Evidence mapPaperPMID 30228187Full record

ArticleThe Journal of biological chemistry2018

Complement 1q-like-3 protein inhibits insulin secretion from pancreatic β-cells via the cell adhesion G protein-coupled receptor BAI3.

Rajesh Gupta, Dan C Nguyen, Michael D Schaid, Xia Lei, Appakalai N Balamurugan, G William Wong, Jeong-A Kim, James E Koltes, Michelle E Kimple, Sushant Bhatnagar

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.3field-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

28 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Unveiling the roles of CTRP family in cardiac remodeling.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  10. Article
  11. Mechanisms of spinophilin-dependent pancreas dysregulation in obesity.American journal of physiology. Endocrinology and metabolism · 2024
    Article
  12. Elucidating the Role of Pelargonidin-3-O-Glucoside onJournal of pharmacy & bioallied sciences · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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 5 institutions in 1 country.

Rajesh GuptaFrom the Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, and Comprehensive Diabetes Center, University of Alabama, Birmingham, Alabama 35294.
Dan C NguyenFrom the Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, and Comprehensive Diabetes Center, University of Alabama, Birmingham, Alabama 35294.
Michael D Schaidthe Interdisciplinary Graduate Program in Nutritional Sciences, University of Wisconsin-Madison, Madison, Wisconsin 53706,; the William S. Middleton Memorial Veterans Hospital, Research Service, Madison, Wisconsin 53705.
Xia Leithe Department of Physiology and Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Appakalai N Balamuruganthe Department of Surgery, University of Louisville, Louisville, Kentucky 40202, and.
G William Wongthe Department of Physiology and Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Jeong-A KimFrom the Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, and Comprehensive Diabetes Center, University of Alabama, Birmingham, Alabama 35294.
James E Koltesthe Department of Animal Science, Iowa State University, Ames, Iowa 50011.
Michelle E Kimplethe Interdisciplinary Graduate Program in Nutritional Sciences, University of Wisconsin-Madison, Madison, Wisconsin 53706,; the William S. Middleton Memorial Veterans Hospital, Research Service, Madison, Wisconsin 53705,; the Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, and the Department of Cell and Regenerative Biology, University of Wisconsin-Madison, Madison, Wisconsin 53705.
Sushant BhatnagarFrom the Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, and Comprehensive Diabetes Center, University of Alabama, Birmingham, Alabama 35294,. Electronic address: sushantbhatnagar@uabmc.edu.
University of Alabama at Birmingham · USJohns Hopkins University · USUniversity of Wisconsin–Madison · USIowa State University · USUniversity of Louisville · US

Funding

Computation and Informatics in Biology and MedicineT15LM007359 · UNIVERSITY OF WISCONSIN-MADISON · 2002 to 2025
$4.7M
CTRP and Metabolic ControlR01DK084171 · NIDDK · JOHNS HOPKINS UNIVERSITY · 2022 to 2025
$1.7M
UAB Diabetes Research CenterP30DK079626 · UNIVERSITY OF ALABAMA AT BIRMINGHAM · 2025 to 2025
$1.3M
NHLBI NIH HHS R01 HL128695NIDDK NIH HHS P30 DK079626NIDDK NIH HHS R00 DK095975NIDDK NIH HHS R01 DK084171NLM NIH HHS T15 LM007359
6 · The paper itself

Abstract

Secreted proteins are important metabolic regulators in both healthy and disease states. Here, we sought to investigate the mechanism by which the secreted protein complement 1q-like-3 (C1ql3) regulates insulin secretion from pancreatic β-cells, a key process affecting whole-body glucose metabolism. We found that C1ql3 predominantly inhibits exendin-4- and cAMP-stimulated insulin secretion from mouse and human islets. However, to a lesser extent, C1ql3 also reduced insulin secretion in response to KCl, the potassium channel blocker tolbutamide, and high glucose. Strikingly, C1ql3 did not affect insulin secretion stimulated by fatty acids, amino acids, or mitochondrial metabolites, either at low or submaximal glucose concentrations. Additionally, C1ql3 inhibited glucose-stimulated cAMP levels, and insulin secretion stimulated by exchange protein directly activated by cAMP-2 and protein kinase A. These results suggest that C1ql3 inhibits insulin secretion primarily by regulating cAMP signaling. The cell adhesion G protein-coupled receptor, brain angiogenesis inhibitor-3 (BAI3), is a C1ql3 receptor and is expressed in β-cells and in mouse and human islets, but its function in β-cells remained unknown. We found that siRNA-mediated

Indexed as

AdipokinesAnimalsCell LineComplement C1qComplement System ProteinsCyclic AMPCyclic AMP-Dependent Protein KinasesGlucagon-Like Peptide 1GlucoseHumansInsulinInsulin-Secreting CellsInsulin SecretionNerve Tissue ProteinsRatsADGRB3 protein, humanAdipokinesC1QL3 protein, humanComplement C1qComplement System ProteinsCyclic AMPCyclic AMP-Dependent Protein KinasesGlucagon-Like Peptide 1GlucoseInsulinNerve Tissue Proteinsbeta cell (B-cell)brain angiogenesis inhibitor 3complement 1q-like 3cyclic AMP (cAMP)glucagon-like peptide-1G protein-coupled receptor (GPCR)insulin secretionobesitysecond messengertype 2 diabetes

Identifiers

PMID30228187
PMCPMC6254345
OpenAlexW2892351430

What Socratic 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 Socratic graph.