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Sökning: WFRF:(Hagström Toft E)

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1.
  • Gustafsson, U O, et al. (författare)
  • Pre-operative carbohydrate loading may be used in type 2 diabetes patients
  • 2008
  • Ingår i: Acta Anaesthesiologica Scandinavica. - Malden, USA : Blackwell Publishing. - 0001-5172 .- 1399-6576. ; 52:7, s. 946-51
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Post-operative insulin resistance and hyperglycaemia are associated with an impaired outcome after surgery. Pre-operative oral carbohydrate loading (CHO) reduces post-operative insulin resistance with a reduced risk of hyperglycaemia during post-operative nutrition. Insulin-resistant diabetic patients have not been given CHO because the effects on pre-operative glycaemia and gastric emptying are unknown.Methods: Twenty-five patients (45-73 years) with type 2 diabetes [glycated haemoglobin (HbA1c) 6.2 +/- 0.2%, mean +/- SEM] and 10 healthy control subjects (45-72 years) were studied. A carbohydrate-rich drink (400 ml, 12.5%) was given with paracetamol 1.5 g for determination of gastric emptying.Results: Peak glucose was higher in diabetic patients than in healthy subjects (13.4 +/- 0.5 vs. 7.6 +/- 0.5 mM; P<0.01) and occurred later after intake (60 vs. 30 min; P<0.01). Glucose concentrations were back to baseline at 180 vs. 120 min in diabetic patients and healthy subjects, respectively (P<0.01). At 120 min, 10.9 +/- 0.7% and 13.3 +/- 1.2% of paracetamol remained in the stomach in diabetic patients and healthy, subjects respectively. Gastric half-emptying time (T50) occurred at 49.8 +/- 2.2 min in diabetics and at 58.6 +/- 3.7 min in healthy subjects (P<0.05). Neither peak glucose, glucose at 180 min, gastric T50, nor retention at 120 min differed between insulin (HbA1c 6.8 +/- 0.7%)- and non-insulin-treated (HbA1c 5.6 +/- 0.4%) patients.Conclusions: Type 2 diabetic patients showed no signs of delayed gastric emptying, suggesting that a carbohydrate-rich drink may be safely administrated 180 min before anaesthesia without risk of hyperglycaemia or aspiration pre-operatively.
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3.
  • Hagström-Toft, E, et al. (författare)
  • Role of phosphodiesterase III in the antilipolytic effect of insulin in vivo
  • 1995
  • Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 44:10, s. 1170-5
  • Tidskriftsartikel (refereegranskat)abstract
    • The effect of three types of phosphodiesterase (PDE) inhibitors on in vivo antilipolysis was investigated in healthy subjects using a 2-h euglycemic, hyperinsulinemic (40 mU · m-2·min) clamp together with microdialysis of abdominal subcutaneous adipose tissue. During hyperinsulinemia (∼330 pmol/l), the circulating glycerol concentration was reduced to ∼50% of the basal level of 53.2 ± 3.6 μmol/l, indicating an antilipolytic effect. The decrease in adipose tissue dialysate glycerol, which mirrors the change in interstitial glycerol concentration, was about 40% during hyperinsulinemia when Ringer's solution alone was perfused. Local perfusion with a selective PDE IV inhibitor, rolipram (10−4) mol/l), did not influence the insulin-induced decrease in dialysate glycerol (F = 0.8 vs. perfusion with Ringer's solution by two-factor analysis of variance [ANOVA]), although rolipram increased the dialysate glycerol level by 144 ± 7% of the baseline value. However, local perfusion with a selective PDE III inhibitor, amrinone (10−3) mol/l), or a nonselective PDE inhibitor, theophylline (10−2) mol/l), abolished the ability of insulin to lower dialysate glycerol (F = 16.5, P &lt; 0.01 and F = 8.5, P &lt; 0.01, respectively, as compared with perfusion with Ringer's solution). The findings could not be explained by changes in the local blood flow (as measured by a microdialysis–ethanol escape technique), which was not affected by hyperinsulinemia in the presence or the absence of PDE inhibitors in the dialysis solvent. We conclude that PDEs play an important role in mediating the antilipolytic effect of insulin in vivo and that PDE III is the dominant isoenzyme modulating this effect.
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4.
  • Hamrin, Kerstin, et al. (författare)
  • Prolonged Exercise-Induced Stimulation of Skeletal Muscle Glucose Uptake Is due to Sustained Increases in Tissue Perfusion and Fractional Glucose Extraction
  • 2011
  • Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 96:4, s. 1085-1092
  • Tidskriftsartikel (refereegranskat)abstract
    • Context: The mechanisms behind the positive effects of physical activity on glucose metabolism in skeletal muscle and the time course of the effects need to be more elucidated. Objective: The aim was to examine the prolonged effects of an acute bout of one-legged exercise on local skeletal muscle glucose utilization and tissue perfusion. Design and Setting: Interstitial glucose concentration, local tissue perfusion, glucose uptake, and effects of insulin infusion were studied 12 h after an acute bout of exercise and without prior exercise. Participants: Ten healthy subjects, five women and five men, participated in the study. Intervention: Microdialysis measurements, (133)Xe clearance, and a 2-h hyperinsulinemic euglycemic clamp were performed on two occasions. Main Outcome Measures: We measured interstitial glucose concentration and tissue perfusion in the quadriceps femoris muscle of both legs. Results: Tissue perfusion (3.3 +/- 0.6 ml x 100 g(-1) x min(-1) vs. 1.4 +/- 0.2 ml x 100 g(-1) x min(-1); P = 0.007) and basal glucose uptake (2.3 +/- 0.5 mu mol x 100 g(-1) x min(-1) vs. 0.9 +/- 0.2 mu mol x 100 g(-1) x min(-1); P = 0.006) were increased in the leg that had exercised compared to the resting leg; the findings in the resting leg were comparable to those in the control experiment without prior exercise. The relative effect of insulin on fractional skeletal muscle glucose uptake was the same in all experimental settings, and insulin did not affect tissue perfusion. Conclusions: The prolonged stimulatory effect of physical exercise on skeletal muscle glucose uptake was mediated via vascular effects combined with an increase in basal glucose transport independent of enhancement of insulin responses.
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