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Choline deficiency and membrane alteration in POTS


PR activist
FASEB J. 2015 May;29(5):1663-75.

Mechanism of choline deficiency and membrane alteration in postural orthostatic tachycardia syndrome primary skin fibroblasts.

Schenkel LC1, Singh RK1, Michel V1, Zeisel SH1, da Costa KA1, Johnson AR1, Mudd HS1, Bakovic M2.

Fibroblasts from a patient with postural orthostatic tachycardia syndrome (POTS), who presented with low plasma choline and betaine, were studied to determine the metabolic characteristics of the choline deficiency. Choline is required for the synthesis of the phospholipid phosphatidylcholine (PC) and for betaine, an important osmoregulator. Here, choline transport, lipid homeostasis, and mitochondria function were analyzed in skin fibroblasts from POTS and compared with control cells. The choline transporter-like protein 1/solute carrier 44A1 (CTL1/SLC44A1) and mRNA expression were 2-3 times lower in POTS fibroblasts, and choline uptake was reduced 60% (P < 0.05). Disturbances of membrane homeostasis were observed by reduced ratios between PC: phosphatidylethanolamine and sphingomyelin:cholesterol, as well as by modified phospholipid fatty acid composition. Choline deficiency also impaired mitochondria function, which was observed by a reduction in oxygen consumption, mitochondrial potential, and glycolytic activity. When POTS cells were treated with choline, transporter was up-regulated, and uptake of choline increased, offering an option for patient treatment. The characteristics of the POTS fibroblasts described here represent a first model of choline and CTL1/SLC44A1 deficiency, in which choline transport, membrane homeostasis, and mitochondrial function are impaired.


Senior Member
Problem i see with this is that POTS patients with hypovolemia may have issues getting nutrients from the GI tract if the POTS is of this variety...

Which according to Dr Bell is what we have.


Senior Member
We concluded that the fatty acid profiles of the major membrane phospholipids and TAG were altered in POTS cells compared to control as a result of broadly modified glycerolipid metabolism and remodeling in POTS cells.

Mitochondrial function is impaired in POTS cells

Because the mitochondrial choline uptake was 50% reduced in the POTS cells (Fig. 2B), we further examined the mitochondrial function and membrane potential of these cells (Fig. 7) We found that the mitochondria potential was reduced by a factor of 1.5 in the POTS cells compared to control cells (Fig. 7A). Mitochondria potential has been related to choline uptake into the mitochondria (36), and the decrease in the potential observed here may contribute to the decrease in choline transport into the mitochondria in POTS cells.
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