Postabsorptive and insulin-stimulated energy homeostasis and leucine turnover in offspring of type 2 diabetic patients

Guido Lattuada, Lucia Piceni Sereni, Dora Ruggieri, Antonella Scollo, Stefano Benedini, Francesca Ragogna, Federica Costantino, Alberto Battezzati, Livio Luzi, Gianluca Perseghin

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15 Citations (Scopus)

Abstract

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. 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 [6,6-2H 2]glucose and [l-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.

Original languageEnglish
Pages (from-to)2716-2722
Number of pages7
JournalDiabetes Care
Volume27
Issue number11
DOIs
Publication statusPublished - Nov 2004

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Leucine
Homeostasis
Insulin
Glucose
Insulin Resistance
Parents
Proteins
Glutamine
Phenylalanine
Lipid Metabolism
Alanine
Fasting
Fatty Acids
X-Rays
Amino Acids

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Internal Medicine

Cite this

Postabsorptive and insulin-stimulated energy homeostasis and leucine turnover in offspring of type 2 diabetic patients. / Lattuada, Guido; Sereni, Lucia Piceni; Ruggieri, Dora; Scollo, Antonella; Benedini, Stefano; Ragogna, Francesca; Costantino, Federica; Battezzati, Alberto; Luzi, Livio; Perseghin, Gianluca.

In: Diabetes Care, Vol. 27, No. 11, 11.2004, p. 2716-2722.

Research output: Contribution to journalArticle

Lattuada, G, Sereni, LP, Ruggieri, D, Scollo, A, Benedini, S, Ragogna, F, Costantino, F, Battezzati, A, Luzi, L & Perseghin, G 2004, 'Postabsorptive and insulin-stimulated energy homeostasis and leucine turnover in offspring of type 2 diabetic patients', Diabetes Care, vol. 27, no. 11, pp. 2716-2722. https://doi.org/10.2337/diacare.27.11.2716
Lattuada, Guido ; Sereni, Lucia Piceni ; Ruggieri, Dora ; Scollo, Antonella ; Benedini, Stefano ; Ragogna, Francesca ; Costantino, Federica ; Battezzati, Alberto ; Luzi, Livio ; Perseghin, Gianluca. / Postabsorptive and insulin-stimulated energy homeostasis and leucine turnover in offspring of type 2 diabetic patients. In: Diabetes Care. 2004 ; Vol. 27, No. 11. pp. 2716-2722.
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abstract = "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. 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 [6,6-2H 2]glucose and [l-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.",
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T1 - Postabsorptive and insulin-stimulated energy homeostasis and leucine turnover in offspring of type 2 diabetic patients

AU - Lattuada, Guido

AU - Sereni, Lucia Piceni

AU - Ruggieri, Dora

AU - Scollo, Antonella

AU - Benedini, Stefano

AU - Ragogna, Francesca

AU - Costantino, Federica

AU - Battezzati, Alberto

AU - Luzi, Livio

AU - Perseghin, Gianluca

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N2 - 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. 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 [6,6-2H 2]glucose and [l-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.

AB - 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. 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 [6,6-2H 2]glucose and [l-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.

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