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 language | English |
|---|---|
| Pages (from-to) | 2716-2722 |
| Number of pages | 7 |
| Journal | Diabetes Care |
| Volume | 27 |
| Issue number | 11 |
| DOIs | |
| Publication status | Published - Nov 2004 |
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ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Internal Medicine
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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 journal › Article
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TY - JOUR
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
PY - 2004/11
Y1 - 2004/11
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.
UR - http://www.scopus.com/inward/record.url?scp=7444247829&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=7444247829&partnerID=8YFLogxK
U2 - 10.2337/diacare.27.11.2716
DO - 10.2337/diacare.27.11.2716
M3 - Article
C2 - 15505010
AN - SCOPUS:7444247829
VL - 27
SP - 2716
EP - 2722
JO - Diabetes Care
JF - Diabetes Care
SN - 1935-5548
IS - 11
ER -