The clinical and epidemiological experience has demonstrated an indisputable association between obesity and diabetes mellitus not insulino salesman and intolerance to theglucose. Moderate degrees of obesity it can raise the risk of diabetes up to 10 times and the risk grows while major is the intensity of the obesity. Also it relates to the type of obesity, as for thedistribution of the corporal fat, being major in obesity of type toracoabdominal.
The studies of sensibility to the insulin and of clamp euglicémico are concordant in demonstrating that the obesitygenerates a resistance to the insulin. This owes to a fault of action insulínica, specially to level postrreceptor, demonstrated specially in the skeletal muscle. The resistance to the insulin generates acompensating hiperinsulinemia, with sobreestímulo of the cells thread of the pancreas and also a reduction of the number of peripheral recipients to the insulin (phenomenon of down regulation). If thisconjugates with a fault genetic or acquired of secretion insulínica, an intolerance appears to the glucose and later a diabetes. On the other hand, the hyperblood sugar of fasting is a consequence ofa major hepatic production of glucose that is not sufficiently inhibida for the insulin. The major liberation of oily free acids from the adipose fabric that the obese individual has (phenomenon thatenclosed is more accentuated in the obesity of abdominal and visceral distribution) stimulates the hepatic neoglucogenia, which uses substrata of 3 carbons for his production.
In synthesis, in thepathogeny of the diabetes mellitus not insulino salesman, who is the most frequent form of primary diabetes, the obesity is the most relevant environmental and possible factor of anticipating andmodifying. In turn, the reduction of weight of an obese diabetic improves glaringly his metabolic condition, facilitating the control of the blood sugar and of the dislipidemia on having reduced the...
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