Evidence map›Paper›PMID 27548523›Full record

ArticleThe Journal of clinical investigation2016

β1-Adrenergic receptor deficiency in ghrelin-expressing cells causes hypoglycemia in susceptible individuals.

Bharath K Mani, Sherri Osborne-Lawrence, Prasanna Vijayaraghavan, Chelsea Hepler, Jeffrey M Zigman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
  2. LEAP2 changes with body mass and food intake in humans and mice.The Journal of clinical investigation · 2019
    Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. β-Adrenergic Signaling Promotes Morphological Maturation of Astrocytes in Female Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  8. Article
  9. Ghrelin receptor signaling in health and disease: a biased view.Trends in endocrinology and metabolism: TEM · 2023
    Review
  10. Article
  11. Unexpected role for IGF-1 in starvation: Maintenance of blood glucose.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Article
  13. Ghrelin mediated regulation of neurosynaptic transmitters in depressive disorders.Current research in pharmacology and drug discovery · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  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

5 authors.

Bharath K Mani
Sherri Osborne-Lawrence
Prasanna Vijayaraghavan
Chelsea Hepler
Jeffrey M Zigman

Funding

Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ALVIN C POWERS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI POWERS, ALVIN C · 1986 to 2011
$28.1M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
Role of the hormone LEAP2 in eating, body weight, blood glucose and survivalR01DK103884 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI ZIGMAN, JEFFREY M · 2015 to 2023
$3.4M
NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P60 DK020593NIDDK NIH HHS R01 DK103884NIDDK NIH HHS U24 DK059637
6 · The paper itself

Abstract

Ghrelin is an orexigenic gastric peptide hormone secreted when caloric intake is limited. Ghrelin also regulates blood glucose, as emphasized by the hypoglycemia that is induced by caloric restriction in mouse models of deficient ghrelin signaling. Here, we hypothesized that activation of β1-adrenergic receptors (β1ARs) localized to ghrelin cells is required for caloric restriction-associated ghrelin release and the ensuing protective glucoregulatory response. In mice lacking the β1AR specifically in ghrelin-expressing cells, ghrelin secretion was markedly blunted, resulting in profound hypoglycemia and prevalent mortality upon severe caloric restriction. Replacement of ghrelin blocked the effects of caloric restriction in β1AR-deficient mice. We also determined that treating calorically restricted juvenile WT mice with beta blockers led to reduced plasma ghrelin and hypoglycemia, the latter of which is similar to the life-threatening, fasting-induced hypoglycemia observed in infants treated with beta blockers. These findings highlight the critical functions of ghrelin in preventing hypoglycemia and promoting survival during severe caloric restriction and the requirement for ghrelin cell-expressed β1ARs in these processes. Moreover, these results indicate a potential role for ghrelin in mediating beta blocker-associated hypoglycemia in susceptible individuals, such as young children.

Indexed as

AnimalsAtenololBlood GlucoseBody WeightCaloric RestrictionFemaleGastric MucosaGene DeletionGhrelinHypoglycemiaInsulinMaleMiceMice, Inbred C57BLMice, TransgenicReceptors, Adrenergic, beta-1Adrb1 protein, mouseAtenololBlood GlucoseGhrelinInsulinReceptors, Adrenergic, beta-1Recombinant Proteins

Identifiers

PMID27548523
PMCPMC5004971
OpenAlexW2510941321

What OpenQuestion 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 OpenQuestion graph.