin action in muscles and/or in liver.
Adiponectin is the only known adipokine whose circulating levels are decreasedin the visceral obesity while others adipokines levels are increased. This abnormallevel of adipokine may promoteobesity-linked metabolic disorders and cardiovascular disease. This abnormallevel of adipokine may lead toobesity-linked cardiometabolic disorders.Hence, the relationships between metabolicsyndrome and adipokines is complex, including a variety of influences likecardiovascular function, metabolic status and behavioural aspects. Thus, thefirst line approach to treat MetS is the prevention of excessive weight gain.