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Growth hormone and adipocyte function in obesity.

S Y Nam1, C Marcus

  • 1Division of Endocrinology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.

Hormone Research
|July 15, 2000
PubMed
Summary

Growth hormone (GH) secretion impairment in obesity is a consequence, not a cause. GH therapy in obesity offers benefits like reduced adiposity and improved lipid profiles, though its impact on insulin sensitivity is debated.

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Area of Science:

  • Endocrinology
  • Metabolism
  • Obesity Research

Background:

  • Obesity is associated with impaired growth hormone (GH) secretion, often considered a consequence rather than a cause.
  • GH influences GH receptor expression and insulin-like growth factor I (IGF-I) synthesis in adipocytes.
  • Obesity may lead to paradoxically normal or high serum-IGF-I and GH-binding protein levels due to increased adipose tissue mass.

Purpose of the Study:

  • To explore the complex interplay between obesity, the GH-IGF-I axis, and the effects of GH treatment.
  • To understand how hyperinsulinemia and altered GH receptor activity impact the GH-IGF-I axis in obesity.
  • To review the established and potential benefits of GH therapy in managing obesity and associated metabolic disturbances.

Main Methods:

  • Review of existing literature on GH secretion, GH receptor activity, and IGF-I regulation in obesity.
  • Analysis of the impact of obesity on the GH-IGF-I axis, considering adipocyte function and adipose tissue mass.
  • Examination of clinical findings regarding the effects of GH treatment on body composition, lipid profiles, and insulin sensitivity in obese individuals.

Main Results:

  • GH hyposecretion in obesity may be compensated by increased IGF-I and GH-binding protein secretion from expanded adipose tissue.
  • GH treatment demonstrates efficacy in reducing adiposity and triglyceride accumulation by modulating enzymes like lipoprotein lipase and hormone-sensitive lipase.
  • GH therapy positively impacts obesity-associated dyslipidemia, but its effects on insulin sensitivity remain inconsistent across studies.

Conclusions:

  • The GH-IGF-I axis is dysregulated in obesity, with GH deficiency being a consequence rather than a primary driver.
  • GH treatment presents a viable therapeutic strategy for improving body composition and lipid profiles in obese individuals.
  • Further research is warranted to clarify the conflicting effects of GH therapy on insulin sensitivity in the context of obesity.

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