Evidence map›Paper›PMID 29300910›Full record

ArticleEndocrinology2018

FoxO1 Is Required for Most of the Metabolic and Hormonal Perturbations Produced by Hepatic Insulin Receptor Deletion in Male Mice.

Alisha V Ling, Mary E Gearing, Ivana Semova, Dong-Ju Shin, Rebecca Clements, Zon W Lai, Sudha B Biddinger

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
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  9. Article
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  13. Article
  14. Role of Insulin Resistance in MAFLD.International journal of molecular sciences · 2021
    Review
  15. Article
  16. Review
  17. Insulin: Trigger and Target of Renal Functions.Frontiers in cell and developmental biology · 2020
    Review
  18. Frontiers in pharmacology · 2018
    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

7 authors at 2 institutions in 1 country.

Alisha V LingDivision of Endocrinology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Mary E GearingDivision of Endocrinology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Ivana SemovaDivision of Endocrinology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Dong-Ju ShinDivision of Endocrinology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Rebecca ClementsDivision of Endocrinology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Zon W LaiDepartment of Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, Massachusetts.
Sudha B BiddingerDivision of Endocrinology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Harvard University · USBoston Children's Hospital · US

Funding

Physiology of Lipid Droplets and Triglyceride StorageR01DK101579 · NIDDK · HARVARD SCHOOL OF PUBLIC HEALTH · PI FARESE, ROBERT V · 2014 to 2018
$2.6M
The microRNA Control of Alcoholic Liver Injury and Hepatic Lipid MetabolismR01AA026322 · NIAAA · UNIVERSITY OF CONNECTICUT STORRS · PI SHIN, DONG JU · 2017 to 2021
$1.8M
Control of lipid metabolism in insulin resistant statesR01DK094162 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI BIDDINGER, SUDHA B · 2012 to 2015
$1.5M
NIAAA NIH HHS R01 AA026322NIDDK NIH HHS L40 DK065607NIDDK NIH HHS R01 DK094162NIDDK NIH HHS R01 DK101579
6 · The paper itself

Abstract

Insulin coordinates the complex response to feeding, affecting numerous metabolic and hormonal pathways. Forkhead box protein O1 (FoxO1) is one of several signaling molecules downstream of insulin; FoxO1 drives gluconeogenesis and is suppressed by insulin. To determine the role of FoxO1 in mediating other actions of insulin, we studied mice with hepatic deletion of the insulin receptor, FoxO1, or both. We found that mice with deletion of the insulin receptor alone showed not only hyperglycemia but also a 70% decrease in plasma insulin-like growth factor 1 and delayed growth during the first 2 months of life, a 24-fold increase in the soluble leptin receptor and a 19-fold increase in plasma leptin levels. Deletion of the insulin receptor also produced derangements in fatty acid metabolism, with a decrease in the expression of the lipogenic enzymes, hepatic diglycerides, and plasma triglycerides; in parallel, it increased expression of the fatty acid oxidation enzymes. Mice with deletion of both insulin receptor and FoxO1 showed a much more modest phenotype, with normal or near-normal glucose levels, growth, leptin levels, hepatic diglycerides, and fatty acid oxidation gene expression; however, lipogenic gene expression remained low. Taken together, these data reveal the pervasive role of FoxO1 in mediating the effects of insulin on not only glucose metabolism but also other hormonal signaling pathways and even some aspects of lipid metabolism.

Indexed as

AnimalsBlood GlucoseFatty AcidsForkhead Box Protein O1Gene ExpressionGluconeogenesisInsulinInsulin-Like Growth Factor ILeptinLipidsLipogenesisLiverMaleMiceMice, Inbred C57BLMice, KnockoutBlood GlucoseFatty AcidsForkhead Box Protein O1InsulinInsulin-Like Growth Factor ILeptinLipidsReceptor, InsulinReceptors, LeptinTriglycerides

Identifiers

PMID29300910
PMCPMC5802805
OpenAlexW2781432559

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.