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Further Lowering of Muscle Lipid Oxidative Capacity in Obese Subjects after Biliopancreatic Diversion

Endocrine-Metabolic Laboratory, (R.F., G.Mil., M.G., A.D.P., A.S., R.S., G.F., R.V.) Internal Medicine, Department of Medical and Surgical Sciences, University of Padova, 35128 Padova, Italy; and Department of Medicine, Catholic University (G.Min., M.M., A.V.G.), 8-00168 Rome, Italy

Address all correspondence and requests for reprints to: Dr. Roberto Vettor, Department of Medical and Surgical Sciences, University of Padova, via Ospedale 105, 35128 Padova, Italy. E-mail: roberto.vettor{at}unipd.it.

A reduced lipid oxidative capacity is considered a risk factor for the development of obesity, but a further impairment of lipid oxidative capacity is observed after weight loss. We aimed to define the mechanisms underlying this phenomenon in skeletal muscle and in particular to study the mitochondrial and peroxisomal lipid oxidative pathways. Thus we measured intramyocellular triglyceride content (IMTG) and the expression of genes of lipid oxidation [peroxisome proliferator-activated receptor-, carnitine palmitoyltransferase 1B, and acyl-coenzyme A (acyl-CoA) oxidase 1] and synthesis (acetyl-CoA carboxylase B) using RT-PCR analysis in muscle biopsies of morbidly obese patients before and after biliopancreatic diversion. Weight reduction significantly decreased IMTG while increasing insulin sensitivity, measured by euglycemic hyperinsulinemic clamp. Moreover, an increase in glucose and a decline in lipid oxidation, as assessed by respiratory chamber, were observed. Weight loss reduced the expression of peroxisome proliferator-activated receptor- (–46.7%), carnitine palmitoyltransferase 1B (–43.1%), acyl-CoA oxidase 1 (–37.8%), and acetyl-CoA carboxylase B (–48.7%). Our results indicate that a defect of both peroxisomal and mitochondrial oxidative pathways at the muscular level may contribute to the reduced fat oxidation in obese subjects after biliopancreatic diversion. They also suggest that a depression of the de novo lipogenesis may account for IMTG depletion.

This work was supported by grants from Ministero della Ricerca Scientifica e Tecnologica (no. 2001065883_003) and Ministero della Salute, Ricerca Finalizzata: OBEIR.

Abbreviations: ACAC, Acetyl-coenzyme A carboxylase; ACOX1, acyl-coenzyme A oxidase 1, palmitoyl; BPD, biliopancreatic diversion; BW, body weight; CoA, coenzyme A; CPT1, carnitine palmitoyltransferase 1; EE, energy expenditure; FFM, fat-free mass; FM, fat mass; IMTG, intramyocellular triglyceride content; NEFA, nonesterified fatty acid; PPAR, peroxisome proliferator-activated receptor-; SREBF, sterol regulatory element-binding factor; TBW, total body water.