By Bernard Testa, Urs A. Meyer
Quantity 27, the 1st thematic quantity within the sequence, presents an outline of current wisdom in regards to the pharmacological and scientific points of antidiabetic medicines. It goals to stimulate extra attention of attainable ideas within the improvement of latest antidiabetic medications.
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Extra resources for Antidiabetic Agents: Recent Advances in their Molecular and Clinical Pharmacology, Volume 27
HGP still remains within normal range because of the suppressive effect of hyperglycaemia. Tissue glucose uptake, however, is markedly reduced. In diabetic subjects, the glucose uptake of muscle tissue is delayed and retarded. While in control subjects muscle glucose uptake accounts for 75% of the total glucose uptake, normal-weight NIDDM patients have a 50% reduction in insulin-mediated peripheral glucose uptake. Thus in the early stages of NIDDM, the site of insulin resistance is not at the level of the liver.
At that time, the early phase of insulin secretion tends to be reduced, priming the insulin target tissues, primarily the liver, that are responsible for the maintenance of glucose homoeostasis. As the first phase of insulin secretion is impaired, the resulting postprandial hyperglycaemia initiates a hyperinsulinaemia, returning blood glucose to normal. In NIDDM, with a fasting glucose concentration up to 120mg/100 ml, insulin secretion is increased to twice normal with a fasting glucose concentration of 80 mg/100 ml.
With a further increase in glucose to more than 160mg/100ml the insulin response becomes 14 ANTIDIABETIC AGENTS insulinopenic, and markedly reduced when basal glucose exceeds 200220 mg/100 ml. e. suppression of hepatic glucose production (HGP), stimulation of splanchnic (hepatic) glucose uptake and peripheral uptake. The tissues responsible for the insulin resistance in the basal state are quite different from those responsible for the insulin resistance in the insulin-stimulated (hyperinsulinaemic) state.