Evidence map›Paper›PMID 30619718›Full record

ReviewJournal of clinical & translational endocrinology2019

Metabolic effects of glucagon in humans.

María M Adeva-Andany, Raquel Funcasta-Calderón, Carlos Fernández-Fernández, Elvira Castro-Quintela, Natalia Carneiro-Freire

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical & translational endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.

  1. Pooled it
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  4. Effects of Glucagon-Like Peptide-1 Receptor Agonists (Mono and Combination Therapy) on Energy Expenditure: A Scoping Review.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
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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.

María M Adeva-AndanyInternal Medicine Department, Hospital General Juan Cardona, c/ Pardo Bazán s/n, 15406 Ferrol, Spain.
Raquel Funcasta-CalderónInternal Medicine Department, Hospital General Juan Cardona, c/ Pardo Bazán s/n, 15406 Ferrol, Spain.
Carlos Fernández-FernándezInternal Medicine Department, Hospital General Juan Cardona, c/ Pardo Bazán s/n, 15406 Ferrol, Spain.
Elvira Castro-QuintelaInternal Medicine Department, Hospital General Juan Cardona, c/ Pardo Bazán s/n, 15406 Ferrol, Spain.
Natalia Carneiro-FreireInternal Medicine Department, Hospital General Juan Cardona, c/ Pardo Bazán s/n, 15406 Ferrol, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes is a common metabolic disorder that involves glucose, amino acids, and fatty acids. Either insulin deficiency or insulin resistance may cause diabetes. Insulin deficiency causes type 1 diabetes and diabetes associated with total pancreatectomy. Glucagon produces insulin resistance. Glucagon-induced insulin resistance promotes type 2 diabetes and diabetes associated with glucagonoma. Further, glucagon-induced insulin resistance aggravates the metabolic consequences of the insulin-deficient state. A major metabolic effect of insulin is the accumulation of glucose as glycogen in the liver. Glucagon opposes hepatic insulin action and enhances the rate of gluconeogenesis, increasing hepatic glucose output. In order to support gluconeogenesis, glucagon promotes skeletal muscle wasting to supply amino acids as gluconeogenic precursors. Glucagon promotes hepatic fatty acid oxidation to supply energy required to sustain gluconeogenesis. Hepatic fatty acid oxidation generates β-hydroxybutyrate and acetoacetate (ketogenesis). Prospective studies reveal that elevated glucagon secretion at baseline occurs in healthy subjects who develop impaired glucose tolerance at follow-up compared with subjects who maintain normal glucose tolerance, suggesting a relationship between elevated glucagon secretion and development of impaired glucose tolerance. Prospective studies have identified animal protein consumption as an independent risk factor for type 2 diabetes and cardiovascular disease. Animal protein intake activates glucagon secretion inducing sustained elevations in plasma glucagon. Glucagon is a major hormone that causes insulin resistance. Insulin resistance is an established cardiovascular risk factor additionally to its pathogenic role in diabetes. Glucagon may be a potential link between animal protein intake and the risk of developing type 2 diabetes and cardiovascular disease.

Indexed as

Animal proteinBCAA, branched-chain amino acidCardiovascular riskDiabetesGlucagonImpaired glucose toleranceInsulin resistanceSGLT2, sodium-glucose co-transporter-2T1D, type 1 diabetesT2D, type 2 diabetesVegetable protein

Identifiers

PMID30619718
PMCPMC6312800
OpenAlexW2906355073

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.