Avaliação das modificações metabolicas durante e apos o emagrecimento em pacientes portadores de obesidade classe III, submetidos a cirurgia de gastroplastia vertical com bandagem e derivação gastro-jejunal

AUTOR(ES)
DATA DE PUBLICAÇÃO

2002

RESUMO

Obesity has a high prevalence and an increasing incidence, being considered epidemic. It is characterized by hyperinsulinemia and insulin resistance, important early metabolic changes in the obese patient. The first has been reported as an independent cardiovascular risk factor. The mechanisms underlying hyperinsulinemia are not clear and it has been associated to a compensatory beta cell mechanism for insulin resistance. The pos-hepatic insulin delivery rate is a result of the rate of insulin secretion and of its metabolic clearance rate. The main sites of insulin resistance in the obese patient are the liver and the muscle. Both insulin action pathways, oxidative and non oxidative glucose utilization - NOGD, seem to be affected. These metabolic changes are more frequent in class III obese patients, responsible, in part, for the high mortality. Weight reduction improves metabolic and cardiovascular parameters, although it is not clear which amount of weight loss is necessary, neither which insulin effects are modified by this procedure. Bariatric surgery has been report as an efficient tool for the weight, reduction and maintain. A group of 13 class III obese patients (4M/9F; BMI=56.3±2.7 kg.m-2) and 13 lean subjects (5M/8F; BMI=22.4±0.5 kg.m-2) were submitted to a metabolic evaluation including euglycemic hyperinsulinemic clamp, oral glucose tolerance test (OGTT) and indirect calorimetry. The obese patients were submitted to a bariatric surgery (Capella?s technique) and the metabolic studies repeated after ~ 20 % of weight loss relative to their initial body weight (study II) and after weight stabilization (study III ? BMI=34.7±02.1 kg.m-2). Insulin secretion during fasting state and under insulin infusion during the euglycemic clamp was assessed using the C-peptide plasma measurements. It was higher in the obese in the first study (6 folders than control) and the decrease, after weight loss, was statistically significant even in the second study, with further reduction in the third study. The hyperinsulinemia was a result of insulin hyper-secretion since pos-hepatic metabolic clearance rate during the clamp was similar to that of the control group and did not change after weight loss. The insulin sensitivity was significantly impaired in the obese (study I: 19.7 ? 1.5 vs. 51.5 ? 2.4 umol/min.kgFFM; p<0.0001) and it increased significantly after weight loss (35.5 ? 3.7 umol/min.kgFFM; p<0.05 vs. CT and study I), but it was still lower than that of lean group (p<0.0001). The insulin stimulated glucose oxidation was lower in the obese group compared to lean and improved slightly after weight loss but it was still lower than that of the former group. The non oxidative glucose disposal was reduced in the obese group and after weight loss it improved significantly reaching levels similar to those of the lean group. Fasting protein oxidation and suppression of protein oxidation by insulin infusion were similar between lean and obese and they were not influenced significantly after weight reduction. The higher fasting lipid oxidation in obese did not change by weight reduction. The insulin infusion did not suppress the lipid oxidation in the first study, but after weight reduction a slight suppression, similar to that of the control group was observed. Insulin infusion under euglycemic conditions at steady state inhibited its own secretion in lean subjects but this insulin action was blunted in the obese group. After weight loss, inhibition of its own secretion was completely reversed to values very similar to those observed in lean controls (about 40% relative to fasting values). In summary, the rapid weight loss in obese class III, after surgery, induced a normalization of the insulin secretion and only an improvement of the insulin sensitivity, almost entirely dependent of glucose storage. The high lipid oxidation did not change with weight loss. The changes in insulin secretion and sensitivity induced by weight loss displayed different degrees and time courses

ASSUNTO(S)

metabolismo obesidade resistencia a insulina

ACESSO AO ARTIGO

Documentos Relacionados