Evidence map›Paper›PMID 26684275›Full record

ArticleThe Journal of clinical endocrinology and metabolism2016

Increased Bile Acid Synthesis and Impaired Bile Acid Transport in Human Obesity.

Rebecca A Haeusler, Stefania Camastra, Monica Nannipieri, Brenno Astiarraga, Jose Castro-Perez, Dan Xie, Liangsu Wang, Manu Chakravarthy, Ele Ferrannini

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
2.6field-weighted citation impact, top 8% 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

77 citing papers in PubMed, 157 citations in OpenAlex.

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  9. Deciphering the Association Between Homeostatic Model Assessment of Insulin Resistance and Chronic Diarrhea and the Mediating Role of Lymphocyte-to-Monocyte Ratio.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026
    Article
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  13. Bile acid metabolism in type 2 diabetes mellitus.Nature reviews. Endocrinology · 2025
    Review
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  17. Effects ofFrontiers in pharmacology · 2025
    Article
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17 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Rebecca A HaeuslerDepartment of Pathology and Cell Biology (R.A.H.), Columbia University, New York, New York 10032; Department of Clinical and Experimental Medicine (S.C., M.N., B.A., E.F.), University of Pisa School of Medicine, 56100 Pisa, Italy; Merck Research Laboratories (J.C.-P., D.X., L.W., M.C.), Cardiometabolic Disease, Kenilworth, New Jersey 07033; and CNR Institute of Clinical Physiology (E.F.), 56100 Pisa, Italy.
Stefania CamastraDepartment of Pathology and Cell Biology (R.A.H.), Columbia University, New York, New York 10032; Department of Clinical and Experimental Medicine (S.C., M.N., B.A., E.F.), University of Pisa School of Medicine, 56100 Pisa, Italy; Merck Research Laboratories (J.C.-P., D.X., L.W., M.C.), Cardiometabolic Disease, Kenilworth, New Jersey 07033; and CNR Institute of Clinical Physiology (E.F.), 56100 Pisa, Italy.
Monica NannipieriDepartment of Pathology and Cell Biology (R.A.H.), Columbia University, New York, New York 10032; Department of Clinical and Experimental Medicine (S.C., M.N., B.A., E.F.), University of Pisa School of Medicine, 56100 Pisa, Italy; Merck Research Laboratories (J.C.-P., D.X., L.W., M.C.), Cardiometabolic Disease, Kenilworth, New Jersey 07033; and CNR Institute of Clinical Physiology (E.F.), 56100 Pisa, Italy.
Brenno AstiarragaDepartment of Pathology and Cell Biology (R.A.H.), Columbia University, New York, New York 10032; Department of Clinical and Experimental Medicine (S.C., M.N., B.A., E.F.), University of Pisa School of Medicine, 56100 Pisa, Italy; Merck Research Laboratories (J.C.-P., D.X., L.W., M.C.), Cardiometabolic Disease, Kenilworth, New Jersey 07033; and CNR Institute of Clinical Physiology (E.F.), 56100 Pisa, Italy.
Jose Castro-PerezDepartment of Pathology and Cell Biology (R.A.H.), Columbia University, New York, New York 10032; Department of Clinical and Experimental Medicine (S.C., M.N., B.A., E.F.), University of Pisa School of Medicine, 56100 Pisa, Italy; Merck Research Laboratories (J.C.-P., D.X., L.W., M.C.), Cardiometabolic Disease, Kenilworth, New Jersey 07033; and CNR Institute of Clinical Physiology (E.F.), 56100 Pisa, Italy.
Dan XieDepartment of Pathology and Cell Biology (R.A.H.), Columbia University, New York, New York 10032; Department of Clinical and Experimental Medicine (S.C., M.N., B.A., E.F.), University of Pisa School of Medicine, 56100 Pisa, Italy; Merck Research Laboratories (J.C.-P., D.X., L.W., M.C.), Cardiometabolic Disease, Kenilworth, New Jersey 07033; and CNR Institute of Clinical Physiology (E.F.), 56100 Pisa, Italy.
Liangsu WangDepartment of Pathology and Cell Biology (R.A.H.), Columbia University, New York, New York 10032; Department of Clinical and Experimental Medicine (S.C., M.N., B.A., E.F.), University of Pisa School of Medicine, 56100 Pisa, Italy; Merck Research Laboratories (J.C.-P., D.X., L.W., M.C.), Cardiometabolic Disease, Kenilworth, New Jersey 07033; and CNR Institute of Clinical Physiology (E.F.), 56100 Pisa, Italy.
Manu ChakravarthyDepartment of Pathology and Cell Biology (R.A.H.), Columbia University, New York, New York 10032; Department of Clinical and Experimental Medicine (S.C., M.N., B.A., E.F.), University of Pisa School of Medicine, 56100 Pisa, Italy; Merck Research Laboratories (J.C.-P., D.X., L.W., M.C.), Cardiometabolic Disease, Kenilworth, New Jersey 07033; and CNR Institute of Clinical Physiology (E.F.), 56100 Pisa, Italy.
Ele FerranniniDepartment of Pathology and Cell Biology (R.A.H.), Columbia University, New York, New York 10032; Department of Clinical and Experimental Medicine (S.C., M.N., B.A., E.F.), University of Pisa School of Medicine, 56100 Pisa, Italy; Merck Research Laboratories (J.C.-P., D.X., L.W., M.C.), Cardiometabolic Disease, Kenilworth, New Jersey 07033; and CNR Institute of Clinical Physiology (E.F.), 56100 Pisa, Italy.
Merck & Co., Inc., Rahway, NJ, USA (United States) · USUniversity of Pisa · ITColumbia University · US

Funding

Clinical and Translational Science AwardUL1TR000040 · NCATS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2012 to 2015
$26.2M
Mechanisms linking insulin action with lipoprotein metabolismR01HL125649 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HAEUSLER, REBECCA ANNE · 2015 to 2023
$4.2M
Role of FoxO1 in Lipid MetabolismR00HL111206 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HAEUSLER, REBECCA ANNE · 2014 to 2016
$747k
Role of FoxO1 in Lipid MetabolismK99HL111206 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HAEUSLER, REBECCA ANNE · 2012 to 2013
$268k
NCATS NIH HHS UL1 TR000040NHLBI NIH HHS K99 HL111206NHLBI NIH HHS R00 HL111206NHLBI NIH HHS R01 HL125649
6 · The paper itself

Abstract

contextAlterations in bile acid (BA) synthesis and transport have the potential to affect multiple metabolic pathways in the pathophysiology of obesity.

objectiveThe objective of the study was to investigate the effects of obesity on serum fluctuations of BAs and markers of BA synthesis.

designWe measured BA fluctuations in 11 nonobese and 32 obese subjects and BA transporter expression in liver specimens from 42 individuals and specimens of duodenum, jejunum, ileum, colon, and pancreas from nine individuals.

main outcome measuresWe analyzed serum BAs and markers of BA synthesis after overnight fasting, during a hyperinsulinemic-euglycemic clamp, or a mixed-meal tolerance test and the association of BA transporter expression with body mass index.

resultsBA synthesis markers were 2-fold higher (P < .01) and preferentially 12α-hydroxylated (P < .05) in obese subjects, and both measures were correlated with clamp-derived insulin sensitivity (r = -0.62, P < .0001, and r = -0.39, P = .01, respectively). Insulin infusion acutely reduced serum BAs in nonobese subjects, but this effect was blunted in obese subjects (δBAs -44.2% vs -4.2%, P < .05). The rise in serum BAs postprandially was also relatively blunted in obese subjects (δBAs +402% vs +133%, P < .01). Liver expression of the Na+-taurocholate cotransporting polypeptide and the bile salt export pump were negatively correlated with body mass index (r = -0.37, P = .02, and r = -0.48, P = .001, respectively).

conclusionsObesity is associated with increased BA synthesis, preferential 12α-hydroxylation, and impaired serum BA fluctuations. The findings reveal new pathophysiological aspects of BA action in obesity that may lend themselves to therapeutic targeting in metabolic disease.

Indexed as

AdultBile Acids and SaltsBiological TransportCarrier ProteinsFemaleGlucose Clamp TechniqueHumansIntestinal MucosaLiverMaleMembrane GlycoproteinsObesityPancreasbile acid binding proteinsBile Acids and SaltsCarrier ProteinsMembrane Glycoproteins

Identifiers

PMID26684275
PMCPMC4870845
OpenAlexW2199066586

What OpenQuestion holds

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Registered trials

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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.