Evidence map›Paper›PMID 31279640›Full record

ArticleMolecular metabolism2019

Adipocyte Gs but not Gi signaling regulates whole-body glucose homeostasis.

Alexandre Caron, Ryan P Reynolds, Carlos M Castorena, Natalie J Michael, Charlotte E Lee, Syann Lee, Rebecca Berdeaux, Philipp E Scherer, Joel K Elmquist

Abstract read
In one paragraph

Article in Molecular metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Article
  2. Review
  3. Glucose sensing and homeostasis by adipocyte GPCR.Frontiers in endocrinology · 2025
    Review
  4. History and future of leptin: Discovery, regulation and signaling.Metabolism: clinical and experimental · 2024
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Adipocyte GNature communications · 2022
    Article
  12. Deletion ofFrontiers in endocrinology · 2022
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Lack of GαMolecular metabolism · 2020
    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

9 authors.

Alexandre CaronDepartment of Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: Alexandre.Caron@UTSouthwestern.edu.
Ryan P ReynoldsDepartment of Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Carlos M CastorenaDepartment of Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Natalie J MichaelDepartment of Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Charlotte E LeeDepartment of Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Syann LeeDepartment of Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Rebecca BerdeauxDepartment of Integrative Biology and Pharmacology, Center for Metabolic and Degenerative Diseases at the Brown Foundation, Institute of Molecular Medicine, McGovern Medical School at The University of Texas Health Science Center at Houston (UTHealth), Graduate Program in Biochemistry and Cell Biology, MD Anderson Cancer Center-UTHealth Graduate School of Biomedical Sciences, Houston, TX, USA.
Philipp E SchererTouchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Joel K ElmquistDepartment of Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: Joel.Elmquist@UTSouthwestern.edu.

Funding

Interactions of Leptin and the Melanocortin SystemR01DK118725 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JOEL K. ELMQUIST · 2018 to 2026
$3.5M
Regulation of glucose utilization by skeletal muscle SIK1R01DK092590 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BERDEAUX, REBECCA L · 2011 to 2021
$3.3M
The role of SIK1 in myogenic differentiation and skeletal muscle repairR01AR059847 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BERDEAUX, REBECCA L · 2011 to 2015
$1.7M
Endocannabinoids: Obesity and Insulin ResistanceK01DK111644 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI CASTORENA, CARLOS MICHEL · 2018 to 2020
$360k
Sympathetic Control of Liver MetabolismK99DK120894 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI CARON, ALEXANDRE · 2019 to 2019
$92k
CIHRNIAMS NIH HHS R01 AR059847NIDDK NIH HHS K01 DK111644NIDDK NIH HHS K99 DK120894NIDDK NIH HHS R01 DK092590NIDDK NIH HHS R01 DK118725
6 · The paper itself

Abstract

objectiveThe sympathetic nervous system (SNS) is a key regulator of the metabolic and endocrine functions of adipose tissue. Increased SNS outflow promotes fat mobilization, stimulates non-shivering thermogenesis, promotes browning, and inhibits leptin production. Most of these effects are attributed to norepinephrine activation of the Gs-coupled beta adrenergic receptors located on the surface of the adipocytes. Evidence suggests that other adrenergic receptor subtypes, including the Gi-coupled alpha 2 adrenergic receptors might also mediate the SNS effects on adipose tissue. However, the impact of acute stimulation of adipocyte Gs and Gi has never been reported.

methodsWe harness the power of chemogenetics to develop unique mouse models allowing the specific and spatiotemporal stimulation of adipose tissue Gi and Gs signaling. We evaluated the impact of chemogenetic stimulation of these pathways on glucose homeostasis, lipolysis, leptin production, and gene expression.

resultsStimulation of Gs signaling in adipocytes induced rapid and sustained hypoglycemia. These hypoglycemic effects were secondary to increased insulin release, likely consequent to increased lipolysis. Notably, we also observed differences in gene regulation and ex vivo lipolysis in different adipose depots. In contrast, acute stimulation of Gi signaling in adipose tissue did not affect glucose metabolism or lipolysis, but regulated leptin production.

conclusionOur data highlight the significance of adipose Gs signaling in regulating systemic glucose homeostasis. We also found previously unappreciated heterogeneity across adipose depots following acute stimulation. Together, these results highlight the complex interactions of GPCR signaling in adipose tissue and demonstrate the usefulness of chemogenetic technology to better understand adipocyte function.

Indexed as

AdipocytesAnimalsGlucoseGTP-Binding Protein alpha Subunits, Gi-GoGTP-Binding Protein alpha Subunits, GsHomeostasisHypoglycemiaInsulinLeptinMaleMice, Inbred C57BLReceptors, G-Protein-CoupledSignal TransductionGlucoseGTP-Binding Protein alpha Subunits, Gi-GoGTP-Binding Protein alpha Subunits, GsInsulinLeptinReceptors, G-Protein-CoupledAdipose tissueDREADDGlucoseInsulinLeptinLipolysis

Identifiers

PMID31279640
PMCPMC6717754

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.