[Decreased first-phase secretion of insulin may play a role in the development of insulin resistance].
Decreased first-phase secretion of insulin may play a role in the development of insulin resistance. In the development of type 2 diabetes an abnormal function of the beta-cells and insulin resistance of liver, fat cells and muscle play the main role. An early sign of beta-cell damage can be the loss of first-phase insulin response. This is supposed to precede the development of insulin resistance. Decrease of first-phase secretion of insulin can induce early postprandial hyperglycaemia and hypertriglyceridaemia damaging endothelium of precapillary arterioles of the nutritive capillaries. Insulin-induced endothelium-dependent dilation of these arterioles is inhibited by high glucose and triglyceride levels preventing metabolic effect of insulin on the parenchymal cells surrounded by nutritive capillaries and leading this way to insulin resistance. Second-phase hyperinsulinaemia develops in the impaired glucose tolerance. With the progression of the disease into the type 2 diabetes, insulin secretion decreases in the second-phase, as well. Because of decrease of first-phase insulin secretion in type 2 diabetic patients, early insulin therapy could be a choice of treatment in type 2 diabetes. Results of the UKPDS suggest that insulin-treated type 2 diabetic patients are longer in the near-euglycaemic state compared to those treated by oral hypoglycaemic agents. Recent data support that early insulin therapy of type 2 diabetic patients retains their own insulin secretion capacity and results in lower haemoglobin A1c. A comparison of before-meal rapid-acting insulin analogue and bedtime NPH insulin regimens verified that rapid-acting insulin analogue decreased haemoglobin A1c compared to NPH insulin treatment in type 2 diabetes. On the basis of these data arises the possibility of the change of the attitude "Oh no, not insulin in type 2 diabetes" to the "early rapid-acting insulin analogue treatment" of these patients.
Wittmann
István
I
Pécsi Tudományegyetem Altalános Orvostudományi Kar, II. Belgyógyászati Klinika és Nephrologiai Centrum, Pécs. istvan.wittmann@aok.pte.hu
Soltész
Gyula
G
Jermendy
György
G
Nagy
Judit
J
D000818:Animals; D001160:Arterioles / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy / Q000378:metabolism*; D018450:Disease Progression; D004334:Drug Administration Schedule; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000378:metabolism*; D015228:Hypertriglyceridemia / Q000097:blood / Q000378:metabolism*; D007328:Insulin / Q000008:administration & dosage / Q000378:metabolism*; D007333:Insulin Resistance; D000078790:Insulin Secretion; D009569:Nitric Oxide / Q000378:metabolism; D016035:Pancreas Transplantation / Q000009:adverse effects; D019518:Postprandial Period
D007328:Insulin; D009569:Nitric Oxide