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Betaine acts as a compatible osmolyte and a methyl donor. High levels of betaine are found in the mammalian kidney, liver and testis. Betaine is either produced from choline or taken up from the intestine. The most studied betaine transporter is the betaine/GABA transporter (BGT1, slc6a12), but this is not the only one. BGT1 has mostly gained attention as a protector against osmolarity changes in the kidney and as a putative controller of brain excitability. The latter role, however, turns out to be insignificant. Most of the BGT1 protein is in hepatocytes where it has received little attention. Hepatocytes also express the only enzyme (BHMT1) that can metabolize betaine suggesting that a major role of BGT1 is to provide betaine to BHMT1. This hepatic BHMT pathway is important for the removal of homocysteine. In the mouse kidney, BGT1 is expressed in the medulla and at the highest concentrations at the renal papilla. This, and the fact that BGT1 is targeted to the basolateral membranes, suggests that another transporter is responsible for the reabsorption of betaine from the glomerular filtrate. This other transporter may be SIT1 (slc6a20), which may also be the main transporter for intestinal betaine uptake. BGT1 does not colocalize with BHMT1 in the kidney. Instead it is primarily located in the inner medulla where the conditions are particularly hostile (hyperosmolarity and high levels of ammonium chloride and urea). In response to the hostile environment, cells trigger osmotic adaption and accumulate osmoprotectants including betaine.

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