Taurine Regulation of Neuroendocrine Function
Taurine (2-aminoethanesulfonic acid) is a sulfur-containing amino acid. It is one of the most abundant free amino acids in many excitable tissues, including the brain, skeletal and cardiac muscles. Physiological actions of taurine are widespread and include regulation of plasma glucose levels, bile acid conjugation, detoxification, membrane stabilization, blood pressure regulation, osmoregulation, neurotransmission, and modulation of mitochondria function and cellular calcium levels. Taurine plays an important role in modulating glutamate and GABA neurotransmission and prevents excitotoxicity in vitro primarily through modulation of intracellular calcium homeostasis. Taurine supplementation prevents age-dependent decline of cognitive functions. Because of the wide spread actions of taurine, its levels are highly regulated through enzymatic biosynthesis or dietary intake. Furthermore, depletion of endogenous or dietary supplementation of exogenous taurine have been shown to induce wide spread actions on multiple organs. Cysteine sulfonic acid decarboxylase (CSAD) was first identified in the liver and is thought to be the rate-limiting enzyme in taurine biosynthesis. CSAD mRNA is expressed in the brain in astrocytes. Homozygous knockout mice lacking CSAD (CSAD-KO) have very reduced taurine content and show severe functional histopathology in the visual system, skeletal system, heart, pancreas and brain. Conversely, dietary supplementation of taurine results in significant health benefits acting through the same organ systems. Fluctuation of taurine bioavailability lead to changes in the expression levels of taurine transporters in neuronal plasma membranes, endothelial cells forming the blood-brain barrier and proximal cells of the kidneys. Suggesting a highly regulated mechanism for maintaining taurine homeostasis and organ systems function. Here we show how alterations in taurine levels directly affect the function of one organ system and through functional interaction and compensatory adaptation; these effects extend to another organ systems with focus on the nervous system.
KeywordsCSAD KO Taurine supplementation Neuroendocrine alteration Glut4 Insulin receptor calbindin Na-K-ATPase
- CSAD KO
cysteine sulfinic acid decarboxylase knock-out mice
cysteine sulfinic acid decarboxylase
glucose transporter 4
voltage sensitive calcium channels
This work was supported by CDN, PSC-CUNY and CSI. The author declares that he has no conflict of interest. This chapter was modified from the paper published by our group in Advances in Experimental Biology and Medicine. The related contents are re-used with the permission.
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