Evidence map›Paper›PMID 23919961›Full record

ArticleDiabetes2013

Adaptive changes of the Insig1/SREBP1/SCD1 set point help adipose tissue to cope with increased storage demands of obesity.

Stefania Carobbio, Rachel M Hagen, Christopher J Lelliott, Marc Slawik, Gema Medina-Gomez, Chong-Yew Tan, Audrey Sicard, Helen J Atherton, Nuria Barbarroja, Mikael Bjursell and 16 more

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
6.4field-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

49 citing papers in PubMed, 97 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. International journal of molecular sciences · 2024
    Article
  12. Article
  13. Adipose Tissue Hypoxia in Obesity: Clinical Reappraisal of Hypoxia Hypothesis.Advances in experimental medicine and biology · 2024
    Review
  14. Mechanism of Obesity-Related Lipotoxicity and Clinical Perspective.Advances in experimental medicine and biology · 2024
    Review
  15. Article
  16. Article
  17. Obesity wars: may the smell be with you.American journal of physiology. Endocrinology and metabolism · 2023
    Review
  18. Article
  19. Article
  20. 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

26 authors at 12 institutions in 8 countries.

Stefania CarobbioUniversity of Cambridge, Metabolic Research Laboratories, Institute of Metabolic Science Addenbrooke's Treatment Centre, Addenbrooke's Hospital, Cambridge, U.K.
Rachel M Hagen
Christopher J Lelliott
Marc Slawik
Gema Medina-Gomez
Chong-Yew Tan
Audrey Sicard
Helen J Atherton
Nuria Barbarroja
Mikael Bjursell
Mohammad Bohlooly-Y
Sam Virtue
Antoinette Tuthill
Etienne Lefai
Martine Laville
Tingting Wu
Robert V Considine
Hubert Vidal
Dominique Langin
Matej Oresic
Francisco J Tinahones
Jose Manuel Fernandez-Real
Julian L Griffin
Jaswinder K Sethi
Miguel López
Antonio Vidal-Puig
AstraZeneca (Sweden) · SEInserm · FRInstituto de Salud Carlos III · ESCentro de Investigación Biomédica en Red · ESHelsinki University Hospital · FIIndiana University School of MedicineLaboratoire CarMeN · FRLudwig-Maximilians-Universität München · DEUniversidade de Santiago de Compostela · ESUniversidad Rey Juan Carlos · ESUniversité Claude Bernard Lyon 1 · FRWellcome Sanger Institute · GB

Funding

Biotechnology and Biological Sciences Research Council BB/H002731/1Biotechnology and Biological Sciences Research Council BB/H013539/1Biotechnology and Biological Sciences Research Council JF16994British Heart Foundation PG/10/38/28359Medical Research Council G0600717Medical Research Council G0802051Medical Research Council MC_G0802535Medical Research Council MC_UP_A090_1006Medical Research Council MC_UU_12012/5
6 · The paper itself

Abstract

The epidemic of obesity imposes unprecedented challenges on human adipose tissue (WAT) storage capacity that may benefit from adaptive mechanisms to maintain adipocyte functionality. Here, we demonstrate that changes in the regulatory feedback set point control of Insig1/SREBP1 represent an adaptive response that preserves WAT lipid homeostasis in obese and insulin-resistant states. In our experiments, we show that Insig1 mRNA expression decreases in WAT from mice with obesity-associated insulin resistance and from morbidly obese humans and in in vitro models of adipocyte insulin resistance. Insig1 downregulation is part of an adaptive response that promotes the maintenance of SREBP1 maturation and facilitates lipogenesis and availability of appropriate levels of fatty acid unsaturation, partially compensating the antilipogenic effect associated with insulin resistance. We describe for the first time the existence of this adaptive mechanism in WAT, which involves Insig1/SREBP1 and preserves the degree of lipid unsaturation under conditions of obesity-induced insulin resistance. These adaptive mechanisms contribute to maintain lipid desaturation through preferential SCD1 regulation and facilitate fat storage in WAT, despite on-going metabolic stress.

Indexed as

Adaptation, Physiological3T3-L1 CellsAdipose Tissue, WhiteAnimalsDown-RegulationHumansInsulin ResistanceLipid MetabolismMembrane ProteinsMiceMice, KnockoutObesityObesity, MorbidRNA, MessengerStearoyl-CoA DesaturaseSterol Regulatory Element Binding Protein 1Insig1 protein, mouseMembrane ProteinsRNA, MessengerScd1 protein, mouseSrebf1 protein, mouseStearoyl-CoA DesaturaseSterol Regulatory Element Binding Protein 1

Identifiers

PMID23919961
PMCPMC3806615
OpenAlexW2134720556

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.