Plasma glucose concentration depends on rate of glucose appearing in circulation ( glucose appearance ) and rate of glucose removal from circulation ( glucose disappearance ). The circulating glucose is derived from three sources-- 1. Intestinal absorption from ingested food. 2. Glycogenolysis 3. Gluconeogenesis .
In non diabetic persons
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In fasting state the blood glucose is derived from glycogenolysis under the influence of glucagon. Basal ( stored ) levels of insulin control glucose disposal . Insulin' s role in suppressing gluconeogenesis and glycogenolysis is minimal due to low secretion of insulin in fasting insulin.
In fed state ( after food ) plasma glucose is derived from ingestion of nutrients. Glucagon secretion is suppressed through the action of ENDOGENOUS INSULIN secretion. This action is facilitated through paracrine route ( communication within the islet cells ). Additionally, insulin suppresses gluconeogenesis and glycogenolysis in the liver and promotes glucose disposal in periphery.
In Diabetic persons
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In fasting state plasma glucose is derived from glycogenolysis and gluconeogenesis under the influence of glucagon. EXOGENOUS Insulin influences the rate of peripheral glucose disappearance and because of its deficiency in portal circulation does not properly regulate the degree to which hepatic glycogenolysis and gluconeogenesis occurs.
After food in diabetics EXOGENOUS INSULIN is ineffective in suppressing glucagon secretion through physiological paracrine route. As a result the appearance of glucose in circulation exceeds the rate of glucose disappearance . THE NET EFFECT IS POST PRANDIAL HYPERGLYCEMIA.