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Review
. 2020 Dec 12;10(12):1665.
doi: 10.3390/biom10121665.

The Influence of Physical Activity on the Bioactive Lipids Metabolism in Obesity-Induced Muscle Insulin Resistance

Monika Imierska  1 , Adam Kurianiuk  1 , Agnieszka Błachnio-Zabielska  1
Affiliations
Review

The Influence of Physical Activity on the Bioactive Lipids Metabolism in Obesity-Induced Muscle Insulin Resistance

Monika Imierska et al. Biomolecules. .

Abstract

High-fat diet consumption and lack of physical activity are important risk factors for metabolic disorders such as insulin resistance and cardiovascular diseases. Insulin resistance is a state of a weakened response of tissues such as skeletal muscle, adipose tissue, and liver to insulin, which causes an increase in blood glucose levels. This condition is the result of inhibition of the intracellular insulin signaling pathway. Skeletal muscle is an important insulin-sensitive tissue that accounts for about 80% of insulin-dependent glucose uptake. Although the exact mechanism by which insulin resistance is induced has not been thoroughly understood, it is known that insulin resistance is most commonly associated with obesity. Therefore, it is believed that lipids may play an important role in inducing insulin resistance. Among lipids, researchers' attention is mainly focused on biologically active lipids: diacylglycerols (DAG) and ceramides. These lipids are able to regulate the activity of intracellular enzymes, including those involved in insulin signaling. Available data indicate that physical activity affects lipid metabolism and has a positive effect on insulin sensitivity in skeletal muscles. In this review, we have presented the current state of knowledge about the impact of physical activity on insulin resistance and metabolism of biologically active lipids.

Keywords: insulin resistance; lipid metabolism; physical activity; skeletal muscle; type 2 diabetes.

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Conflict of interest statement

The authors declare no conflict of interest

Figures

Figure 1
Figure 1
Insulin signaling pathway; Insulin stimulates the insulin receptor (IR), leading to phosphorylation of insulin receptor substrate (IRS). Recruitment of phosphatidylinositol 3-kinase (PI3K), generated of the second messenger PIP3, leading to the recruitment of Akt and subsequent phosphorylation by the upstream mediators PDK1 and mTORC2. PDK1 phosphorylates and activates PKC-ζ and α isoforms. Activated Akt phosphorylates Akt substrate 160 (AS160), thereby inactivating its Rab-GAP domain and preventing the hydrolysis of GTP to GDP by Rab proteins. This results in processes promoting the translocation of GLUT4 to the cell surface.
Figure 2
Figure 2
Effects of physical activity on lipid metabolism and insulin sensitivity. Orange arrows—impact of exercise on lipid metabolism; green arrows—impact of physical activity on glucose metabolism.
See this image and copyright information in PMC

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