The PI3K/AKT pathway in obesity and type 2 diabetes

Area of Science:

• Metabolic diseases
• Molecular signaling pathways

Background:

• Obesity and type 2 diabetes mellitus (T2DM) are complex metabolic disorders impacting multiple organs.
• Current treatments for obesity and T2DM lack stability and efficacy, necessitating identification of underlying mechanisms and novel therapeutic strategies.
• The phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway is integral to normal metabolism, and its dysregulation is implicated in obesity and T2DM pathogenesis.

Purpose of the Study:

• To review the role of the PI3K/AKT signaling pathway in key metabolic tissues.
• To elucidate how PI3K/AKT pathway dysregulation contributes to obesity and T2DM.
• To summarize emerging therapeutic targets within the PI3K/AKT pathway for treating these metabolic diseases.

Main Methods:

• Literature review of existing evidence on PI3K/AKT signaling in metabolism.
• Analysis of the pathway's involvement in skeletal muscle, adipose tissue, liver, brain, and pancreas.
• Synthesis of data on therapeutic targets related to the PI3K/AKT pathway.

Main Results:

• Imbalance in the PI3K/AKT pathway is a significant factor in the development of obesity and T2DM.
• Insulin resistance exacerbates PI3K/AKT pathway damage, creating a detrimental feedback loop.
• The PI3K/AKT pathway's role in insulin resistance is evident across multiple metabolic tissues.

Conclusions:

• The PI3K/AKT pathway is a critical regulator of metabolism, and its disruption is central to obesity and T2DM.
• Targeting the PI3K/AKT pathway presents a promising therapeutic avenue for managing obesity and T2DM.
• Understanding the interplay between insulin resistance and the PI3K/AKT pathway is key to developing effective treatments.