Abstract

Obesity and type 2 diabetes mellitus are complicated metabolic diseases that affect multiple organs and are characterized by hyperglycaemia. Currently, stable and effective treatments for obesity and type 2 diabetes mellitus are not available. Therefore, the mechanisms leading to obesity and diabetes and more effective ways to treat obesity and diabetes should be identified. Based on accumulated evidences, the PI3K/AKT signalling pathway is required for normal metabolism due to its characteristics, and its imbalance leads to the development of obesity and type 2 diabetes mellitus. This review focuses on the role of PI3K/AKT signalling in the skeletal muscle, adipose tissue, liver, brain and pancreas, and discusses how this signalling pathway affects the development of the aforementioned diseases. We also summarize evidences for recently identified therapeutic targets of the PI3K/AKT pathway as treatments for obesity and type 2 diabetes mellitus. PI3K/AKT pathway damaged in various tissues of the body leads to obesity and type 2 diabetes as the result of insulin resistance, and in turn, insulin resistance exacerbates the PI3K/AKT pathway, forming a vicious circle.

Keywords

Insulin resistancePI3K/AKT/mTOR pathwayDiabetes mellitusProtein kinase BObesityType 2 diabetesMedicineEndocrinologyType 2 Diabetes MellitusInternal medicineAdipose tissueInsulinType 1 diabetesBioinformaticsBiologySignal transductionCell biology

MeSH Terms

AnimalsDiabetes MellitusType 2HumansInsulin ResistanceObesityPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal Transduction

Affiliated Institutions

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Publication Info

Year
2018
Type
review
Volume
14
Issue
11
Pages
1483-1496
Citations
1475
Access
Closed

Social Impact

Social media, news, blog, policy document mentions

Citation Metrics

1475
OpenAlex
36
Influential
1314
CrossRef

Cite This

Xingjun Huang, Guihua Liu, Jiao Guo et al. (2018). The PI3K/AKT pathway in obesity and type 2 diabetes. International Journal of Biological Sciences , 14 (11) , 1483-1496. https://doi.org/10.7150/ijbs.27173

Identifiers

DOI
10.7150/ijbs.27173
PMID
30263000
PMCID
PMC6158718

Data Quality

Data completeness: 86%