This Article Full Text Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Spampinato, D. Articles by Frittitta, L. Search for Related Content PubMed PubMed Citation Articles by Spampinato, D. Articles by Frittitta, L.

Insulin/Insulin-Like Growth Factor I Hybrid Receptors Overexpression Is Not an Early Defect in Insulin-Resistant Subjects

Istituto di Medicina Interna, Endocrinologia e Malattie del Metabolismo, Ospedale Garibaldi, Università di Catania (D.S., G.P., R.V., L.F.), 95123 Catania; Clinica Chirurgica, Ospedale Vitt. Emanuele, Università di Catania (A.I.), 95123 Catania; and Divisione ed Unità di Ricerca di Endocrinologia, Istituto Scientifico Casa Sollievo della Sofferenza, San Giovanni Rotondo (V.T.), 71013 Foggia, Italy

Address correspondence and requests for reprints to: Lucia Frittitta, M.D., Endocrinologia, Ospedale Garibaldi, P.zza S. M. Gesù, 95123 Catania, Italy. E-mail segmeint{at}mbox.unict.it

Hybrid receptors (HRs), insulin receptor (IR)/insulin-like growth factor I receptor (IGF-I-R) heterodimers have been reported increased in skeletal muscle of obese and type 2 diabetic patients and to contribute to the patient insulin resistance. To investigate whether or not the increased expression of hybrid receptors is an early defect (probably genetic) of insulin resistance, we measured by specific enzyme-linked immunosorbent assays both IR, IGF-I-R, and HR content in skeletal muscle of healthy nonobese, nondiabetic subjects either insulin sensitive or insulin resistant, and also in patients with moderate obesity.

IR content was significantly reduced in insulin-resistant subjects both nonobese and obese, compared with insulin-sensitive subjects (2.32 ± 0.26, 2.36 ± 0.18, and 3.45 ± 0.42 ng/mg protein, respectively, P = 0.002). In contrast, IGF-I-R content was similar in the three groups. Muscle HR content was not different in insulin-sensitive vs. insulin-resistant subjects (both nonobese and obese) (4.90 ± 0.46, 4.69 ± 0.29, and 4.91 ± 0.25 ng/mg protein, respectively, P = not significant). These studies indicate that, in insulin-resistant subjects without diabetes or severe obesity, muscle IR content but not IGF-I-R or HR content is reduced. They do not suggest, therefore, a primary (genetic) role of increased HR as a cause of IR decrease and insulin resistance.

This article has been cited by other articles:

				K. Raile, J. Klammt, A. Schneider, A. Keller, S. Laue, R. Smith, R. Pfaffle, J. Kratzsch, E. Keller, and W. Kiess Clinical and Functional Characteristics of the Human Arg59Ter Insulin-Like Growth Factor I Receptor (IGF1R) Mutation: Implications for a Gene Dosage Effect of the Human IGF1R J. Clin. Endocrinol. Metab., June 1, 2006; 91(6): 2264 - 2271. [Abstract] [Full Text] [PDF]

				G. Pandini, F. Frasca, R. Mineo, L. Sciacca, R. Vigneri, and A. Belfiore Insulin/Insulin-like Growth Factor I Hybrid Receptors Have Different Biological Characteristics Depending on the Insulin Receptor Isoform Involved J. Biol. Chem., October 11, 2002; 277(42): 39684 - 39695. [Abstract] [Full Text] [PDF]

				J. Nakae, Y. Kido, and D. Accili Distinct and Overlapping Functions of Insulin and IGF-I Receptors Endocr. Rev., December 1, 2001; 22(6): 818 - 835. [Abstract] [Full Text] [PDF]