Recombinant human insulin-like growth factor-I (IGF-I) therapy decreases plasma leptin concentration in patients with chronic renal insufficiency
Abstract
Objective To determine the relationship between plasma leptin and insulin-like growth factor-I (IGF-I) levels in healthy subjects and patients with chronic renal insufficiency at baseline, and during administration of recombinant human IGF-I in the renal impaired patients.Subjects 20 healthy subjects (six men, 14 women, age: 42.7 +/- 3.2 y) and nine subjects with chronic renal insufficiency (five men, four women, age: 53.6 +/- 3.7 y).Intervention Daily s.c. injection of recombinant human IGF-I (50 micrograms/kg) for 24 d.Measurements Fasting plasma levels of leptin, IGF-I, growth hormone, C-peptide, glucagon and IGF binding proteins by specific radioimmunoassays at baseline in all subjects and serially during IGF-I therapy in the renal impaired subjects.Results Baseline leptin levels were correlated with body mass index (BMI, R = 0.72, P = 0.0001) but not IGF-I levels (R = 0.02). During IGF-I therapy, plasma IGF-I levels increased from 128 +/- 17.4 ng/ml at baseline to 250 +/- 36.8 ng/ml on day 3 (P = 0.003) and 323 +/- 61.6 ng/ml on day 24 (P = 0.01), whereas leptin levels declined: 24.4 +/- 10.3 ng/ml (baseline), 19.5 +/- 6.2 ng/ml (day 3, P = 0.028), and 17.2 +/- 4.9 ng/ml (day 24, P = 0.05).Conclusion Basal plasma leptin and IGF-I levels are not correlated; however, chronic administration of recombinant IGF-I is associated with an early and sustained decrease in plasma leptin levels. IGF-I may have an inhibitory effect on leptin secretion in humans.
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IGF-I treatment leads to marked suppression of leptin levels in both rodents and humans.
“IGF-I treatment leads to marked suppression of leptin levels in both rodents and humans (33, 34).”
From Phenotypic effects of leptin replacement on morbid obesity, diabetes mellitus, hypogonadism, and behavior in leptin-deficient adults (2004) · cites this paper as [34]
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“This suggested that IGF-I might have an inhibitory effect on leptin secretion in humans by directly reducing leptin release from adipocytes [23, 24].”
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- Authors
- Dagogo-Jack, S., Franklin, S., Vijayan, A., Liu, J., Askari, H., & Miller, S.
- Affiliations
- Washington University in St. Louis (US)
- Venue
- International Journal of Obesity
- Published
- 1998-10-29
- Volume
- 22
- Issue
- 11
- Pages
- 1110-1115
- ISSN
- 0307-0565 (ISSN-L)
- 1476-5497
- OpenAlex
- W2316760999
- Cited by
- 26
- References
- 0
- Citations by year
- 2018: 1 · 2016: 1 · 2014: 2
- FWCI
- 2.47
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- International Journal of Obesity (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p60dk020579-35)
- National Institute of Diabetes and Digestive and Kidney Diseases (2P60-DK-20579)
- National Center for Research Resources (MO1RR00036, M01RR000036)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal and reproductive studies
- Keywords
- recombinant human insulin-like growth factor I, leptin, chronic renal insufficiency, IGF-I therapy, plasma leptin, IGF-I binding proteins, growth hormone, body mass index
- MeSH terms
- Adult, Binding Sites, C-Peptide, Female, Glucagon, Humans, Insulin-Like Growth Factor I, Kidney Failure, Chronic, Male, Middle Aged, Proteins, Radioimmunoassay, Recombinant Proteins, Body Mass Index, Receptor, IGF Type 1, Insulin-Like Growth Factor Binding Proteins, Leptin, Receptors, Leptin
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