Evidence map›Paper›PMID 18852327›Full record

Trial reportDiabetes2009

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 Singh, Michael Sarr, Robert A Rizza

Erratum issuedOpen access · hybridAbstract readClinical Trial
In one paragraph

Trial report in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 63 citations in OpenAlex.

  1. Trial
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  8. Reduced cortisol metabolism during critical illness.The New England journal of medicine · 2013
    Trial
  9. Trial
  10. Article
  11. Article
  12. Newly discovered endocrine functions of the liver.World journal of hepatology · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Rita BasuDivision of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Ananda Basu
Meagan Grudzien
Paul Jung
Peer Jacobson
Michael Johnson
Ravinder Singh
Michael Sarr
Robert A Rizza
Mayo Clinic · USAbbott Fund · US

Funding

MAYO CLINIC CENTER FOR TRANSLATIONAL SCIENCE ACTIVITIESUL1RR024150 · NCRR · MAYO CLINIC ROCHESTER · PI RIZZA, ROBERT A. · 2006 to 2011
$66.4M
ZESTRIL VS. VERAPAMIL IN THE TREATMENT OF HYPERTENSIONM01RR000585 · NCRR · MAYO CLINIC ROCHESTER · PI RIZZA, ROBERT A. · 1985 to 2006
$30.4M
MECHANISMS OF INSULIN RESISTANCE IN MANR01DK029953 · NIDDK · UNIVERSITY OF VIRGINIA · PI BASU, RITA · 1986 to 2024
$11.5M
MECHANISMS OF INSULIN RESISTANCE in ManR37DK029953 · NIDDK · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI RIZZA, ROBERT A. · 1996 to 2003
$1.8M
NCRR NIH HHS M01 RR000585NCRR NIH HHS RR-00585NCRR NIH HHS U-54RR-24150-1NCRR NIH HHS UL1 RR024150NIDDK NIH HHS DK-29953NIDDK NIH HHS R01 DK029953NIDDK NIH HHS R37 DK029953
6 · The paper itself

Abstract

objectiveTo determine the contribution of liver and viscera to splanchnic cortisol production in humans. RESEARCH DESIGN AND

methodsD4 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.

resultsRatios of arterial and portal vein D4 cortisol/cortisol(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 11beta-hydroxysteroid dehydrogenase type 1 (11beta-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 microg/min) or D3 cortisol (-0.2 +/- 0.1 microg/min). In contrast, the liver produced both cortisol (22.7 +/- 3.90 microg/min) and D3 cortisol (1.9 +/- 0.4 microg/min) and accounted for all splanchnic cortisol and D3 cortisol production. Additionally, 11beta-HSD-1 mRNA was approximately ninefold higher (P < 0.01) in liver than in visceral fat. Although 11beta-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.

conclusionsThe 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.

Indexed as

FemaleHumansHydrocortisoneIntra-Abdominal FatLiverMaleMiddle AgedObesitySplanchnic CirculationHydrocortisone

Identifiers

PMID18852327
PMCPMC2606891
OpenAlexW2146550902

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.