Monitoring Of Blood Sugar

Posted Mar 12, 2009 by Spill / comments 0 comments / Print / Font Size Decrease font size Increase font size

Read about the beginnings of monitoring blood sugar.

One plausible way for the body to regulate food intake would be through the level of glucose (blood sugar) in the circulatory system, since most foods are at least partially reduced to glucose after digestion. Jean Mayer (1953) proposed that the changing level of glucose is monitored by "gluocostats" in the brain. The mechanism has to be a fairly complex one, though-not one that simply equates hunger with low glucose levels and satiety with high levels. Diabetics have elevated glucose levels, yet they tend to eat more not less than healthy people.

The mechanism postulated by Mayer would keep track of the rate at which glucose is being used by the body's cells; A low rate would produce hunger! a Nigh rate satiety. The rate can be measured (in the laboratory and, theoretically, in the body) by comparing the amount of glucose in the outgoing blood in the arteries with that in the incoming blood in the veins. Mayer found that the difference between these two measurements was largest a little while after a big meal then gradually grew smaller. Subjects reports of hunger coincided with the times when the difference was minimal. According to this theory, diabetics feel hungry because they have a lot of glucose in both arterial and venous blood so the difference is small. Similarly, injections of insulin, which lower glucose levels in both arterial and venous blood, also produce hunger. Nondiabetic rats given daily injections of insulin overeat and become fat.

There apparently are other subspaces in the blood besides glucose that help to regulate intake of food. If blood from a satiated rat is transfused into a hungry one, the hungry rat eats much less than usual. Transfusions in the opposite direction, however, have no effect: The satiated rat does not begin to eat again after receiving blood from a hungry animal (Davis Gallagher, & Ladlove, 1967). One candidate for this mysterious ''satiety factor'' is a hormone called cholecysokinin which is produced by the small intestine soon after a meal. When this hormone is injected into hungry animals it temporarily inhibits eating (Gibbs. Young, & Smith, 1973).

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