Cited by 929Metabolism, Diabetes, and CancerAdipokines, Inflammation, and Metabolic DiseasesPancreatic function and diabetes

Insulin resistance: review of the underlying molecular mechanisms

Yaribeygi, Habib, Farrokhi, Farin Rashid, Butler, Alexandra E., Sahebkar, Amirhossein·2019·Journal of Cellular Physiology

Abstract

Most human cells utilize glucose as the primary substrate, cellular uptake requiring insulin. Insulin signaling is therefore critical for these tissues. However, decrease in insulin sensitivity due to the disruption of various molecular pathways causes insulin resistance (IR). IR underpins many metabolic disorders such as type 2 diabetes and metabolic syndrome, impairments in insulin signaling disrupting entry of glucose into the adipocytes, and skeletal muscle cells. Although the exact underlying cause of IR has not been fully elucidated, a number of major mechanisms, including oxidative stress, inflammation, insulin receptor mutations, endoplasmic reticulum stress, and mitochondrial dysfunction have been suggested. In this review, we consider the role these cellular mechanisms play in the development of IR.

Integrity signals

Registry

Crossref · 10.1002/jcp.27603

Cites

100 of 100 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Yaribeygi, H., Farrokhi, F. R., Butler, A. E., & Sahebkar, A.
Affiliations
  • Shahid Beheshti University (IR)
  • Diabetes Research Center, Qatar Biomedical Research Institute Doha Qatar
  • Mashhad University of Medical Sciences (IR)
Corresponding author
Sahebkar, Amirhossein
Venue
Journal of Cellular Physiology
Publisher
Wiley
Published
2018-10-14
Volume
234
Issue
6
Pages
8152-8161
ISSN
  • 0021-9541 (ISSN-L)
  • 1097-4652
OpenAlex
W2897277000
Cited by
929
References
100
Citations by year
2026: 76 · 2025: 119 · 2024: 187 · 2023: 164 · 2022: 168 · 2021: 116 · 2020: 66 · 2019: 30 · 2018: 2
FWCI
5.26
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Cellular Physiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
insulin resistance, insulin signaling, type 2 diabetes, metabolic syndrome, oxidative stress, inflammation, insulin receptor mutations, endoplasmic reticulum stress, mitochondrial dysfunction, glucose uptake, adipocytes, skeletal muscle
MeSH terms
Diabetes Mellitus, Type 2, Glucose, Humans, Inflammation, Insulin, Insulin Resistance, Mitochondria, Signal Transduction, Oxidative Stress, Muscle, Skeletal, Metabolic Syndrome, Endoplasmic Reticulum Stress

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review