Evidence map›Paper›PMID 27814523›Full record

ArticleCell2016

Hematopoietic-Derived Galectin-3 Causes Cellular and Systemic Insulin Resistance.

Pingping Li, Shuainan Liu, Min Lu, Gautum Bandyopadhyay, Dayoung Oh, Takeshi Imamura, Andrew M F Johnson, Dorothy Sears, Zhufang Shen, Bing Cui and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed
12.6field-weighted citation impact, top 1% 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

179 citing papers in PubMed, 298 citations in OpenAlex.

  1. Trial
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  10. PerturbingCells · 2026
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. The Role of Galectin-3 in Liver Inflammation and Fibrosis.Journal of inflammation research · 2026
    Review
  18. Article
  19. Article
  20. Article

119 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 4 institutions in 3 countries.

Pingping LiState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China; Diabetes Research Center of Chinese Academy of Medical Sciences, Beijing 100050, China; Division of Endocrinology and Metabolism, UC, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA. Electronic address: lipp@imm.ac.cn.
Shuainan LiuState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China; Diabetes Research Center of Chinese Academy of Medical Sciences, Beijing 100050, China.
Min LuDivision of Endocrinology and Metabolism, UC, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA; Diabetes Early Discovery, Merck Research Laboratories, 33 Avenue Louis Pasteur, Boston, MA 02115, USA.
Gautum BandyopadhyayDivision of Endocrinology and Metabolism, UC, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Dayoung OhDivision of Endocrinology and Metabolism, UC, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Takeshi ImamuraPharmacology, Department of Medicine, Shiga University of Medical Science, 1 Tsukinowa, Seta, Otsu-city, Shiga 520-2192, Japan.
Andrew M F JohnsonDivision of Endocrinology and Metabolism, UC, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Dorothy SearsDivision of Endocrinology and Metabolism, UC, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Zhufang ShenState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China; Diabetes Research Center of Chinese Academy of Medical Sciences, Beijing 100050, China.
Bing CuiState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China; Diabetes Research Center of Chinese Academy of Medical Sciences, Beijing 100050, China.
Lijuan KongState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China; Diabetes Research Center of Chinese Academy of Medical Sciences, Beijing 100050, China.
Shaocong HouState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China; Diabetes Research Center of Chinese Academy of Medical Sciences, Beijing 100050, China.
Xiao LiangState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China; Diabetes Research Center of Chinese Academy of Medical Sciences, Beijing 100050, China.
Salvatore IovinoDiabetes Early Discovery, Merck Research Laboratories, 33 Avenue Louis Pasteur, Boston, MA 02115, USA.
Steven M WatkinsLipomics Technologies, Inc., West Sacramento, CA 95691, USA.
Wei YingDivision of Endocrinology and Metabolism, UC, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Olivia OsbornDivision of Endocrinology and Metabolism, UC, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Joshua WollamDivision of Endocrinology and Metabolism, UC, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Martin BrennerDiabetes Early Discovery, Merck Research Laboratories, 33 Avenue Louis Pasteur, Boston, MA 02115, USA.
Jerrold M OlefskyDivision of Endocrinology and Metabolism, UC, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA. Electronic address: jolefsky@ucsd.edu.
University of California San Diego · USChinese Academy of Medical Sciences & Peking Union Medical College · CNMerck & Co., Inc., Rahway, NJ, USA (United States) · USShiga University of Medical Science · JP

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PETER J TONTONOZ · 2003 to 2026
$40.4M
Project# 4: INTERACTIONS OF ANCHORING PROTEINS WITH THEIR TARGETSP01DK054441 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TAYLOR, SUSAN S. · 1999 to 2017
$27.3M
Transcriptional Genomics CoreP01DK074868 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASS, CHRISTOPHER K · 2007 to 2016
$16.6M
INSULIN RECEPTORS AND THE GLUCOSE TRANSPORT SYSTEMR37DK033651 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OLEFSKY, JERROLD MICHAEL · 2000 to 2010
$6.1M
INSULIN RECEPTORS AND THE GLUCOSE TRANSPORT SYSTEMR01DK033651 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OLEFSKY, JERROLD MICHAEL · 1986 to 2013
$2.2M
Molecular Mechanisms of Inflammation, Steatosis and Hepatic Insulin ResistanceR24DK090962 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OLEFSKY, JERROLD MICHAEL · 2010 to 2011
$1.5M
PHOSPHOCALMODULIN AND INSULIN ACTIONF32DK009062 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI JOYAL, JOHN LOUIS · 1994 to 1996
–
NIDDK NIH HHS F32 DK009062NIDDK NIH HHS P01 DK054441NIDDK NIH HHS P01 DK074868NIDDK NIH HHS P30 DK063491NIDDK NIH HHS R01 DK033651NIDDK NIH HHS R24 DK090962NIDDK NIH HHS R37 DK033651
6 · The paper itself

Abstract

In obesity, macrophages and other immune cells accumulate in insulin target tissues, promoting a chronic inflammatory state and insulin resistance. Galectin-3 (Gal3), a lectin mainly secreted by macrophages, is elevated in both obese subjects and mice. Administration of Gal3 to mice causes insulin resistance and glucose intolerance, whereas inhibition of Gal3, through either genetic or pharmacologic loss of function, improved insulin sensitivity in obese mice. In vitro treatment with Gal3 directly enhanced macrophage chemotaxis, reduced insulin-stimulated glucose uptake in myocytes and 3T3-L1 adipocytes and impaired insulin-mediated suppression of glucose output in primary mouse hepatocytes. Importantly, we found that Gal3 can bind directly to the insulin receptor (IR) and inhibit downstream IR signaling. These observations elucidate a novel role for Gal3 in hepatocyte, adipocyte, and myocyte insulin resistance, suggesting that Gal3 can link inflammation to decreased insulin sensitivity. Inhibition of Gal3 could be a new approach to treat insulin resistance.

Indexed as

AdipocytesAnimalsChemotaxisDiabetes Mellitus, Type 2Galectin 3HepatocytesHumansInsulinInsulin ResistanceMacrophagesMiceMice, KnockoutMuscle CellsObesityGalectin 3Insulingalectin-3inflammationinsulin resistance

Identifiers

PMID27814523
PMCPMC5179329
OpenAlexW2548399475

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.