Magic™ Anti-FABPs monoclonal antibody, clone N29723GC2

The FABP (adipocyte fatty acid-binding protein) genes play an important role in intracellular fatty acid transport and considered to be candidate genes for fatness traits in domestic animal. In this study, we cloned the cDNA sequences of goat FABP family genes and their expression patterns were detected by semi-quantitative RTPCR and quantitative real time RT-PCR. Expression analysis showed that goat FABP1 gene was predominantly expressed in liver, kidney and large intestine. While FABP4 was widely expressed in many tissues with a high expression level was observed in the fat, skeletal muscle, stomach and lung. Notably, FABP2 gene was expressed specifically in small intestine. Moreover, goat FABP3 was expressed at 60 day with the highest level, then significantly (p < 0.01) decreased at the 90 day. No significant expression differences were observed in longissimus dorsi muscles among 3 day, 30 day and 60 day. Goat FABP4 was expressed at 3 day with the lowest level, then significantly (p < 0.01) increased to a peak at the 60 day. In addition, a significant relationship between FABP3 mRNA expression levels and intramuscular fat (IMF) content was observed. These results suggest that the FABP3 and FABP4 may be important genes for meat quality and provides useful information for further studies on their roles in skeletal muscle IMF deposit.

Nonalcoholic fatty liver disease (NAFLD) is one of the most prevalent diseases worldwide. Exercise is a first-line therapy and an important preventive measure for patients with NAFLD, but the underlying mechanisms are not clear. C57BL/6 mice were fed a high-fat diet (HFD) and subjected to 12 wk swimming exercise. Exercise protected against hepatic lipid accumulation and alleviated hepatocyte damage in HFD mice. Tandem mass tag- based quantitative proteomic analyses and ingenuity pathway analysis revealed that exercise down-regulated fatty acid-binding protein (FABP)1 signaling pathway, which was most closely associated with lipid metabolism. Moreover, exercise significantly decreased FABP1 expression, and liver-specific overexpression of FABP1 abolished the protective effect of exercise in NAFLD mice. Specifically, exercise significantly increased autophagic flux via restoring lysosomal function, including lysosomal proteolysis and lysosomal acidification maintenance, contributing to enhancement in autophagic clearance and subsequently alleviation of hepatic steatosis. Conversely, Fabp1 overexpression in the mouse liver blocked the protective effect of exercise via inhibiting autophagy flux. The present study identified FABP1 inhibition-mediated replenishment of the autophagy-lysosomal machinery as a novel endogenous mechanism whereby long-term exercise improves lipid homeostasis and ameliorates hepatic steatosis in NAFLD.