Evidence map›Paper›PMID 30598026›Full record

ReviewInternational journal of molecular sciences2018

The Effects of Systemic and Local Acidosis on Insulin Resistance and Signaling.

Nicola Baldini, Sofia Avnet

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

31 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Chronic NHScientific reports · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Insulin Resistance and Urolithiasis as a Challenge for a Dietitian.International journal of environmental research and public health · 2022
    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

2 authors at 1 institution in 1 country.

Nicola BaldiniOrthopaedic Pathophysiology and Regenerative Medicine Unit, Istituto Ortopedico Rizzoli IRCCS, 40136 Bologna, Italy. nicola.baldini@ior.it.
Sofia AvnetOrthopaedic Pathophysiology and Regenerative Medicine Unit, Istituto Ortopedico Rizzoli IRCCS, 40136 Bologna, Italy. sofia.avnet@ior.it.ORCID 0000-0002-7843-0591
Istituto Ortopedico Rizzoli · IT

Funding

financial support for Scientific Research "5 per mille 2015" noneItalian Association for Cancer Research 15608
6 · The paper itself

Abstract

Most pathological conditions that cause local or systemic acidosis by overcoming the buffering activities of body fluids overlap with those diseases that are characterized by glucose metabolic disorders, including diabetes mellitus, inflammation, and cancer. This simple observation suggests the existence of a strong relationship between acidosis and insulin metabolism or insulin receptor signaling. In this review, we summarized the current knowledge on the activity of insulin on the induction of acidosis and, vice versa, on the effects of changes of extracellular and intracellular pH on insulin resistance. Insulin influences acidosis by promoting glycolysis. Although with an unclear mechanism, the lowering of pH, in turn, inhibits insulin sensitivity or activity. In addition to ketoacidosis that is frequently associated with diabetes, other important and more complex factors are involved in this delicate feedback mechanism. Among these, in this review we discussed the acid-mediated inhibiting effects on insulin binding affinity to its receptor, on glycolysis, on the recycling of glucose transporters, and on insulin secretion via transforming growth factor β (TGF-β) activity by pancreatic β-cells. Finally, we revised current data available on the mutual interaction between insulin signaling and the activity of ion/proton transporters and pH sensors, and on how acidosis may enhance insulin resistance through the Nuclear Factor kappa B (NF-κB) inflammatory pathway.

Indexed as

Insulin ResistanceSignal TransductionAcidosisAnimalsHumansInsulinIon TransportReceptor, InsulinInsulinReceptor, Insulinacidosisacid-sensing ion channelsglucose metabolisminsulin receptorion/proton transporters

Identifiers

PMID30598026
PMCPMC6337415
OpenAlexW2907478018

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.