obesity: complications 1 - The metabolic syndrome - obesity
metabolic syndrome is defined as the association between impaired glucose tolerance (or diabetes mellitus type II) and insulin resistance with at least two of: Hypertension, hypertriglyceridemia, central obesity, microalbuminuria.
The fasting hyperinsulinemia predicts the onset of changes due to the metabolic syndrome (and thus the development of cardiovascular risk factors). Moreover, hyperinsulinemia in fasting and after oral glucose load in itself is predictive of coronary heart disease.
Insulin resistance is one of the fundamental changes in states of impaired glucose tolerance and diabetes mellitus type II. It translates to:
- In muscle: reduced utilization of glucose, reduction of glycogen synthesis, decreased glucose oxidation;
- In adipose tissue: reduced utilization of glucose, increased lipolysis and release of lactate;
- In the liver : increased gluconeogenesis and ketogenesis, increased extraction of free fatty acids and substrates neoglucogenetici. The increased
influx of free fatty acids to the liver contributes to the exaltation hepatic glucose production, the first expression is the fasting hyperglycemia.
On the other hand, increased concentrations of free fatty acids and their increased oxidation, result in reduced utilization of glucose in muscle, resulting in worsening of hyperglycemia.
In turn, the increased blood glucose tends to reduce tissue sensitivity to insulin, through the downstream control of GLUT-4.
(for type II diabetes have reduced insulin secretion is also required).
In individuals with the metabolic syndrome, insulin resistance and hyperinsulinemia coexist.
To identify the metabolic syndrome, it is important to note nell'anamnesi:
- Family history of obesity. Diabetes, hypertension, hyperlipidemia, gout, cardiovascular disease early;
- individual weight at birth (low birth weight = predictive of diabetes mellitus type II, macrosomia = predictor of metabolic syndrome);
- Evolution of the weight in childhood and during puberty;
- Lifestyle.
course, be investigated chemical correlates of the syndrome (impaired glucose tolerance, diabetes mellitus type II, hypertension, abnormal lipid metabolism and purine).
The first project involves minimizing the cardiovascular risk through the elimination of risk factors (eg smoking). We must then arrange to normalize the glucose metabolism, purine and lipid normalize pressure.
The weight reduction is accompanied by improvement of insulin resistance.
In particular, avoid alcohol and reduction of animal fat is effective central obesity.
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