Decreased sensitivity to insulin-like growth factor I in Turner's syndrome: a study of monocytes and T lymphocytes
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Turner's syndrome is characterized, amongst other things, by growth retardation with high serum levels of insulin-like growth factor 1 (IGF-I) in relation to growth, by a tendency to autoimmune disease and by insulin resistance with hyperlipidaemia. Assuming a role for IGF-I subresponsiveness in the last two features, the present study was designed to evaluate in patients with Turner's syndrome their monocyte/macrophage response to growth hormone (GH) and to IGF-I with respect to low-density lipoprotein (LDL) degradation and to the monocyte-dependent lymphocyte proliferation. Nineteen patients with Turner's syndrome and puberty-matched control subjects were studied. Monocytes were isolated from the blood of the patients and the control group, and cultured to develop into macrophages. The cells were then incubated with 125I-labelled LDL (25 micrograms of protein mL-1) in the absence or presence of 50 ng mL-1 IGF-I or GH, and cellular lipoprotein degradation was determined. GH and IGF-I effects on T-cell proliferation were measured in autologous mixed lymphocyte reaction Monocytes/macrophages degradation of LDL was lower in Turner's syndrome patients than in control subjects (P < 0.05). IGF-I stimulated LDL degradation by 42 +/- 8% in the control subjects and by only 16 +/- 7% in Turner's syndrome patients (P < 0.05). Control lymphocyte proliferation in AMLR was significantly augmented by 50-100 ng mL-1 GH or IGF-I. Lymphocytes derived from peripheral blood of Turner's syndrome patients remained almost unaffected by either GH or IGF-I. Measurement of IL-2 secretion by purified blastoid T lymphocytes-I. revealed a significant augmentation by 100 ng mL-1 GH and by 50-100 ng mL-1 IGF-I in control subjects, and almost no response in Turner's0 ng syndrome. Turner's syndrome is associated with decreased sensitivity of peripheral blood mononuclear cells to GH and to IGF-I, as is evident by the reduction in LDL degradation, monocyte-stimulated T-lymphocyte proliferation and IL-2 secretion by blastoid T cells.
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Perturbations in GH and IGF-I physiology, including IGF-I resistance and estrogen deficiency, may also contribute to impaired linear growth.
“However, perturbations in GH and insulin-like growth factor-I (IGF-I) physiology,146,147 including resistance to IGF-I,148-150 and estrogen deficiency151 may also contribute to impaired linear growth.”
From Clinical practice guidelines for the care of girls and women with Turner syndrome. (2024) · cites this paper as [149]
Multiple lines of evidence have demonstrated relative IGF-I resistance in girls with TS.
“multiple lines of evidence have demonstrated relative IGF-I resistance in girls with TS.148-151,162”
From Clinical practice guidelines for the care of girls and women with Turner syndrome. (2024) · cites this paper as [149]
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- Stanescu V, Stanescu R, Szirmai JA. Microchemical analysis of human tibial growth cartilage in various forms of dwarfism. Acta Endocrinol 1972;69:659-88.
- Almquist S, Lindsten J, Lindvall N. Linear growth, sulphation factor activity and chromosome constitution in 22 subjects with Turner syndrome. Acta Endocrinol 1962;42:168-86.
- Ranke MB, Blum WF, Haug F. Growth hormone, somatomedin levels and growth regulation in Turner's syndrome. Acta Endocrinol 1987;118:305-13.
- Saenger P, Schwartz E, Wiedemann E, Levine LS, Tsai M, New MI. The interaction of growth hormone, somatomedin and estrogen in patients with Turner's syndrome. Acta Endocrinol 1976;81:9-18.
- Bergmann P, Valsamis J, Van Perborgh J, De Schepper J, Van Vliet G. Comparative study of the changes in insulin-like growth factor-I, precollagen-III N-terminal extension peptide, bone Gla-protein, and bone mineral content in children with Turner's syndrome treated with recombinant growth hormone. J Clin Endocrinol Metab 1990;71:1461-7.
- Hochberg Z, Hertz P, Maor G, Oiknine J, Aviram M. Growth hormone and insulin like growth factor-I increase macrophage uptake and degradation of low density lipoprotein. Endocrinology 1992;131:430-5. 546
- HOCHBERG et al. ᭧ 1997 Blackwell Science Ltd, European Journal of Clinical Investigation, 27, 543-547 Figure 3. IL-2 activity in Turner's syndrome patients and control subjects. Blastoid T cells were incubated with PHA (blank), GH (diagonal) or IGF-I (cross-hatched), and IL-2 activity was measured in the culture medium.
- Raviv D. The influence of recombinant growth hormone and insulin-like growth factor-I on in vitro immune function: regulation of T-cell proliferation stimulated by MHC-2 antigens and mitogens. Research thesis, Technion-Israel Institute of Technology, 1990.
- Pollack S, Raviv D, Etzioni A, Hochberg Z. Enhancement of in vitro IL-2 secretion by rGH: direct and indirect effect on activated T- cells. Cytokine 1991;3:467.
- Aviram M. Plasma lipoprotein separation by discontinuous density lipoprotein gradient ultracentrifugation in hyperlipoproteinemic patients. Biochem Med 1983;30:111-18.
- Aviram M, Keidar S, Rosenblat M, Brook GJ. Reduced uptake of cholesterol esterase-modified low density lipoprotein by macrophages. J Biol Chem 1991;266:11567-74.
- Brown MS, Goldstein JL. A receptor mediated pathway for cholesterol. Science 1986;232:34-9.
- Smolen SJ, Chused MT, Novotny AE, Steinberg DA. The human autologous mixed lymphocyte reaction. J Immunol 1982;129: 1050-3.
- Gillis S, Ferm MM, Ou W, Smith AK, Janeway AC. T-cell growth factor: parameter of production and a quantitation microassay for activity. J Immunol 1978;120:2027-32.
- Aviram M. Low density lipoprotein modification be cholesterol oxidase induces enhanced uptake and cholesterol accumulation in cells. J Biol Chem 1988;267:218-25.
- Steinbrecher UP, Zhang H, Laugheed M. Role of oxidatively modified LDL in atherosclerosis. Free Rad Biol Med 1990;9:155- 68.
- Berliner JA, Navab M, Fogelman AM et al. Atherosclerosis: basic mechanisms oxidation, inflammation and genetics. Circulation 1995;91:2488-96.
- Steinberg D, Parthasarathy S, Carew TE, Khoo JC, Witztum JL. Beyond cholesterol: modification of low-density lipoprotein that increase its atherogenicity. N Engl J Med 1989;320:915-24.
- Rosenfeld R, Dollar LA, Hintz RL, Conover C. Normal somato- medin-C/insulin-like growth factor I binding and action in cultured human fibroblasts from Turner syndrome. Acta Endocrinol 1983;104:502-9.
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Clinical practice guidelines for the care of girls and women with Turner syndrome.
Gravholt, C. H., Andersen, N. H., Christin-Maitre, S., Davis, S. M., Duijnhouwer, A., Gawlik, A., Maciel-Guerra, A. T., Gutmark-Little, I., Fleischer, K., Hong, D., et al. (2024) · European Journal of Endocrinology · doi:10.1093/ejendo/lvae050 · Cited by 224 · see citing works
- Authors
- Hochberg, Z., Aviram, M., Rubin, D., & Pollack, S.
- Affiliations
- Rambam Health Care Campus (IL)
- Technion – Israel Institute of Technology (IL)
- Corresponding author
- Hochberg, Z.
- Venue
- European Journal of Clinical Investigation
- Publisher
- Wiley
- Published
- 1997-07
- Volume
- 27
- Issue
- 7
- Pages
- 543-547
- ISSN
- 0014-2972 (ISSN-L)
- 1365-2362
- OpenAlex
- W2016083071
- Cited by
- 29
- References
- 0
- Citations by year
- 2025: 1 · 2024: 2 · 2021: 1 · 2020: 1 · 2016: 1 · 2014: 1
- FWCI
- 1.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- European Journal of Clinical Investigation (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic and Clinical Aspects of Sex Determination and Chromosomal Abnormalities
- Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
- Keywords
- insulin-like growth factor I, IGF-I resistance, growth hormone, monocytes, macrophages, T cell proliferation, interleukin-2, hyperlipidemia, insulin resistance, growth retardation
- MeSH terms
- Adolescent, Child, Child, Preschool, Female, Humans, Insulin-Like Growth Factor I, Interleukin-2, Lymphocyte Culture Test, Mixed, Lipoproteins, LDL, Lymphocyte Activation, Monocytes, Puberty, Growth Hormone, T-Lymphocytes, Turner Syndrome
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