Evidence map›Paper›PMID 32167208›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

RBP4 increases lipolysis in human adipocytes and is associated with increased lipolysis and hepatic insulin resistance in obese women.

Murat Kilicarslan, Barbara A de Weijer, Kotryna Simonyté Sjödin, Pratik Aryal, Kasper W Ter Horst, Hamit Cakir, Johannes A Romijn, Mariëtte T Ackermans, Ignace M Janssen, Frits J Berends and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

40 citing papers in PubMed, 65 citations in OpenAlex.

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  18. Cornelian Cherry (International journal of molecular sciences · 2024
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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

14 authors at 7 institutions in 2 countries.

Murat KilicarslanDepartment of Endocrinology & Metabolism, Amsterdam University Medical Centers, Amsterdam, the Netherlands.
Barbara A de WeijerDepartment of Endocrinology & Metabolism, Amsterdam University Medical Centers, Amsterdam, the Netherlands.
Kotryna Simonyté SjödinDivision of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Pratik AryalDivision of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Kasper W Ter HorstDepartment of Endocrinology & Metabolism, Amsterdam University Medical Centers, Amsterdam, the Netherlands.
Hamit CakirDepartment of Surgery, Northwest Clinics, Alkmaar, the Netherlands.
Johannes A RomijnDepartment of Endocrinology & Metabolism, Amsterdam University Medical Centers, Amsterdam, the Netherlands.
Mariëtte T AckermansClinical Chemistry, Laboratory of Endocrinology, Amsterdam University Medical Centers, Amsterdam, the Netherlands.
Ignace M JanssenDepartment of Surgery, Rijnstate Hospital, Arnhem, the Netherlands.
Frits J BerendsDepartment of Surgery, Rijnstate Hospital, Arnhem, the Netherlands.
Arnold W van de LaarDepartment of Surgery, Spaarne Hospital, Hoofddorp, the Netherlands.
Alexander P HoudijkDepartment of Surgery, Northwest Clinics, Alkmaar, the Netherlands.
Barbara B KahnDivision of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Mireille J SerlieDepartment of Endocrinology & Metabolism, Amsterdam University Medical Centers, Amsterdam, the Netherlands.
Amsterdam University Medical Centers · NLHarvard University · USRijnstate Hospital · NLBeth Israel Deaconess Medical Center · USMedisch Centrum Alkmaar · NLNorthwest Hospital · USSpaarne Ziekenhuis · NL

Funding

Transgenic CoreP30DK046200 · NIDDK · TUFTS MEDICAL CENTER · PI GREENBERG, ANDREW S, PERISSI, VALENTINA · 1992 to 2021
$25.0M
GLUCOSE TRANSPORTER REGULATION IN OBESITY AND DIABETESR01DK043051 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B. · 1992 to 2020
$4.4M
HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) R01 DK43051NIDDK NIH HHS P30 DK046200NIDDK NIH HHS R01 DK043051
6 · The paper itself

Abstract

Retinol-binding protein-4 (RBP4) is elevated in serum and adipose tissue (AT) in obesity-induced insulin resistance and correlates inversely with insulin-stimulated glucose disposal. But its role in insulin-mediated suppression of lipolysis, free fatty acids (FFA), and endogenous glucose production (EGP) in humans is unknown. RBP4 mRNA or protein levels were higher in liver, subcutaneous adipose tissue (SAT), and visceral adipose tissue (VAT) in morbidly obese subjects undergoing Roux-en-Y gastric bypass surgery compared to lean controls undergoing elective laparoscopic cholecystectomy. RBP4 mRNA expression in SAT correlated with the expression of several macrophage and other inflammation markers. Serum RBP4 levels correlated inversely with glucose disposal and insulin-mediated suppression of lipolysis, FFA, and EGP. Mechanistically, RBP4 treatment of human adipocytes in vitro directly stimulated basal lipolysis. Treatment of adipocytes with conditioned media from RBP4-activated macrophages markedly increased basal lipolysis and impaired insulin-mediated lipolysis suppression. RBP4 treatment of macrophages increased TNFα production. These data suggest that elevated serum or adipose tissue RBP4 levels in morbidly obese subjects may cause hepatic and systemic insulin resistance by stimulating basal lipolysis and by activating macrophages in adipose tissue, resulting in release of pro-inflammatory cytokines that impair lipolysis suppression. While we have demonstrated this mechanism in human adipocytes in vitro, and correlations from our flux studies in humans strongly support this, further studies are needed to determine whether this mechanism explains RBP4-induced insulin resistance in humans.

Indexed as

Insulin ResistanceLipolysisAdipose TissueAdultBlood GlucoseFemaleGlucose IntoleranceHumansLiverMiddle AgedObesity, MorbidRetinol-Binding Proteins, PlasmaBlood GlucoseRBP4 protein, humanRetinol-Binding Proteins, Plasmaendogenous glucose productioninflammationinsulin resistancelipolysisobesityRBP4

Identifiers

PMID32167208
PMCPMC7317205
OpenAlexW3012325810

What OpenQuestion holds

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LicenceCC BY-NC
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.