Mouse Fabp6(Gastrotropin) ELISA Kit

Fatty acid-binding proteins (Fabps) make up a family of widely distributed cytoplasmic lipid-binding proteins. The small intestine contains three predominant Fabp species, Fabp1, Fabp2, and Fabp6. Our previous studies showed thatFabp2andFabp6gene-disrupted mice exhibited sexually dimorphic phenotypes. In this study, we carried out a systematic comparative analysis of the small intestinal transcriptomes of 10 week-old wild-type (WT) and Fabp gene-disrupted male and female mice. We found that the small intestinal transcriptome of male and female mice showed key differences in the gene expression profiles that affect major biological processes. The deletion of specific Fabp genes induced unique and sex-specific changes in the gene expression program, although some differentially expressed genes in certain genotypes were common to both sexes. Functional annotation and interaction network analyses revealed that the number and type of affected pathways, as well as the sets of interacting nodes in each of the Fabp genotypes, are partitioned by sex. To our knowledge, this is the first time that sex differences were identified and categorized at the transcriptome level in mice lacking different intestinal Fabps. The distinctive transcriptome profiles of WT male and female small intestine may predetermine the nature of transcriptional reprogramming that manifests as sexually dimorphic responses to the ablation of intestinal Fabp genes.

Liver-type fatty acid-binding protein (L-FABP) is a key regulator of fatty acid metabolism, but serum L-FABP levels are not well investigated in chronic liver diseases. We aimed to elucidate the prognostic ability of serum L-FABP in human chronic liver diseases and compare it with the albumin-bilirubin (ALBI) score. In 242 chronic liver disease patients, including chronic hepatitis (CH, n=100), liver cirrhosis (LC, n=142), and presence of hepatocellular carcinoma (HCC, n=144), serum L-FABP levels were correlated with liver function (P<0.0001), increased in LC compared with CH (P<0.01), and correlated to ALBI score (P<0.0001). Serum L-FABP levels were increased in the presence of HCC (P<0.0001), correlating to des-gamma-carboxy prothrombin (P<0.0001), alpha-fetoprotein (P=0.009), and Barcelona-Clinic Liver Cancer stage. In the average follow-up period of 1,054 days, serum L-FABP levels were elevated (P<0.0001) in patients who eventually died. The area under the curve (AUC) of serum L-FABP (0.764) was higher than that of ALB (0.709), and the patients with serum L-FABP6.8 ng/mL had significantly longer rates of survival (P<0.0001). Serum L-FABP (hazard ratio [HR] 4.0; P<0.001), HCC (HR 3.7; P=0.001), ALBI score (HR 2.7; P<0.001), and age (HR 1.0; P=0.049) were independent predictors of survival. In the subgroup who maintained liver function, the AUC of serum L-FABP (0.751) was higher than that of ALB (0.643). In this subgroup, serum L-FABP (HR 4.4; P=0.002) and HCC (HR 13.9; P<0.001) were independent predictors of survival. Conclusion: Serum L-FABP is a possible predictor of survival in chronic liver diseases from CH to LC and HCC, including any subgroup that maintains liver function.