Aim: 

Endocannabinoids are orexigenic mediators acting at multiple peripheral sites, including adipose tissue, liver and skeletal muscle to promote lipogenesis, limit fat elimination and reduce energy expenditure. The two major endocannabinoids, anandamide (AEA) and 2 arachidonoyl-glycerol (2-AG) derive from arachidonic acid (AA). Particularly, AEA and 2-AG derive from phospholipid AA in position sn-1 and sn-2 respectively. We aim to verify whether dietary fatty acid composition may modulate endocannabinoid biosynthesis by modifying arachidonic incorporation in tissue phospholipids.

Methods: 

Fatty acid phospholipids, and their incorporation in position sn-1 and sn-2, AEA and 2-AG were measured by HPLC-MS in mouse adipocytes incubated with different polyunsaturated fatty acids (PUFAs) and in visceral and subcutaneous adipose tissue, liver and heart of obese rats fed with different dietary fatty acids.

Results: 

In vitro and in vivo data show that AEA and 2-AG tissue concentration were strongly influenced by tissue AA incorporation in position sn-1 and sn-2 phospholipids. In particular, dietary n-3 fatty acids and conjugated linoleic acid were the most active in modulating endocannabinoid tissue concentration, improving metabolic consequences of obesity in visceral adipose tissue liver and heart.

Conclusion: 

Our data clearly show that dietary fatty acids strongly affect tissue endocannabinoids and thereby modulating lipid metabolism and tissue fat distribution, resulting in an overall improvement of obesity metabolic consequences such as abnormal fat deposition in liver and heart.