Cited by 45Growth Hormone and Insulin-like Growth FactorsRegulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic Diseases

Leptin is suppressed during infusion of recombinant human insulin-like growth factor I (rhIGF I) in normal rats

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Böni-Schnetzler, M., Hauri, C., Zapf, J.·1999·Diabetologia

Abstract

To examine whether insulin-like growth factor I (IGF I) or growth hormone (GH) influences leptin in vivo we measured leptin mRNA in epididymal fat pads and serum leptin of normal rats infused subcutaneously for 6 days with recombinant human (rh)IGF I (1 mg/day), rhGH (200 mU/day), or vehicle. In addition, we determined fat pad weight and food consumption as well as IGF I, insulin, glucose, non-esterified fatty acid (NEFA), glycerol, beta-hydroxybutyrate and triglyceride (TG) serum concentrations. Food intake was identical during all three treatments. RhIGF I but not rhGH raised IGF I serum concentrations, reduced fat pad weight (60.3 +/- 7.4% of control rats, p = 0.019), and suppressed leptin mRNA (38.8 +/- 11.9% of control rats, p = 0.002), serum leptin (51.6 +/- 10.5% of control rats, p = 0.0028) and serum triglycerides (39.3 +/- 8.0% of control rats, p = 2.6 x 10(-6)). Both rhIGF I and rhGH reduced non-esterified fatty acids (NEFA) (p = 0.00001 and 0.0007, respectively), whereas serum glycerol, beta-OH butyrate and glucose concentrations remained unchanged. Serum insulin concentrations during rhIGF I were lower than during rhGH infusion and correlated with leptin mRNA (r = 0.589, p = 0.016) and fat pad weight (r = 0.643, p = 0.007). Reduction of adipose tissue mass and suppression of leptin by IGF I appear to be due to reduced circulating insulin leading to enhanced fat mobilization and NEFA oxidation as well as to increased gluconeogenesis from glycerol. In contrast, decreased NEFA concentrations during rhGH in the presence of unchanged fat pad weight, serum glycerol and triglycerides might result from more efficient re-esterification of released fatty acids within the triglyceride-fatty acid cycle. The results also show that exogenously infused IGF I and GH act on lipid metabolism by different mechanisms and suggest an IGF-independent, probably direct, metabolic effect of GH. Finally, in agreement with previous studies in GH-infused hypophysectomized rats, it appears unlikely that GH regulates leptin in the rat.

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Authors
Böni-Schnetzler, M., Hauri, C., & Zapf, J.
Affiliations
University Hospital Zurich (CH)
Venue
Diabetologia
Published
1999-01-21
Volume
42
Issue
2
Pages
160-166
ISSN
  • 0012-186X (ISSN-L)
  • 1432-0428
OpenAlex
W2035285457
Cited by
45
References
39
Citations by year
2021: 1 · 2018: 1 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 3 · 2013: 1
FWCI
4.38
Type
journal article
Language
en
Open access
Locations
  • Diabetologia (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Science Foundation
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
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 › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
leptin, insulin-like growth factor I, recombinant human growth hormone, adipose tissue, leptin mRNA, serum leptin, fat pad weight, insulin, free fatty acids, triglycerides, glycerol, gluconeogenesis, lipid metabolism, lipid mobilization, rats
MeSH terms
Adipose Tissue, Animals, Blood Glucose, Body Weight, Fatty Acids, Nonesterified, Glycerol, Humans, Insulin, Insulin-Like Growth Factor I, Male, Organ Size, Proteins, Recombinant Proteins, RNA, Messenger, Triglycerides, Human Growth Hormone, 3-Hydroxybutyric Acid, Leptin, Rats

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