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Diabetes Care 27:2716-2722, 2004
© 2004 by the American Diabetes Association, Inc.

Metabolic Syndrome/Insulin Resistance Syndrome/Pre-Diabetes
Original Article

Postabsorptive and Insulin-Stimulated Energy Homeostasis and Leucine Turnover in Offspring of Type 2 Diabetic Patients

Guido Lattuada, PHD1, Lucia Piceni Sereni, MD1, Dora Ruggieri, PHD1, Antonella Scollo, RN1, Stefano Benedini, MD, PHD1, Francesca Ragogna, PHD1, Federica Costantino, PHD1, Alberto Battezzati, MD, PHD1,2, Livio Luzi, MD1,2,3,4 and Gianluca Perseghin, MD1,3

1 Internal Medicine, Section of Nutrition/Metabolism, Istituto Scientifico H San Raffaele, Milan, Italy
2 International Center for the Assessment of Nutritional Status, Milan, Italy
3 Unit of Clinical Spectroscopy, Istituto Scientifico H San Raffaele, Milan Italy
4 Faculty of Exercise Sciences, Università degli Studi di Milano, Milan, Italy

Address correspondence and reprint requests to Gianluca Perseghin, MD, Istituto Scientifico H San Raffaele, Internal Medicine, Section of Nutrition/Metabolism & Unit of Clinical Spectroscopy via Olgettina 60, 20132, Milan, Italy. E-mail: perseghin.gianluca{at}hsr.it

OBJECTIVE—This study was performed to ascertain whether insulin resistance with respect to protein metabolism is an additional primary metabolic abnormality affecting insulin-resistant offspring of type 2 diabetic parents, along with insulin resistance with respect to glucose and lipid metabolism.

RESEARCH DESIGN AND METHODS—We studied 18 young, nonobese offspring of type 2 diabetic parents and 27 healthy matched (by means of dual-energy X-ray absorption) individuals with the bolus plus continuous infusion of [6,6-2H2]glucose and [1-13C]leucine in combination with the insulin clamp (40 mU · m–2 · min–1).

RESULTS—Fasting plasma leucine, phenylalanine, alanine, and glutamine concentrations, as well as the glucose and leucine turnover (reciprocal pool model: 155 ± 10 vs. 165 ± 5 µmol · kg lean body mass–1 · h–1 in offspring of type 2 diabetic patients and healthy matched individuals, respectively), were also not different. During the clamp, glucose turnover rates were significantly reduced in offspring of type 2 diabetic patients (7.1 ± 0.5) in comparison with healthy matched individuals (9.9 ± 0.6 mg · kg lean body mass–1 · min–1; P < 0.01). Also, the suppression of leucine turnover was impaired in offspring of type 2 diabetic patients (12 ± 1%) in comparison with healthy matched individuals (17 ± 1%; P = 0.04) and correlated with the degree of the impairment of insulin-stimulated glucose metabolism (R2 = 0.13; P = 0.02).

CONCLUSIONS—Nonobese, nondiabetic, insulin-resistant offspring of type 2 diabetic patients were characterized by an impairment of insulin-dependent suppression of protein breakdown, which was proportional to the impairment of glucose metabolism. These results demonstrate that in humans, a primary in vivo impairment of insulin action affects glucose and fatty acid metabolism as previously shown and also protein/amino acid metabolism.

Abbreviations: ELF, endogenous leucine flux • FFA, free fatty acid • REE, resting energy expenditure • {alpha}-TNF-R2, {alpha}-tumor necrosis factor receptor-2


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