AMP-activated protein kinase, fatty acid metabolism, and insulin sensitivity

作者：Smith Brennan K; Steinberg Gregory R

来源：Current Opinion in Clinical Nutrition and Metabolic Care, 2017, 20(4): 248-253.

DOI：10.1097/MCO.0000000000000380

• AMP-activated protein kinase
• acetyl-CoA carboxylase
• de novo lipogenesis
• fatty acid metabolism
• insulin resistance
• mitochondria

Purpose of review
Insulin resistance is an important risk factor for metabolic diseases such as type 2 diabetes, cardiovascular disease and certain cancers. A common characteristic of strategies that improve insulin sensitivity involves the activation of the energy sensing enzyme of the cell, AMP-activated protein kinase (AMPK). The purpose of this review is to explore the mechanisms associated with AMPK activation to improve insulin sensitivity with a focus on fatty acid metabolism. We will also discuss the literature surrounding direct AMPK activators to improve insulin resistance and important considerations for the design of direct AMPK activators.
Recent findings
AMPK activation can decrease de novo lipogenesis, increase fatty acid oxidation and promote mitochondrial integrity to improve insulin sensitivity. Drugs targeted to directly activate AMPK show therapeutic promise, yet in vivo data is lacking.
Summary
Designing a drug to directly activate AMPK may improve insulin resistance by reducing liver de novo lipogenesis and increasing brown and white adipose tissue mitochondrial function. However, in vivo experimental procedures to support this notion are not extensive and more research is required.

• 出版日期2017-7