Adipogenic genes expression in relation to hepatic steatosis in the liver of two duck species. (3rd May 2018)

• Record Type: Journal Article
• Authors: Hérault, F.; Duby, C.; Baéza, E.; Diot, C.
• Is Part Of: Animal. Volume 12:Number 12(2018)
• Page Start: 2571
• Page End: 2577
• Publication Date: 2018-05-03
• Subjects: adipokines, -- proliferator-activated receptor gamma, -- leptin receptor, -- fatty liver, -- waterfowls; Animal breeding -- Periodicals; Animal genetics -- Periodicals; Animal nutrition -- Periodicals; Animal physiology -- Periodicals; Environmental sciences -- Periodicals; 636.005
• DOI: 10.1017/S1751731118000897
• Languages: English
• ISSNs: 1751-7311

Abstract

Abstract : Some studies have shown that expression of peroxisome proliferator-activated receptor gamma ( PPARG ), a key regulator of adipogenesis, and of some adipocyte-specific genes or adipokines are expressed in hepatic steatosis, leading to the concept of 'adipogenic hepatic steatosis' or 'hepatic adiposis.' Most of these studies were conducted in genetic obese mouse models or after manipulation of gene expression. The relevance of this concept to other species and more physiological models was here addressed in ducks which are able to develop hepatic steatosis after overfeeding. The expression of PPARG and other adipocyte-specific genes was thus analyzed in the liver of ducks fed ad libitum or overfed and compared with those observed in adipose tissues. Pekin ( Anas platyrhynchos ) and Muscovy ducks ( Cairina moschata ) were analyzed, as metabolic responses to overfeeding differ according to these two species, Muscovy ducks having a greater ability to synthesize and store lipids in the liver than Pekin ducks. Our results indicate that adipocyte-specific genes are expressed in the liver of ducks, PPARG and fatty acid-binding protein 4 being upregulated and adiponectin and leptin receptor downregulated by overfeeding. However, these expression levels are much lower than those observed in adipose tissue suggesting that fatty liver cells are not transformed to adipocytes, although some hepato-specific functions are decreased in fatty liver when compared with normal liver.