Evidence map›Paper›PMID 32872570›Full record

ReviewInternational journal of molecular sciences2020

Pathophysiology of Type 2 Diabetes Mellitus.

Unai Galicia-Garcia, Asier Benito-Vicente, Shifa Jebari, Asier Larrea-Sebal, Haziq Siddiqi, Kepa B Uribe, Helena Ostolaza, César Martín

Registry-linked trialOpen access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06059833 (Serum Magnesium Level in Type 2 Diabetes Mellitus), which is not on this map. Cited by 1,418 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,418citing papers in PubMed, 3 pooled it
140.6field-weighted citation impact, top 1% 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.

NCT06059833 unknown statusnot on this mapstarted 2023, after this paper: background citation

Serum Magnesium Level in Type 2 Diabetes Mellitus

TypeobservationalSponsorSohag UniversityRan2023 to 2024Enrolled120ConditionsDiabetes MellitusArmsMagnesium
3 · Its place in the literature

Who cites it

1,418 citing papers in PubMed, 3 syntheses or guidelines pooled it, 2,963 citations in OpenAlex.

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1,358 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

8 authors at 4 institutions in 2 countries.

Unai Galicia-GarciaFundación Biofisika Bizkaia, Barrio Sarriena s/n., 48940 Leioa (Bizkaia), Spain.
Asier Benito-VicenteBiofisika Institute (UPV/EHU, CSIC), Barrio Sarriena s/n., 48940 Leioa (Bizkaia), Spain.
Shifa JebariBiofisika Institute (UPV/EHU, CSIC), Barrio Sarriena s/n., 48940 Leioa (Bizkaia), Spain.
Asier Larrea-SebalFundación Biofisika Bizkaia, Barrio Sarriena s/n., 48940 Leioa (Bizkaia), Spain.
Haziq SiddiqiHavard Medical School, 25 Shattuck St, Boston, MA 02115, USA.
Kepa B UribeCenter for Cooperative Research in Biomaterials (CIC biomaGUNE), Basque Research and Technology Alliance (BRTA), Paseo de Miramon 182, 20014 Donostia San Sebastián, Spain.
Helena OstolazaBiofisika Institute (UPV/EHU, CSIC), Barrio Sarriena s/n., 48940 Leioa (Bizkaia), Spain.
César MartínBiofisika Institute (UPV/EHU, CSIC), Barrio Sarriena s/n., 48940 Leioa (Bizkaia), Spain.ORCID 0000-0002-4087-8729
University of the Basque Country · ESInstituto Biofisika · ESCIC biomaGUNE · ESLemuel Shattuck Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 Diabetes Mellitus (T2DM), one of the most common metabolic disorders, is caused by a combination of two primary factors: defective insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond appropriately to insulin. Because insulin release and activity are essential processes for glucose homeostasis, the molecular mechanisms involved in the synthesis and release of insulin, as well as in its detection are tightly regulated. Defects in any of the mechanisms involved in these processes can lead to a metabolic imbalance responsible for the development of the disease. This review analyzes the key aspects of T2DM, as well as the molecular mechanisms and pathways implicated in insulin metabolism leading to T2DM and insulin resistance. For that purpose, we summarize the data gathered up until now, focusing especially on insulin synthesis, insulin release, insulin sensing and on the downstream effects on individual insulin-sensitive organs. The review also covers the pathological conditions perpetuating T2DM such as nutritional factors, physical activity, gut dysbiosis and metabolic memory. Additionally, because T2DM is associated with accelerated atherosclerosis development, we review here some of the molecular mechanisms that link T2DM and insulin resistance (IR) as well as cardiovascular risk as one of the most important complications in T2DM.

Indexed as

HomeostasisInsulin SecretionAnimalsBlood GlucoseDiabetes Mellitus, Type 2HumansBlood Glucoseadipocytecardiovascular diseaseinsulin resistancelivermusclepathophysiologytype 2 diabetes mellitusβ-cell

Identifiers

PMID32872570
PMCPMC7503727
OpenAlexW3081655479

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.