Evidence map›Paper›PMID 26910308›Full record

ArticleEndocrinology2016

Essential Role of IGFIR in the Onset of Male Brown Fat Thermogenic Function: Regulation of Glucose Homeostasis by Differential Organ-Specific Insulin Sensitivity.

Vanesa Viana-Huete, Carlos Guillén, Ana García-Aguilar, Gema García, Silvia Fernández, C R Kahn, Manuel Benito

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Signaling Pathways Regulating Thermogenesis.Frontiers in endocrinology · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Pathogenesis of hypothyroidism-induced NAFLD is driven by intra- and extrahepatic mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  11. Article
  12. 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

7 authors at 4 institutions in 2 countries.

Vanesa Viana-HueteDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Complutense University-Madrid, Madrid 28040, Spain; Spanish Diabetes and Metabolic Research Network (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Institute of Health Carlos III, Madrid 28029, Spain; and Joslin Diabetes Center (C.R.K.), Harvard Medical School, Boston, MA 02215.
Carlos GuillénDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Complutense University-Madrid, Madrid 28040, Spain; Spanish Diabetes and Metabolic Research Network (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Institute of Health Carlos III, Madrid 28029, Spain; and Joslin Diabetes Center (C.R.K.), Harvard Medical School, Boston, MA 02215.
Ana García-AguilarDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Complutense University-Madrid, Madrid 28040, Spain; Spanish Diabetes and Metabolic Research Network (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Institute of Health Carlos III, Madrid 28029, Spain; and Joslin Diabetes Center (C.R.K.), Harvard Medical School, Boston, MA 02215.
Gema GarcíaDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Complutense University-Madrid, Madrid 28040, Spain; Spanish Diabetes and Metabolic Research Network (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Institute of Health Carlos III, Madrid 28029, Spain; and Joslin Diabetes Center (C.R.K.), Harvard Medical School, Boston, MA 02215.
Silvia FernándezDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Complutense University-Madrid, Madrid 28040, Spain; Spanish Diabetes and Metabolic Research Network (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Institute of Health Carlos III, Madrid 28029, Spain; and Joslin Diabetes Center (C.R.K.), Harvard Medical School, Boston, MA 02215.
C R KahnDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Complutense University-Madrid, Madrid 28040, Spain; Spanish Diabetes and Metabolic Research Network (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Institute of Health Carlos III, Madrid 28029, Spain; and Joslin Diabetes Center (C.R.K.), Harvard Medical School, Boston, MA 02215.
Manuel BenitoDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Complutense University-Madrid, Madrid 28040, Spain; Spanish Diabetes and Metabolic Research Network (V.V.-H., C.G., A.G.-A., G.G., S.F., M.B.), Institute of Health Carlos III, Madrid 28029, Spain; and Joslin Diabetes Center (C.R.K.), Harvard Medical School, Boston, MA 02215.
Instituto de Salud Carlos III · ESSpanish Clinical Research Network · ESUniversidad Complutense de Madrid · ESHarvard University · US

Funding

The Insulin Receptor and Its Signaling MechanismsR01DK031036 · NIDDK · JOSLIN DIABETES CENTER · PI C RONALD KAHN · 1986 to 2026
$4.2M
NIDDK NIH HHS R01 DK031036
6 · The paper itself

Abstract

Brown fat is a thermogenic tissue that generates heat to maintain body temperature in cold environments and dissipate excess energy in response to overfeeding. We have addressed the role of the IGFIR in the brown fat development and function. Mice lacking IGFIR exhibited normal brown adipose tissue/body weight in knockout (KO) vs control mice. However, lack of IGFIR decreased uncoupling protein 1 expression in interscapular brown fat and beige cells in inguinal fat. More importantly, the lack of IGFIR resulted in an impaired cold acclimation. No differences in the total fat volume were found in the KO vs control mice. Epididymal fat showed larger adipocytes but with a lower number of adipocytes in KO vs control mice at age 12 months. In addition, KO mice showed a sustained moderate hyperinsulinemia and hypertriglyceridemia upon time and hepatic insulin insensitivity associated with lipid accumulation, with the outcome of a global insulin resistance. In addition, we found that the expression of uncoupling protein 3 in the skeletal muscle was decreased and its expression was increased in the heart in parallel with the expression of beta-2 adrenergic receptors. Upon nonobesogenic high-fat diet, we found a severe insulin resistance in the liver and in the skeletal muscle, but unchanged insulin sensitivity in the heart. In conclusion, our data suggest that IGFIR it is not an essential growth factor in the brown fat development in the presence of the IR and very high plasma levels of IGF-I, but it is indispensable for full brown fat functionality.

Indexed as

Insulin ResistanceThermogenesisAcclimatizationAdipocytesAdipose Tissue, BrownAnimalsBlotting, WesternCold TemperatureEpididymisGene ExpressionGlucoseHomeostasisHyperinsulinismHypertriglyceridemiaInsulin-Like Growth Factor IMaleGlucoseinsulin-like growth factor-1, mouseInsulin-Like Growth Factor IReceptor, IGF Type 1

Identifiers

PMID26910308
PMCPMC6285213
OpenAlexW2277072337

What OpenQuestion holds

Textmetadata
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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.