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S Efendic

Publications and source records attributed to S Efendic.

204 records · Page 12Linked to original sources
PubMedDate not supplied

Overview of incretin hormones.

Incretins are hormones released by nutrients from the GI tract. They amplify glucose-induced insulin release. By raising circulating incretin levels, oral glucose provokes a higher insulin response than that resulting from intravenous glucose. The two most important incretin hormones are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). In patients with type 2 diabetes, the incretin effect is decreased, mainly due to loss of the GIP-regulated second phase of insulin secretion, and because of a decreased secretion of GLP-1. In addition to its insulinotropic effect, GLP-1 inhibits glucagon release, prolongs gastric emptying, and leads to decreases in body-weight, all of which explain the marked antidiabetogenic effect of this incretin hormone.

Amino Acid Sequence↗
PubMedDate not supplied

Insulin release in type 2 diabetes mellitus.

Impaired insulin response is a characteristic feature of Type 2 diabetes. Overt diabetes develops when beta-cells fail to release enough insulin to compensate for decreased insulin sensitivity. However, a subgroup of normal weight patients demonstrates a pronounced beta-cell secretory defect and a normal insulin sensitivity. The molecular basis behind the impaired insulin response in Type 2 diabetes is not clear. Our studies in two animal models of this disease (GK rat and ob/ob mouse) suggest that an impaired glucose metabolism may be a primary defect in the stimulus-secretion coupling in the beta-cells in Type 2 diabetes. In the GK rat, three major alterations in the islet metabolism of glucose have been demonstrated: 1) increased glucose utilization but unchanged glucose oxidation; 2) increased glucose cycling and 3) decreased activity of the glycerol phosphate shuttle. In ob/ob animals we have found an increased rate of glucose cycling. These derangements might result in an incomplete closure of ATP-sensitive K(+)-channels with a decreased insulin response as a consequence.

Animals↗
PubMedDate not supplied

Development of postoperative insulin resistance is associated with the magnitude of operation.

OBJECTIVE: To study the development of insulin resistance and changes in stress hormone concentrations in patients undergoing elective operations of different magnitude. DESIGN: Prospective open study. SETTING: University hospital, Sweden. SUBJECTS: 12 otherwise healthy patients, undergoing elective surgery for cholecystectomy (n = 6) and inguinal hernia repair (n = 6). INTERVENTIONS: Insulin sensitivity was measured by the normoglycaemic, hyperinsulinaemic glucose clamp technique before operation (control) and on the first postoperative day. MAIN OUTCOME MEASURE: Relative insulin sensitivity (compared with preoperative) on the day after each operation. Changes in stress hormone concentrations in relation to the relative change in insulin sensitivity. RESULTS: After hernia repair, mean (SEM) insulin sensitivity was reduced by 32 (4)%, p < 0.05 compared with baseline, and after open cholecystectomy by 56 (3)%, (p < 0.05). The difference between the two groups was highly significant (p < 0.01). The changes in concentrations of catecholamines, glucagon, cortisol and growth hormone after operation were only small, and did not correlate with the relative changes in insulin sensitivity. CONCLUSIONS: Insulin resistance develops even after a minor elective operation, (inguinal hernia repair). The degree of postoperative insulin resistance was more pronounced after open cholecystectomy. The alteration in insulin sensitivity could not be related to simultaneous changes in the hormones studied.

Catecholamines↗