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Sökning: WFRF:(Gutniak M)

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  • Ahren, B, et al. (författare)
  • No correlation between insulin and islet amyloid polypeptide after stimulation with glucagon-like peptide-1 in type 2 diabetes
  • 1997
  • Ingår i: European journal of endocrinology. - : Oxford University Press (OUP). - 0804-4643 .- 1479-683X. ; 137:6, s. 643-649
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: To examine whether glucagon-like peptide-1 (GLP-1), which has been suggested as a new therapeutic agent in type 2 diabetes, affects circulating islet amyloid polypeptide (IAPP), a B-cell peptide of potential importance for diabetes pathophysiology. DESIGN: GLP-1 was administered in a buccal tablet (400 micrograms) to seven healthy subjects and nine subjects with type 2 diabetes. Serum IAPP and insulin levels were measured before and after GLP-1 administration. RESULTS: In the fasting state, serum IAPP was 4.1 +/- 0.3 pmol/l in the controls vs 9.8 +/- 0.9 pmol/l in the subjects with type 2 diabetes (P < 0.001). IAPP correlated with insulin only in controls (r = 0.74, P = 0.002) but not in type 2 diabetes (r = 0.26, NS). At 15 min after GLP-1, circulating IAPP increased to (6.0 +/- 0.5 pmol/l in controls P = 0.009) and to 13.8 +/- 1.2 pmol/l in type 2 diabetes (P = 0.021). In both groups, serum insulin increased and blood glucose decreased compared with placebo. In controls serum IAPP increased in parallel with insulin (r = 0.79, P = 0.032), whereas in type 2 diabetes the increase in IAPP did not correlate with the increase in insulin. CONCLUSION: Type 2 diabetes is associated with elevated circulating IAPP; GLP-1stimulates IAPP secretion both in healthy human subjects and in type 2 diabetes; IAPP secretion correlates with insulin secretion only in healthy subjects and not in type 2 diabetes.
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  • Gutniak, M, et al. (författare)
  • GLP-1 tablet in NIDDM
  • 1997
  • Ingår i: DIABETOLOGIA. - 0012-186X. ; 40, s. 172-172
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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  • Ljungqvist, Olle, 1954-, et al. (författare)
  • Glucose infusion instead of preoperative fasting reduces postoperative insulin resistance
  • 1994
  • Ingår i: Journal of the American College of Surgeons. - 1072-7515 .- 1879-1190. ; , s. 329-336
  • Tidskriftsartikel (refereegranskat)abstract
    • In severe catabolic states, such as burn injury, sepsis and accidental injury, a state of marked insulin resistance is encountered. Insulin resistance is also present after elective surgical treatment, more pronounced with increasingly greater magnitude of operation performed. Results of recent animal experiments have shown that even short periods of food deprivation, reducing carbohydrate reserves, alter responses to stress. This notion resulted in our questioning the rationale of carbohydrate depletion associated with overnight preoperative fasting. Twelve patients undergoing elective open cholecystectomy were randomly given no infusion (control group) or 5 milligrams per kilogram per minute of glucose infusion (glucose group) during preoperative overnight fasting. Insulin sensitivity (M value, milligram per kilogram per minute) was determined using the hyperinsulinemic normoglycemic clamp (plasma insulin level, 65 microunits per milliliter and blood glucose level, 4.5 millimoles per liter) before and the first postoperative day. Preoperative insulin sensitivity was similar in the two groups. Postoperatively, M values decreased by 55±3 percent (control group) and by 32±5 percent (glucose group) (p<0.01). Plasma levels of insulin, c- peptide, glucagon, growth hormone, catecholamines and cortisol in connection with clamps were similar in both groups preoperatively and postoperatively. The present results indicate that active preoperative carbohydrate preservation may improve postoperative metabolism because postoperative occurrence of insulin resistance was reduced with preoperative glucose infusion.
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