Evidence map›Paper›PMID 25740694›Full record

ArticleDiabetologia2015

The role of mouse Akt2 in insulin-dependent suppression of adipocyte lipolysis in vivo.

Shlomit Koren, Lisa M DiPilato, Matthew J Emmett, Abigail L Shearin, Qingwei Chu, Bob Monks, Morris J Birnbaum

Open access · bronzeAbstract read
In one paragraph

Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Anti-Lipolysis Induced by Insulin in Diverse Pathophysiologic Conditions of Adipose Tissue.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. The Akt pathway in oncology therapy and beyond (Review).International journal of oncology · 2018
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  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

7 authors at 1 institution in 1 country.

Shlomit KorenThe Institute for Diabetes, Obesity and Metabolism, University of Pennsylvania, Philadelphia, PA, USA.
Lisa M DiPilato
Matthew J Emmett
Abigail L Shearin
Qingwei Chu
Bob Monks
Morris J Birnbaum
University of Pennsylvania · US

Funding

The regulation of adipocyte lipolysis by insulinR01DK093959 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SEALE, PATRICK · 2011 to 2014
$1.4M
Control of Brown Adipose Physiology Via Genomic Recruitment of Histone Deacetylase 3F30DK104513 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI EMMETT, MATTHEW J · 2014 to 2016
$106k
Metabolic defects in mice with adipocyte-specific deletion of Akt2F30DK100123 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SHEARIN, ABIGAIL · 2013 to 2015
$88k
NIDDK NIH HHS F30 DK100123NIDDK NIH HHS F30DK100123NIDDK NIH HHS F30 DK104513NIDDK NIH HHS F30DK104513NIDDK NIH HHS F32DK884442NIDDK NIH HHS R01 DK093959NIDDK NIH HHS R01DK093959
6 · The paper itself

Abstract

aim/hypothesisThe release of fatty acids from adipocytes, i.e. lipolysis, is maintained under tight control, primarily by the opposing actions of catecholamines and insulin. A widely accepted model is that insulin antagonises catecholamine-dependent lipolysis through phosphorylation and activation of cAMP phosphodiesterase 3B (PDE3B) by the serine-threonine protein kinase Akt (protein kinase B). Recently, this hypothesis has been challenged, as in cultured adipocytes insulin appears, under some conditions, to suppress lipolysis independently of Akt.

methodsTo address the requirement for Akt2, the predominant isoform expressed in classic insulin target tissues, in the suppression of fatty acid release in vivo, we assessed lipolysis in mice lacking Akt2.

resultsIn the fed state and following an oral glucose challenge, Akt2 null mice were glucose intolerant and hyperinsulinaemic, but nonetheless exhibited normal serum NEFA and glycerol levels, suggestive of normal suppression of lipolysis. Furthermore, insulin partially inhibited lipolysis in Akt2 null mice during an insulin tolerance test (ITT) and hyperinsulinaemic-euglycaemic clamp, respectively. In support of these in vivo observations, insulin antagonised catecholamine-induced lipolysis in primary brown fat adipocytes from Akt2-deficient mice. CONCLUSIONS/

interpretationThese data suggest that suppression of lipolysis by insulin in hyperinsulinaemic states can take place in the absence of Akt2.

Indexed as

AdipocytesAnimalsHypoglycemic AgentsInsulinInsulin ResistanceLipolysisMicePhosphorylationProto-Oncogene Proteins c-aktSignal TransductionAkt2 protein, mouseHypoglycemic AgentsInsulinProto-Oncogene Proteins c-akt

Identifiers

PMID25740694
PMCPMC4393789
OpenAlexW2069508779

What OpenQuestion holds

Textmetadata
LicenceTDM
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.