Changes in BA metabolism, producing more secondary BA, can be the result of dysbiosis in the colonic microbiome, but overall these results are inconsistent, with increased proportions of primary and not secondary BA in the feces having been described in NASH and in BAD.[9, 31] Also, obesity and insulin resistance have been shown to affect FGF19 sensing in the liver through increased miRNA-34a interference of the transcription of hepatic FGF19 co-receptor klotho-β.[25]Physiologically, this could produce hepatic FGF19 resistance, with the increased C4 levels reported here. The gene discussed is KLB; the disease is obesity disorder.