Evidence map›Paper›PMID 21824265›Full record

ReviewDiabetes, obesity & metabolism2011

Physiologic action of glucagon on liver glucose metabolism.

C J Ramnanan, D S Edgerton, G Kraft, A D Cherrington

Open access · bronzeAbstract readReview
In one paragraph

Review in Diabetes, obesity & metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed, 3 pooled it
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

143 citing papers in PubMed, 3 syntheses or guidelines pooled it, 287 citations in OpenAlex.

  1. Pooled it
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  9. Effect of Pramlintide on Postprandial Glucose Fluxes in Type 1 Diabetes.The Journal of clinical endocrinology and metabolism · 2016
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  14. Article
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  16. Review
  17. The evolving landscape of obesity pharmacotherapy.Nature reviews. Drug discovery · 2026
    Review
  18. Article
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  20. Article

83 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

C J RamnananDepartment of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232-0615, USA.
D S Edgerton
G Kraft
A D Cherrington
Vanderbilt University · US

Funding

Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ALVIN C POWERS · 2012 to 2026
$29.3M
GLUCONEOGENESIS &GLYCOGENOLYSIS:ROLE &REGULATIONR01DK018243 · NIDDK · VANDERBILT UNIVERSITY · PI Alan D Cherrington, Dale S Edgerton · 1986 to 2026
$12.2M
NIDDK NIH HHS P30 DK020593NIDDK NIH HHS R01 DK018243NIDDK NIH HHS R01-DK-18243
6 · The paper itself

Abstract

Glucagon is a primary regulator of hepatic glucose production (HGP) in vivo during fasting, exercise and hypoglycaemia. Glucagon also plays a role in limiting hepatic glucose uptake and producing the hyperglycaemic phenotype associated with insulin deficiency and insulin resistance. In response to a physiological rise in glucagon, HGP is rapidly stimulated. This increase in HGP is entirely attributable to an enhancement of glycogenolysis, with little to no acute effect on gluconeogenesis. This dramatic rise in glycogenolysis in response to hyperglucagonemia wanes with time. A component of this waning effect is known to be independent of hyperglycemia, though the molecular basis for this tachyphylaxis is not fully understood. In the overnight fasted state, the presence of basal glucagon secretion is essential in countering the suppressive effects of basal insulin, resulting in the maintenance of appropriate levels of glycogenolysis, fasting HGP and blood glucose. The enhancement of glycogenolysis in response to elevated glucagon is critical in the life-preserving counterregulatory response to hypoglycaemia, as well as a key factor in providing adequate circulating glucose for working muscle during exercise. Finally, glucagon has a key role in promoting the catabolic consequences associated with states of deficient insulin action, which supports the therapeutic potential in developing glucagon receptor antagonists or inhibitors of glucagon secretion.

Indexed as

AnimalsBlood GlucoseDogsFastingGlucagonGluconeogenesisInsulinLiverPhysical Conditioning, AnimalBlood GlucoseGlucagonInsulin

Identifiers

PMID21824265
PMCPMC5371022
OpenAlexW2013438463

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.