Metabolic syndrom

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Metabolic syndrom

The constellation of metabolic abnormalities is known as the metabolic syndrome. The constellation of metabolic abnormalities includes glucose intolerance (type 2 diabetes, impaired glucose tolerance, or impaired fasting glycaemia), insulin resistance, central obesity, dyslipidaemia, and hypertension, all well documented risk factors for cardiovascular disease. These conditions co-occur in an individual more often than might be expected by chance. The metabolic syndrome is also known as syndrome X, the insulin resistance syndrome, and the deadly quartet. According to the new definition, for a person to be defined as having the metabolic syndrome, they must have central obesity plus any two of four additional factors. These four factors are: i) raised triglyceride level; ii) reduced high-density lipoprotein cholesterol; iii) raised blood pressure (or treatment of previously diagnosed hypertension); iiii) raised fasting plasma glucose (or previously diagnosed type 2 diabetes).

While the pathogenesis of the MetS and each of its components is complex and not fully elucidated, two features appear to stand out as potential causative factors: insulin resistance and abnormal fat distribution (central obesity). Other factors have also been implicated in the development of the MetS, including genetic profile, physical inactivity, ageing, a proinflammatory state and hormonal dysregulation. It has been suggested that the role of these causal factors may vary depending on ethnic group. Insulin resistance is a key feature of these diseases and is defined as a state that requires more insulin to obtain the biological effects achieved by a lower amount of insulin in the normal state. Thus, any defects in the insulin signaling cascade can cause insulin resistance.

Besides insulin, two other hormones have been associated with the development of the metabolic syndrome. These are leptin and adiponectin. Both are peptide hormones produced from adipose tissue. Leptin levels closely follow the amount of total adiposity. Leptin produces anorexia and increased metabolism, thus attempting to decrease the increased adiposity. Testosterone decreases leptin levels in males and leads to a decline in body fat. Thus, the age-related decline in testosterone in males may play a role in the pathogenesis of the metabolic syndrome. With increasing obesity, resistance to the effects of leptin occurs. This resistance appears to be due to hypertriglyceridemia. Adiponectin has been shown to enhance insulin sensitivity and decrease triglycerides. Low levels of adiponectin are closely associated with the development of insulin resistance. The metabolic syndrome is directly related to the accumulation of visceral adiposity in middle age associated with overeating and a decline in exercise.