Evidence map›Paper›PMID 27797907›Full record

ArticleDiabetes2017

Hepatocytes Are the Principal Source of Circulating RBP4 in Mice.

Spencer J Thompson, Ashot Sargsyan, Seung-Ah Lee, Jason J Yuen, Jinjin Cai, Rana Smalling, Norbert Ghyselinck, Manuel Mark, William S Blaner, Timothy E Graham

Abstract read
In one paragraph

Article in Diabetes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Reduced Esterification Rather Than Increased Hydrolysis Is Causative for Loss of Hepatic Retinoids Upon CClLiver international : official journal of the International Association for the Study of the Liver · 2025
    Article
  6. Review
  7. Sex and Age but Not Body Mass Index (BMI) Predict Serum Retinol Binding Protein 4 (RBP4) and Transthyretin (TTR) Concentrations.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  8. Advances and therapeutic opportunities in visual cycle modulation.Progress in retinal and eye research · 2025
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Role of vitamins in the metabolic syndrome and cardiovascular disease.Pflugers Archiv : European journal of physiology · 2022
    Review
  20. Review
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

10 authors at 4 institutions in 2 countries.

Spencer J ThompsonMolecular Medicine Program, Department of Medicine, Division of Endocrinology, Metabolism, and Diabetes, Department of Nutrition, and Department of Biological Chemistry, University of Utah School of Medicine, Salt Lake City, UT.
Ashot SargsyanMolecular Medicine Program, Department of Medicine, Division of Endocrinology, Metabolism, and Diabetes, Department of Nutrition, and Department of Biological Chemistry, University of Utah School of Medicine, Salt Lake City, UT.
Seung-Ah LeeDepartment of Medicine and Institute of Human Nutrition, Columbia University College of Physicians and Surgeons, New York, NY.
Jason J YuenDepartment of Medicine and Institute of Human Nutrition, Columbia University College of Physicians and Surgeons, New York, NY.
Jinjin CaiMolecular Medicine Program, Department of Medicine, Division of Endocrinology, Metabolism, and Diabetes, Department of Nutrition, and Department of Biological Chemistry, University of Utah School of Medicine, Salt Lake City, UT.
Rana SmallingGeorge E. Wahlen Department of Veterans Affairs Medical Center, Salt Lake City, UT.
Norbert GhyselinckDépartement de Génétique Fonctionnelle et Cancer, Institut de Génétique et de Biologie Moléculaire et Cellulaire; Centre National de la Recherche Scientifique; INSERM; and Université de Strasbourg, Illkirch, France.
Manuel MarkDépartement de Génétique Fonctionnelle et Cancer, Institut de Génétique et de Biologie Moléculaire et Cellulaire; Centre National de la Recherche Scientifique; INSERM; and Université de Strasbourg, Illkirch, France.
William S BlanerDepartment of Medicine and Institute of Human Nutrition, Columbia University College of Physicians and Surgeons, New York, NY.
Timothy E GrahamMolecular Medicine Program, Department of Medicine, Division of Endocrinology, Metabolism, and Diabetes, Department of Nutrition, and Department of Biological Chemistry, University of Utah School of Medicine, Salt Lake City, UT tim.graham@progenitorlifesciences.com.
Columbia University · USUniversity of Utah · USGeorge E. Wahlen Department of VA Medical Center · USInserm · FR

Funding

POSTDOCTORAL TRAINING IN ARTERIOSCLEROSIS RESEARCHT32HL007343 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI HENRY N GINSBERG, Muredach P Reilly · 1985 to 2026
$12.7M
Postprandial Vitamin AR01DK068437 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BLANER, WILLIAM S · 2004 to 2023
$7.0M
Post-Developmental Adipocyte Autophagy in Control of Insulin-Glucose HomeostasisR01DK100826 · NIDDK · UNIVERSITY OF UTAH · PI BOUDINA, SIHEM · 2013 to 2017
$1.6M
Vitamin A Homeostasis: Retinyl Ester StoresR01DK101251 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BLANER, WILLIAM S, HARRISON, EARL HOWARD · 2016 to 2018
$1.4M
Tissue specific production of RBP4 and mechanism of insulin resistanceI01BX000937 · VA · VA SALT LAKE CITY HEALTHCARE SYSTEM · PI GRAHAM, TIMOTHY E. · 2011 to 2013
–
BLRD VA I01 BX000937NHLBI NIH HHS T32 HL007343NIDDK NIH HHS R01 DK068437NIDDK NIH HHS R01 DK100826NIDDK NIH HHS R01 DK101251
6 · The paper itself

Abstract

RBP4 is produced mainly by hepatocytes. In type 2 diabetes and obesity, circulating RBP4 is increased and may act systemically to cause insulin resistance and glucose intolerance. Observations that adipocyte RBP4 mRNA increases in parallel with circulating RBP4 in these conditions, whereas liver RBP4 mRNA does not, led to a widely held hypothesis that elevated circulating RBP4 is a direct result of increased production by adipocytes. To test this, we generated mice with hepatocyte-specific deletion of RBP4 (liver RBP4 knockout or LRKO mice). Adipose tissue RBP4 expression and secretion remained intact in LRKO mice and increased as expected in the setting of diet-induced insulin resistance. However, circulating RBP4 was undetectable in LRKO mice. We conclude that adipocyte RBP4 is not a significant source of circulating RBP4, even in the setting of insulin resistance. Adipocyte RBP4, therefore, may have a more important autocrine or paracrine function that is confined within the adipose tissue compartment.

Indexed as

AdipocytesAnimalsBlotting, WesternFemaleGenotypeHepatocytesInsulin ResistanceMaleMiceMice, Inbred C57BLMice, KnockoutRetinol-Binding Proteins, PlasmaReverse Transcriptase Polymerase Chain ReactionRNA, MessengerRbp4 protein, mouseRetinol-Binding Proteins, PlasmaRNA, Messenger

Identifiers

PMID27797907
PMCPMC5204311
OpenAlexW2532093754

What OpenQuestion holds

Textmetadata
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.