Evidence map›Paper›PMID 23257358›Full record

ArticleThe Journal of clinical investigation2013

Direct control of hepatic glucose production by interleukin-13 in mice.

Kristopher J Stanya, David Jacobi, Sihao Liu, Prerna Bhargava, Lingling Dai, Matthew R Gangl, Karen Inouye, Jillian L Barlow, Yewei Ji, Joseph P Mizgerd and 4 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

80 citing papers in PubMed, 137 citations in OpenAlex.

  1. Soluble interleukin-13rα1: a circulating regulator of glucose.American journal of physiology. Endocrinology and metabolism · 2017
    Trial
  2. Interleukin13 Ameliorates Hepatocellular Steatosis via IL13Rα1/JNK/FOSL2 Signaling Pathway.Cellular and molecular gastroenterology and hepatology · 2026
    Article
  3. Article
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  9. Sinusoidal communication in chronic liver disease.Clinical and molecular hepatology · 2025
    Review
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  15. Article
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20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 6 institutions in 4 countries.

Kristopher J StanyaDepartment of Genetics and Complex Diseases, Harvard School of Public Health, 665 Huntington Ave., Boston, Massachusetts 02115, USA.
David Jacobi
Sihao Liu
Prerna Bhargava
Lingling Dai
Matthew R Gangl
Karen Inouye
Jillian L Barlow
Yewei Ji
Joseph P Mizgerd
Ling Qi
Hang Shi
Andrew N J McKenzie
Chih-Hao Lee
Harvard University Press · USCornell University · USMedical Research Council · GBCentral South University · CNGeorgia State University · USUniversité de Tours · FR

Funding

Interdisciplinary Training in Genes and the EnvironmentT32ES016645 · NIEHS · HARVARD SCHOOL OF PUBLIC HEALTH · PI LEE, CHIH-HAO · 2008 to 2018
$4.0M
Regulation and function of STAT3 during pneumoniaR01HL079392 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI MIZGERD, JOSEPH P · 2005 to 2015
$4.0M
PPAR Delta Functions in LiverR01DK075046 · NIDDK · HARVARD SCHOOL OF PUBLIC HEALTH · PI LEE, CHIH-HAO · 2007 to 2015
$3.0M
Medical Research Council MC_U105178805NHLBI NIH HHS R01 HL079392NIDDK NIH HHS R01 DK075046NIDDK NIH HHS R01DK075046NIEHS NIH HHS T32 ES016645NIEHS NIH HHS T32ES016645
6 · The paper itself

Abstract

Hyperglycemia is a result of impaired insulin action on glucose production and disposal, and a major target of antidiabetic therapies. The study of insulin-independent regulatory mechanisms of glucose metabolism may identify new strategies to lower blood sugar levels. Here we demonstrate an unexpected metabolic function for IL-13 in the control of hepatic glucose production. IL-13 is a Th2 cytokine known to mediate macrophage alternative activation. Genetic ablation of Il-13 in mice (Il-13-/-) resulted in hyperglycemia, which progressed to hepatic insulin resistance and systemic metabolic dysfunction. In Il-13-/- mice, upregulation of enzymes involved in hepatic gluconeogenesis was a primary event leading to dysregulated glucose metabolism. IL-13 inhibited transcription of gluconeogenic genes by acting directly on hepatocytes through Stat3, a noncanonical downstream effector. Consequently, the ability of IL-13 to suppress glucose production was abolished in liver cells lacking Stat3 or IL-13 receptor α1 (Il-13rα1), which suggests that the IL-13Rα1/Stat3 axis directs IL-13 signaling toward metabolic responses. These findings extend the implication of a Th1/Th2 paradigm in metabolic homeostasis beyond inflammation to direct control of glucose metabolism and suggest that the IL-13/Stat3 pathway may serve as a therapeutic target for glycemic control in insulin resistance and type 2 diabetes.

Indexed as

AnimalsDiabetes Mellitus, Type 2GluconeogenesisGlucoseHyperglycemiaInsulin ResistanceInterleukin-13Interleukin-13 Receptor alpha1 SubunitLiverMiceMice, Inbred BALB CMice, KnockoutSTAT3 Transcription FactorTh1 CellsTh2 CellsGlucoseIl13ra1 protein, mouseInterleukin-13Interleukin-13 Receptor alpha1 SubunitStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID23257358
PMCPMC3533296
OpenAlexW2108003067

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.