syndrome is a worldwide epidemic disorder. MetS is a cluster of risk factors
i.e. abdominal obesity, dyslipidemia, high blood pressure, insulin resistance
and proinflammatory states. It is a strong, independent contributor to the
onset of coronary heart disease and type 2 diabetes (T2D). Metabolic syndrome is defined by the WHO as the presence of insulin
resistance (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 developing
CVD compared with those without the syndrome, and experience a five-fold
increased risk of type 2 diabetes.
tissue acts in an autocrine, paracrine or endocrine fashion to control various
metabolic functions and may contribute to the development of obesity mediated
MetS. Adipose tissue also participates in the regulation of energy homeostatis
as an important endocrine organ that secretes a number of bioactive mediators
with diverse functions termed as “adipokine” or “adipocytokine”
such as IL-6, TNF-?, resistin, resistin binding protein-4, leptin, adiponectin,
is accumulating evidence that excess visceral fat (often referred to as
abdominal or central obesity) is especially predictive of the MetS and
increased risk of metabolic risk factors. Central obesity is linked with
hyperinsulinemia, insulin resistance, diabetes, dyslipidemia, hypertension,
albuminuria, and proinflammatory and prothrombotic clinical states. Waist
circumference (WC) and waist-to-hip ratio (WHR) are widely accepted modes of
defining central obesity. Optimum waist circumferences are lower for Asians
compared with white people. It has been hypothesized that adipokines are a
possible link between obesity and the other components of the MetS.
identified adipokines include Adipocyte Fatty
Acid Binding Protein (A-FABP), visfatin, Lipocalin-2 Chemerin,
Omentin, Progranulin, Apelin. These adipokines are postulated
as a potential link between abdominal obesity and the vasculature, and have
been shown to mediate insulin resistance. The increasing visceral fat
accumulation 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 decreased
in the visceral obesity while others adipokines levels are increased. This abnormal
level of adipokine may promote
obesity-linked metabolic disorders and cardiovascular disease. This abnormal
level of adipokine may lead to
obesity-linked cardiometabolic disorders.
Hence, the relationships between metabolic
syndrome and adipokines is complex, including a variety of influences like
cardiovascular function, metabolic status and behavioural aspects. Thus, the
first line approach to treat MetS is the prevention of excessive weight gain.