Estradiol decreases taurine level by reducing cysteine sulfinic acid decarboxylase via the estrogen receptor-α in female mice liver

Abstract

Cysteine sulfinic acid decarboxylase (CSAD) and cysteine dioxygenase (CDO) are two rate-limiting enzymes in taurine de novo synthesis, and their expressions are associated with estrogen concentration. The present study was designed to determine the relationship between 17β-estradiol (E₂) and taurine in female mice liver. We initially observed the mice had lower levels of CSAD, CDO, and taurine during estrus than diestrus. We then, respectively, treated the ovariectomized mice, the cultured hepatocytes, and Hep G2 cells with different doses of E₂, and the CSAD and CDO expressions and taurine levels were analyzed. The results showed that E₂ decreased taurine level in the serum and the cultured cells by inhibiting CSAD and CDO expressions. Furthermore, we identified the molecular receptor types through which E₂ plays its role in regulating taurine synthesis, and our results showed that estrogen receptor-α (ERα) expression was much higher than estrogen receptor-β (ERβ) in the liver and hepatocytes, and the inhibiting effects of E₂ on CSAD, CDO, and taurine level were partially abrogated in the ICI-182,780-pretreated liver and hepatocytes, and in ERα knockout mice. These results indicate that estradiol decreases taurine content by reducing taurine biosynthetic enzyme expression in mice liver.

RNA-Seq reveals common and unique PXR- and CAR-target gene signatures in the mouse liver transcriptome

“…This may contribute to PCN-mediated increase in cell proliferation. PCN also down-regulated multiple genes involved in intermediary metabolism, such as cysteine sulfinic acid decarboxylase (Csad), which is a rate-limiting enzyme in taurine de novo synthesis (Ma et al, 2015b); phospholipid scramblase 1 (Plscr1), which is involved in movement of phospholipids, immune-activation, and cell proliferation (Lu et al, 2007); peroxiredoxin 4 (Prdx4), which reduces oxidative-stress induced liver injury (Nabeshima et al, 2013), as well as the chemokine Cxcl9 and hemoglobin. Conversely, the uniquely up-regulated genes by PCN include the phase-I enzyme Aldh1b1; the antimicrobial peptide hepcidin 2 (hamp2), which is involved in inflammation, infection, and iron homeostasis (Lu et al, 2015); inositol polyphosphate multikinase (Ipmk), which regulates the central metabolic enzyme AMP-activated protein kinase (Ampk) for energy sensing (Dailey and Kim, 2012); the sodium/lithum/calcium exchanger Slc8b1; and immunoglobulin-like domain containing receptor 2 (Ildr2), which is an endoplasmic reticulum (ER) resident molecule mediating hepatic lipid homeostasis during ER stress (Watanabe et al, 2013).…”

Methionine and choline supply alter transmethylation, transsulfuration, and cytidine 5′-diphosphocholine pathways to different extents in isolated primary liver cells from dairy cows

“…The marked increase in mRNA and protein abundance of CBS in response to Met supplementation indicated the potential for greater flux of homocysteine into cysteine followed by synthesis of glutathione and taurine (Brosnan and Brosnan, 2006). The enzymes CDO1 and CSAD are 2 rate-limiting enzymes in de novo taurine synthesis (Park et al, 2014), and their expression is positively associated with taurine levels in the liver (Ma et al, 2015). Despite the lack of change in abundance of CDO1 in response to Met or Chol, the marked upregulation of CSAD abundance in Met-supplemented PHEP suggests that synthesis of taurine might have been increased (Osorio et al, 2014a).…”

Taurine, energy drinks, and neuroendocrine effects

“…Taurine may have effects on human sex hormones, based on the limited observations in rodents. [89][90][91][92][93][94] Although human salivary cortisol concentrations were purportedly assessed in response to 2,000 mg of oral taurine, 95 the methods and reported data are not adequate to draw any conclusions.…”