Increased expression of regulator of G protein signaling 2 explains how choline supplementation increases visceral fat mass in phosphatidylethanolamine N-methyltransferase deficient mice

Choline is an essential nutrient, acquired from the diet or synthesized via phosphatidylethanolamine N-methyltransferase (PEMT) pathway. Pemt-/- mice exhibited reduced weight gain and visceral fat mass after being fed the high fat (HF) diet for 1 week. Surprisingly, dietary choline supplementation reversed the phenotype of Pemt-/- mice fed the HF diet.;Compared to Pemt-/- mice, Pemt -/- mice had reduced amount of choline in plasma, liver and gastrocnemius muscle after fed the HF diet. Gonadal fat pads from Pemt-/- mice took up less oleate for triglyceride (TG) biosynthesis and exhibited increased lipolysis. However, choline supplementation reduced lipolysis and induced the expression of regulator of G protein signaling 2 (RGS2) in the fat pads of Pemt-/- mice. RGS2 can attenuate beta-adrenergic signaling that is the primary initiator of TG mobilization in adipose tissue.;Hence, we hypothesize that increased expression of RGS2 would present a potential mechanism for how choline supplementation revered visceral fat mass in Pemt-/- mice.