An article “Specific collagen XVIII isoforms promote adipose tissue accrual via mechanisms determining adipocyte number and affect fat deposition” from the Pihlajaniemi Group with Mari Aikio as the first author was recently published in PNAS. Researchers describe a previously unidentified role for collagen XVIII—a ubiquitous, structurally complex basement membrane proteoglycan- in supporting preadipocyte differentiation and the maintenance of this differentiated state, and hence the size and lipid-clearing/storage functions of white adipose tissue depots. Specific lack of medium/long isoforms of this nonfibrillar collagen in mice led to reduced adiposity, ectopic deposition of fat in liver, and elevated very low-density lipoprotein-triglyceride levels.
Human genetic linkage studies have returned robust statistical evidence of linkage between the chromosome 21 interval housing COL18A1 and the Familial Combined Hyperlipidemia-Triglyceride trait. In this study, scientists found a positive correlation between expression of medium/long isoforms of collagen XVIII in visceral fat and serum free fatty acid levels, suggesting that collagen α1 (XVIII) expression contributes to regulation of adipose tissue metabolism in visceral obesity.
The finding of a previously unidentified extracellular mechanism contributing to control of adipogenesis is expected to promote understanding of the molecular and functional bases of human hyperlipidemic syndromes associated with fatty liver.
The article by Aikio et al. can be found here.
Last updated: 2.9.2016