Bileopancreatic diversion with duodenal switch lowers both early and late phases of glucose, insulin and proinsulin responses after meal.
ABSTRACT Hyperproinsulinemia is associated with obesity and type 2 diabetes. We explored the after-meal dynamics of proinsulin and insulin and postprandial effects on glucose and lipids in patients treated with bileopancreatic diversion with duodenal switch (BPD-DS) surgery compared with normal-weight controls [body mass index (BMI)+/-SD, 23.2 +/- 2.4 kg/m(2)].
Ten previously morbidly obese (BMI+/-SD, 53.5 +/- 3.8 kg/m(2)) patients free from diabetes who had undergone BPD-DS (BMI+/-SD, 29.0 +/- 5.2 kg/m(2)) 2 years earlier were recruited. A standardised meal (2400 kJ) was ingested, and glucose, proinsulin, insulin, free fatty acids and triglycerides (TGs) were determined during 180 min. Follow-up characteristics yearly on glucose, lipids, creatinine and uric acid over 3 years after BPD-DS are presented.
Fasting glucose and insulin were lower, 0.4 mmol/L and 4.6 pmol/L, respectively, in the BPD-DS group despite higher BMI. Fasting proinsulin was similar in both groups. Postprandial area under the curve (AUC) for glucose, proinsulin and insulin did not differ between the two groups (p = 0.106-734). Postprandial changes in glucose, proinsulin and insulin were essentially similar but absolute concentrations of proinsulin and insulin were lower in the later phases in the BPD-DS group (p = 0.052-0.001). Postprandial AUC for TGs was lower in the BPD-DS group (p = 0.005). Postprandial changes in TGs were lowered in the intermediate phase (p = 0.07-0.08) and in the late phase (0.002). Follow-up data showed markedly lowered creatinine and uric acid after BPD-DS.
BPD-DS surgery induces a large weight loss and lowers, close to normal, postprandial responses of glucose, proinsulin and insulin but with marked lowering of TGs.
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ABSTRACT: Insulin-mediated glucose metabolism (euglycemic insulin clamp at plasma insulin concentration of 100 microU/mL) and glucose-stimulated insulin secretion (hyperglycemic clamp) were examined in 42 obese subjects (ideal body weight [IBW], 158 +/- 4%) with normal glucose tolerance and in 36 normal weight (IBW, 102% +/- 1%) age-matched controls. In 10 obese and eight control subjects, insulin was infused at six rates to increase plasma insulin concentration by approximately 10, 20, 40, 80, 2,000, and 20,000 microU/mL. Throughout the physiologic range of plasma insulin concentrations, both the increase in total body glucose uptake and the suppression of hepatic glucose production (HGP) were significantly impaired in the obese group (P less than .001 to .01). At the two highest plasma insulin concentrations, inhibition of HGP and the stimulation of glucose disposal were similar in both the obese and control groups. Insulin secretion during the hyperglycemic (+/- 125 mg/dL) clamp was twofold greater in obese subjects than in controls (P less than .01) and was inversely related to the rate of glucose uptake during the insulin clamp (r = -.438, P less than .05), but was still unable to normalize glucose disposal (P less than .05). In conclusion, our results indicate that insulin resistance is a common accompaniment of obesity and can be overcome at supraphysiological insulin concentrations. Both in the basal state and following a hyperglycemic stimulus obese people display hyperinsulinemia, which correlates with the degree of insulin resistance. However, endogenous hyperinsulinemia fails to fully compensate for the insulin resistance.Metabolism 06/1990; 39(5):452-9. · 3.10 Impact Factor
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ABSTRACT: Currently, there are no data in the literature regarding the pathophysiological mechanisms involved in the rapid resolution of type 2 diabetes after bariatric surgery, which was reported as an additional benefit of the surgical treatment for morbid obesity. With this question in mind, insulin sensitivity, using euglycemic-hyperinsulinemic clamp, and insulin secretion, by the C-peptide deconvolution method after an oral glucose load, together with the circulating levels of intestinal incretins and adipocytokines, have been studied in 10 diabetic morbidly obese subjects before and shortly after biliopancreatic diversion (BPD) to avoid the weight loss interference. Diabetes disappeared 1 week after BPD, while insulin sensitivity (32.96 +/- 4.3 to 65.73 +/- 3.22 mumol . kg fat-free mass(-1) . min(-1) at 1 week and to 64.73 +/- 3.42 mumol . kg fat-free mass(-1) . min(-1) at 4 weeks; P < 0.0001) was fully normalized. Fasting insulin secretion rate (148.16 +/- 20.07 to 70.0.2 +/- 8.14 and 83.24 +/- 8.28 pmol/min per m(2); P < 0.01) and total insulin output (43.76 +/- 4.07 to 25.48 +/- 1.69 and 30.50 +/- 4.71 nmol/m(2); P < 0.05) dramatically decreased, while a significant improvement in beta-cell glucose sensitivity was observed. Both fasting and glucose-stimulated gastrointestinal polypeptide (13.40 +/- 1.99 to 6.58 +/- 1.72 pmol/l at 1 week and 5.83 +/- 0.80 pmol/l at 4 weeks) significantly (P < 0.001) decreased, while glucagon-like peptide 1 significantly increased (1.75 +/- 0.16 to 3.42 +/- 0.41 pmol/l at 1 week and 3.62 +/- 0.21 pmol/l at 4 weeks; P < 0.001). BPD determines a prompt reversibility of type 2 diabetes by normalizing peripheral insulin sensitivity and enhancing beta-cell sensitivity to glucose, these changes occurring very early after the operation. This operation may affect the enteroinsular axis function by diverting nutrients away from the proximal gastrointestinal tract and by delivering incompletely digested nutrients to the ileum.Diabetes 08/2006; 55(7):2025-31. · 7.90 Impact Factor
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ABSTRACT: The objective of this study was to evaluate changes in resting energy expenditure (REE), body composition and metabolic parameters, and to investigate predictors of the results in seriously obese patients after Roux-en-Y gastric bypass (RYGBP). 31 patients (BMI 44.4 +/- 4.8 kg/m2; 27 female, 4 male; 37.3 +/- 11.1 y) were evaluated at baseline and 6 months after RYGBP. Weight, REE, waist circumference (WC), fat mass (FM) and fat-free mass (FFM), physical activity, food intake, fasting glucose (GLU), insulin (INS), HOMA-IR and lipid concentrations were measured. At 6 months, percentage of weight loss (%WL) was 29.0 +/- 4.4% and percentage of excess weight loss was (%EWL) 59.7 +/- 12.3%. FM loss corresponded to 77.1 +/- 12.2% of the weight loss. REE decreased from 33.4 +/- 4.1 to 30.1 +/- 2.6 kcal/kg FFM (P<0.05). Significant decreases (P<0.001) were observed in GLU, INS, HOMA-IR, LDL-cholesterol and triglycerides. %EWL was correlated with baseline INS (r=0.44; P=0.014), baseline HOMA (r=0.43; P=0.017), change in %FM (r=0.67; P<0.001) and change in WC (r=0.5; P<0.01). Decrease in REE/FFM (%) was positively correlated with baseline REE/FFM% (r=0.51; P<0.005) and change in %FM (r=0.69; P<0.001). Initial REE/FFM, baseline energy balance and FM change explain 90% of REE/FFM decrease. RYGBP was an effective procedure to induce significant weight loss, fat mass loss and improvement in metabolic parameters in the short term. Metabolic adaptation was not related to FFM wasting but to a higher baseline REE. Fasting hyperinsulinemia was the best single predictor of weight loss after RYGBP.Obesity Surgery 05/2007; 17(5):608-16. · 3.10 Impact Factor