Hormonal regulation of human leptin in vivo

Effects of hydrocortisone and insulin

H. Askari, J. Liu, Samuel Dagogo-Jack

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

OBJECTIVE: To investigate the effects of continuous i.v. infusion of hydrocortisone or insulin on leptin secretion in humans. SUBJECTS: Six, nonfasting healthy adults (four women, two men), aged (mean ± s.e.m.) 36.6 ± 1.7 y; body mass index (BMI) 27.6 ± 0.9 kg/rn2. DESIGN: Randomized, placebo-controlled, cross-over study, with a 2-week 'wash-out' period. INTERVENTIONS: Intravenous infusion of hydrocortisone (3.3 μg/(kg min)), insulin (1 mU/(kg min)) or normal saline (placebo) for 24. h. MEASUREMENTS: Blood sampling every 1-2 h for measurement of glucose, insulin, cortisol and leptin; subcutaneous abdominal fat biopsy for determination of leptin mRNA expression. RESULTS: Plasma cortisol increased to 50.0 ± 0.4 μg/dl during hydrocortisone infusion, but was unaltered during saline or insulin infusion. The plasma insulin levels were: 28.5 ± 4.7 μU/ml (placebo), 40.8 ± 9.2 μU/ml (hydrocortisone, P = 0.214), and 243 ± 23.0 μU/ml (insulin, P=0.0002). Peak hyperleptinemia occurred after 16 h of insulin and 20 h of hydrocortisone infusion; peak/baseline plasma leptin levels (ng/ml) were 18.2 ± 4.2/15.1 ± 3.3 (placebo, P = 0.056), 42.1 ± 7.0/16.0 ± 3.8 (hydrocortisone, + 163%, P = 0.008) and 30.2 ± 4.3/16.6 ± 2.7 (insulin, + 83%, P = 0.024). Adipocyte leptin mRNA increased by 350% after the hydrocortisone infusion. CONCLUSION: Hydrocortisone, a natural glucocorticoid, induces hyperleptinemia in vivo, with a potency greater than that of insulin. The interaction between glucocorticoids and leptin may be of metabolic significance in humans.

Original languageEnglish (US)
Pages (from-to)1254-1259
Number of pages6
JournalInternational Journal of Obesity
Volume24
Issue number10
DOIs
StatePublished - Jan 1 2000
Externally publishedYes

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Leptin
Hydrocortisone
Insulin
Placebos
Glucocorticoids
Abdominal Subcutaneous Fat
Messenger RNA
Adipocytes
Intravenous Infusions
Cross-Over Studies
Body Mass Index
Biopsy
Glucose

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics

Cite this

Hormonal regulation of human leptin in vivo : Effects of hydrocortisone and insulin. / Askari, H.; Liu, J.; Dagogo-Jack, Samuel.

In: International Journal of Obesity, Vol. 24, No. 10, 01.01.2000, p. 1254-1259.

Research output: Contribution to journalArticle

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abstract = "OBJECTIVE: To investigate the effects of continuous i.v. infusion of hydrocortisone or insulin on leptin secretion in humans. SUBJECTS: Six, nonfasting healthy adults (four women, two men), aged (mean ± s.e.m.) 36.6 ± 1.7 y; body mass index (BMI) 27.6 ± 0.9 kg/rn2. DESIGN: Randomized, placebo-controlled, cross-over study, with a 2-week 'wash-out' period. INTERVENTIONS: Intravenous infusion of hydrocortisone (3.3 μg/(kg min)), insulin (1 mU/(kg min)) or normal saline (placebo) for 24. h. MEASUREMENTS: Blood sampling every 1-2 h for measurement of glucose, insulin, cortisol and leptin; subcutaneous abdominal fat biopsy for determination of leptin mRNA expression. RESULTS: Plasma cortisol increased to 50.0 ± 0.4 μg/dl during hydrocortisone infusion, but was unaltered during saline or insulin infusion. The plasma insulin levels were: 28.5 ± 4.7 μU/ml (placebo), 40.8 ± 9.2 μU/ml (hydrocortisone, P = 0.214), and 243 ± 23.0 μU/ml (insulin, P=0.0002). Peak hyperleptinemia occurred after 16 h of insulin and 20 h of hydrocortisone infusion; peak/baseline plasma leptin levels (ng/ml) were 18.2 ± 4.2/15.1 ± 3.3 (placebo, P = 0.056), 42.1 ± 7.0/16.0 ± 3.8 (hydrocortisone, + 163{\%}, P = 0.008) and 30.2 ± 4.3/16.6 ± 2.7 (insulin, + 83{\%}, P = 0.024). Adipocyte leptin mRNA increased by 350{\%} after the hydrocortisone infusion. CONCLUSION: Hydrocortisone, a natural glucocorticoid, induces hyperleptinemia in vivo, with a potency greater than that of insulin. The interaction between glucocorticoids and leptin may be of metabolic significance in humans.",
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N2 - OBJECTIVE: To investigate the effects of continuous i.v. infusion of hydrocortisone or insulin on leptin secretion in humans. SUBJECTS: Six, nonfasting healthy adults (four women, two men), aged (mean ± s.e.m.) 36.6 ± 1.7 y; body mass index (BMI) 27.6 ± 0.9 kg/rn2. DESIGN: Randomized, placebo-controlled, cross-over study, with a 2-week 'wash-out' period. INTERVENTIONS: Intravenous infusion of hydrocortisone (3.3 μg/(kg min)), insulin (1 mU/(kg min)) or normal saline (placebo) for 24. h. MEASUREMENTS: Blood sampling every 1-2 h for measurement of glucose, insulin, cortisol and leptin; subcutaneous abdominal fat biopsy for determination of leptin mRNA expression. RESULTS: Plasma cortisol increased to 50.0 ± 0.4 μg/dl during hydrocortisone infusion, but was unaltered during saline or insulin infusion. The plasma insulin levels were: 28.5 ± 4.7 μU/ml (placebo), 40.8 ± 9.2 μU/ml (hydrocortisone, P = 0.214), and 243 ± 23.0 μU/ml (insulin, P=0.0002). Peak hyperleptinemia occurred after 16 h of insulin and 20 h of hydrocortisone infusion; peak/baseline plasma leptin levels (ng/ml) were 18.2 ± 4.2/15.1 ± 3.3 (placebo, P = 0.056), 42.1 ± 7.0/16.0 ± 3.8 (hydrocortisone, + 163%, P = 0.008) and 30.2 ± 4.3/16.6 ± 2.7 (insulin, + 83%, P = 0.024). Adipocyte leptin mRNA increased by 350% after the hydrocortisone infusion. CONCLUSION: Hydrocortisone, a natural glucocorticoid, induces hyperleptinemia in vivo, with a potency greater than that of insulin. The interaction between glucocorticoids and leptin may be of metabolic significance in humans.

AB - OBJECTIVE: To investigate the effects of continuous i.v. infusion of hydrocortisone or insulin on leptin secretion in humans. SUBJECTS: Six, nonfasting healthy adults (four women, two men), aged (mean ± s.e.m.) 36.6 ± 1.7 y; body mass index (BMI) 27.6 ± 0.9 kg/rn2. DESIGN: Randomized, placebo-controlled, cross-over study, with a 2-week 'wash-out' period. INTERVENTIONS: Intravenous infusion of hydrocortisone (3.3 μg/(kg min)), insulin (1 mU/(kg min)) or normal saline (placebo) for 24. h. MEASUREMENTS: Blood sampling every 1-2 h for measurement of glucose, insulin, cortisol and leptin; subcutaneous abdominal fat biopsy for determination of leptin mRNA expression. RESULTS: Plasma cortisol increased to 50.0 ± 0.4 μg/dl during hydrocortisone infusion, but was unaltered during saline or insulin infusion. The plasma insulin levels were: 28.5 ± 4.7 μU/ml (placebo), 40.8 ± 9.2 μU/ml (hydrocortisone, P = 0.214), and 243 ± 23.0 μU/ml (insulin, P=0.0002). Peak hyperleptinemia occurred after 16 h of insulin and 20 h of hydrocortisone infusion; peak/baseline plasma leptin levels (ng/ml) were 18.2 ± 4.2/15.1 ± 3.3 (placebo, P = 0.056), 42.1 ± 7.0/16.0 ± 3.8 (hydrocortisone, + 163%, P = 0.008) and 30.2 ± 4.3/16.6 ± 2.7 (insulin, + 83%, P = 0.024). Adipocyte leptin mRNA increased by 350% after the hydrocortisone infusion. CONCLUSION: Hydrocortisone, a natural glucocorticoid, induces hyperleptinemia in vivo, with a potency greater than that of insulin. The interaction between glucocorticoids and leptin may be of metabolic significance in humans.

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