Insulin resistance: Review of the underlying molecular mechanisms
By Habib Yaribeygi, F. R. Farrokhi, A. Butler, Amirhossein Sahebkar. Journal of Cellular Physiology, 2018
765 citations recorded by the source corpus.
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.
Subfields: Molecular Biology, Physiology, Surgery
View Paper: https://www.semanticscholar.org/paper/b783d96c71371dc390d68f5086d89c5cd25a651b
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- Yiwen Li
- T. Sathyapalan
- Yanfei Liu
- S. Atkin
- Shiwei Liu
- Amirhossein Sahebkar
- Habib Yaribeygi
- Mengqi Gao
Citations in the corpus
- Molecular Mechanisms Linking Oxidative Stress and Diabetes Mellitus (2020, background): “Although there are several studies to elucidate the molecular mechanisms underlying the development of diabetes complications [5–8], their precise pathophysiology is not completely understood [8].”
- Diabetic vascular diseases: molecular mechanisms and therapeutic strategies (2023, background): “Insulin resistance is the most common and widespread molecular mechanism of diabetic complications, not only in the high glucose state with extensive activation of insulin receptor signaling pathways, such as the regulation of glucose uptake by GLUT.438 Even in the presence of normal blood glucose, ”