Liver is the site of splanchnic cortisol production in obese nondiabetic humans

Rita Basu, Ananda Basu, Meagan Grudzien, Paul Jung, Peer Jacobson, Michael Johnson, Ravinder Jit Singh, Michael Sarr, Robert A. Rizza

Research output: Contribution to journalArticle

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Abstract

OBJECTIVE-To determine the contribution of liver and viscera to splanchnic cortisol production in humans. RESEARCH DESIGN AND METHODS-D4 cortisol was infused intravenously; arterial, portal venous, and hepatic venous blood was sampled; and liver and visceral fat were biopsied in subjects undergoing bariatric surgery. RESULTS-Ratios of arterial and portal vein D4 cortisol/corti-sol total (0.06 ± 0.01 vs. 0.06 ± 0.01) and D4 cortisol/D3 cortisol (1.80 ± 0.14 vs. 1.84 ± 0.14) did not differ, indicating that no visceral cortisol production or conversion of D4 cortisol to D3 cortisol via 11β-hydroxysteroid dehydrogenase type 1 (11β- HSD-1) occurred. Conversely, ratios of both D4 cortisol to cortisol total (0.05 ± 0.01; P < 0.05) and D4 cortisol to D3 cortisol (1.33 ± 0.11; P ≤0.001) were lower in the hepatic vein than in the portal vein, indicating production of both cortisol and D3 cortisol by the liver. The viscera did not produce either cortisol (-8.1 ± 2.6 (μg/min) or D3 cortisol (-0.2 ± 0.1 xg/min). In contrast, the liver produced both cortisol (22.7 ± 3.90 μg/min) and D3 cortisol (1.9 ± 0.4 μg/min) and accounted for all splanchnic cortisol and D3 cortisol production. Additionally, 11fβ-HSD-1 mRNA was approximately ninefold higher (P < 0.01) in liver than in visceral fat. Although 11fβ-HSD-2 gene expression was very low in visceral fat, the viscera released cortisone (P < 0.001) and D3 cortisone (P < 0.01) into the portal vein. CONCLUSIONS-The liver accounts for all splanchnic cortisol production in obese nondiabetic humans. In contrast, the viscera releases cortisone into the portal vein, thereby providing substrate for intrahepatic cortisol production.

Original languageEnglish (US)
Pages (from-to)39-45
Number of pages7
JournalDiabetes
Volume58
Issue number1
DOIs
StatePublished - Jan 2009

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Viscera
Hydrocortisone
Liver
Cortisone
Portal Vein
Intra-Abdominal Fat
11-beta-Hydroxysteroid Dehydrogenases

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Basu, R., Basu, A., Grudzien, M., Jung, P., Jacobson, P., Johnson, M., ... Rizza, R. A. (2009). Liver is the site of splanchnic cortisol production in obese nondiabetic humans. Diabetes, 58(1), 39-45. https://doi.org/10.2337/db08-1079

Liver is the site of splanchnic cortisol production in obese nondiabetic humans. / Basu, Rita; Basu, Ananda; Grudzien, Meagan; Jung, Paul; Jacobson, Peer; Johnson, Michael; Singh, Ravinder Jit; Sarr, Michael; Rizza, Robert A.

In: Diabetes, Vol. 58, No. 1, 01.2009, p. 39-45.

Research output: Contribution to journalArticle

Basu, R, Basu, A, Grudzien, M, Jung, P, Jacobson, P, Johnson, M, Singh, RJ, Sarr, M & Rizza, RA 2009, 'Liver is the site of splanchnic cortisol production in obese nondiabetic humans', Diabetes, vol. 58, no. 1, pp. 39-45. https://doi.org/10.2337/db08-1079
Basu R, Basu A, Grudzien M, Jung P, Jacobson P, Johnson M et al. Liver is the site of splanchnic cortisol production in obese nondiabetic humans. Diabetes. 2009 Jan;58(1):39-45. https://doi.org/10.2337/db08-1079
Basu, Rita ; Basu, Ananda ; Grudzien, Meagan ; Jung, Paul ; Jacobson, Peer ; Johnson, Michael ; Singh, Ravinder Jit ; Sarr, Michael ; Rizza, Robert A. / Liver is the site of splanchnic cortisol production in obese nondiabetic humans. In: Diabetes. 2009 ; Vol. 58, No. 1. pp. 39-45.
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title = "Liver is the site of splanchnic cortisol production in obese nondiabetic humans",
abstract = "OBJECTIVE-To determine the contribution of liver and viscera to splanchnic cortisol production in humans. RESEARCH DESIGN AND METHODS-D4 cortisol was infused intravenously; arterial, portal venous, and hepatic venous blood was sampled; and liver and visceral fat were biopsied in subjects undergoing bariatric surgery. RESULTS-Ratios of arterial and portal vein D4 cortisol/corti-sol total (0.06 ± 0.01 vs. 0.06 ± 0.01) and D4 cortisol/D3 cortisol (1.80 ± 0.14 vs. 1.84 ± 0.14) did not differ, indicating that no visceral cortisol production or conversion of D4 cortisol to D3 cortisol via 11β-hydroxysteroid dehydrogenase type 1 (11β- HSD-1) occurred. Conversely, ratios of both D4 cortisol to cortisol total (0.05 ± 0.01; P < 0.05) and D4 cortisol to D3 cortisol (1.33 ± 0.11; P ≤0.001) were lower in the hepatic vein than in the portal vein, indicating production of both cortisol and D3 cortisol by the liver. The viscera did not produce either cortisol (-8.1 ± 2.6 (μg/min) or D3 cortisol (-0.2 ± 0.1 xg/min). In contrast, the liver produced both cortisol (22.7 ± 3.90 μg/min) and D3 cortisol (1.9 ± 0.4 μg/min) and accounted for all splanchnic cortisol and D3 cortisol production. Additionally, 11fβ-HSD-1 mRNA was approximately ninefold higher (P < 0.01) in liver than in visceral fat. Although 11fβ-HSD-2 gene expression was very low in visceral fat, the viscera released cortisone (P < 0.001) and D3 cortisone (P < 0.01) into the portal vein. CONCLUSIONS-The liver accounts for all splanchnic cortisol production in obese nondiabetic humans. In contrast, the viscera releases cortisone into the portal vein, thereby providing substrate for intrahepatic cortisol production.",
author = "Rita Basu and Ananda Basu and Meagan Grudzien and Paul Jung and Peer Jacobson and Michael Johnson and Singh, {Ravinder Jit} and Michael Sarr and Rizza, {Robert A.}",
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T1 - Liver is the site of splanchnic cortisol production in obese nondiabetic humans

AU - Basu, Rita

AU - Basu, Ananda

AU - Grudzien, Meagan

AU - Jung, Paul

AU - Jacobson, Peer

AU - Johnson, Michael

AU - Singh, Ravinder Jit

AU - Sarr, Michael

AU - Rizza, Robert A.

PY - 2009/1

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N2 - OBJECTIVE-To determine the contribution of liver and viscera to splanchnic cortisol production in humans. RESEARCH DESIGN AND METHODS-D4 cortisol was infused intravenously; arterial, portal venous, and hepatic venous blood was sampled; and liver and visceral fat were biopsied in subjects undergoing bariatric surgery. RESULTS-Ratios of arterial and portal vein D4 cortisol/corti-sol total (0.06 ± 0.01 vs. 0.06 ± 0.01) and D4 cortisol/D3 cortisol (1.80 ± 0.14 vs. 1.84 ± 0.14) did not differ, indicating that no visceral cortisol production or conversion of D4 cortisol to D3 cortisol via 11β-hydroxysteroid dehydrogenase type 1 (11β- HSD-1) occurred. Conversely, ratios of both D4 cortisol to cortisol total (0.05 ± 0.01; P < 0.05) and D4 cortisol to D3 cortisol (1.33 ± 0.11; P ≤0.001) were lower in the hepatic vein than in the portal vein, indicating production of both cortisol and D3 cortisol by the liver. The viscera did not produce either cortisol (-8.1 ± 2.6 (μg/min) or D3 cortisol (-0.2 ± 0.1 xg/min). In contrast, the liver produced both cortisol (22.7 ± 3.90 μg/min) and D3 cortisol (1.9 ± 0.4 μg/min) and accounted for all splanchnic cortisol and D3 cortisol production. Additionally, 11fβ-HSD-1 mRNA was approximately ninefold higher (P < 0.01) in liver than in visceral fat. Although 11fβ-HSD-2 gene expression was very low in visceral fat, the viscera released cortisone (P < 0.001) and D3 cortisone (P < 0.01) into the portal vein. CONCLUSIONS-The liver accounts for all splanchnic cortisol production in obese nondiabetic humans. In contrast, the viscera releases cortisone into the portal vein, thereby providing substrate for intrahepatic cortisol production.

AB - OBJECTIVE-To determine the contribution of liver and viscera to splanchnic cortisol production in humans. RESEARCH DESIGN AND METHODS-D4 cortisol was infused intravenously; arterial, portal venous, and hepatic venous blood was sampled; and liver and visceral fat were biopsied in subjects undergoing bariatric surgery. RESULTS-Ratios of arterial and portal vein D4 cortisol/corti-sol total (0.06 ± 0.01 vs. 0.06 ± 0.01) and D4 cortisol/D3 cortisol (1.80 ± 0.14 vs. 1.84 ± 0.14) did not differ, indicating that no visceral cortisol production or conversion of D4 cortisol to D3 cortisol via 11β-hydroxysteroid dehydrogenase type 1 (11β- HSD-1) occurred. Conversely, ratios of both D4 cortisol to cortisol total (0.05 ± 0.01; P < 0.05) and D4 cortisol to D3 cortisol (1.33 ± 0.11; P ≤0.001) were lower in the hepatic vein than in the portal vein, indicating production of both cortisol and D3 cortisol by the liver. The viscera did not produce either cortisol (-8.1 ± 2.6 (μg/min) or D3 cortisol (-0.2 ± 0.1 xg/min). In contrast, the liver produced both cortisol (22.7 ± 3.90 μg/min) and D3 cortisol (1.9 ± 0.4 μg/min) and accounted for all splanchnic cortisol and D3 cortisol production. Additionally, 11fβ-HSD-1 mRNA was approximately ninefold higher (P < 0.01) in liver than in visceral fat. Although 11fβ-HSD-2 gene expression was very low in visceral fat, the viscera released cortisone (P < 0.001) and D3 cortisone (P < 0.01) into the portal vein. CONCLUSIONS-The liver accounts for all splanchnic cortisol production in obese nondiabetic humans. In contrast, the viscera releases cortisone into the portal vein, thereby providing substrate for intrahepatic cortisol production.

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