Perturbation of glycerol metabolism in hepatocytes from n3-PUFA-depleted rats

• Published in: International journal of molecular medicine Vol. 29; no. 6; pp. 1121 - 1126
• Main Authors: Portois, Laurence, Zhang, Ying, Ladrière, Laurence, Perret, Jason, Louchami, Karim, Gaspard, Nathalie, Hupkens, Emeline, Bolaky, Nargis, Delforge, Valérie, Beauwens, Renaud, Malaisse, Willy, Sener, Abdullah, Carpentier, Yvon, Delporte, Christine
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01-06-2012
• Subjects: Animals; Aquaporins - genetics; Aquaporins - metabolism; Carbon Radioisotopes; Fatty Acids, Unsaturated - deficiency; Female; Gene Expression Regulation; Glycerol - metabolism; Glycerol Kinase - metabolism; Hepatocytes - metabolism; Intracellular Space - metabolism; Liver - enzymology; Mice; Phospholipids - metabolism; Rats; RNA, Messenger - genetics; RNA, Messenger - metabolism; Time Factors; Triglycerides - metabolism
• ISSN: 1107-3756; 1791-244X
• DOI: 10.3892/ijmm.2012.943

Second generation n3-PUFA-depleted rats represent a good animal model of
metabolic syndrome as they display several features of the disease such as liver
steatosis, visceral obesity and insulin resistance. The goal of our study was
to investigate the influence of n3-PUFA deficiency on hepatic glycerol metabolism.
Aquaglyceroporin 9 (AQP9) allows hepatic glycerol transport and consequently contributes
to neoglucogenesis. AQP9 knockout mice display hypertriacyl-glycerolemia, one
of the hallmarks of the metabolic syndrome. Our data show reduced AQP9 expression
at the protein level in n3-PUFA-depleted rats, without any changes at the mRNA
levels. [U-14C]glycerol uptake was increased in hepatocytes from n3-PUFA-depleted
animal cells. The apparent discrepancy between decreased AQP9 protein expression,
and increased [U-14C]glycerol uptake could be explained by an observed increase
in glycerol kinase activity.