{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPhosphatidylethanolamine N‐methyltransferase (PEMT) is a key enzyme that catalyzes the sequential methylation of phosphatidylethanolamine to form phosphatidylcholine, an essential phospholipid for cell membranes and lipoprotein secretion. Structural and biochemical studies have delineated its polytopic membrane topology and subcellular localization—primarily at the endoplasmic reticulum and mitochondria‐associated membranes—and have shown that its catalytic function is directly linked to the generation of methyl donors, with consequential effects on homocysteine homeostasis. These fundamental investigations establish the biochemical basis for PEMT’s role in ensuring adequate endogenous choline production when dietary choline is limited."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nNumerous genetic studies have identified PEMT variants that impair enzyme activity and modify disease susceptibility. For example, loss‐of‐function mutations and promoter polymorphisms have been associated with reduced phosphatidylcholine synthesis, thereby predisposing individuals to nonalcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis (NASH), and choline‐deficiency syndromes. Variants such as a V175M substitution and SNPs in regulatory regions have been linked not only to hepatic steatosis but also to broader issues in choline metabolism—including alterations in homocysteine levels and potential risks for breast cancer—while meta‐analyses further support a role for these polymorphisms in NAFLD susceptibility."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "4", "end_ref": "11"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nThe regulation of PEMT is tightly influenced by hormonal and nutritional factors. Estrogen has been shown to increase PEMT transcription in both human and animal hepatocytes, providing a molecular explanation for sex differences in choline requirements—premenopausal women are relatively protected from choline deficiency compared with men and postmenopausal women. In addition, studies in lactating women have demonstrated that enhanced PEMT activity helps increase the supply of PEMT‐derived choline metabolites to breast milk, while research in pregnant cohorts indicates that PEMT genetic polymorphisms alter choline metabolite profiles and may affect fetal outcomes. Other investigations have linked variations in PEMT to differences in red blood cell polyunsaturated fatty acid composition, suggesting that its regulation extends into broader metabolic adaptations."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "18"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its central role in choline and lipid metabolism, PEMT genetic variation has been implicated in a range of developmental, neuropsychiatric, reproductive, and vascular phenotypes. Altered PEMT function has been associated with schizophrenia and Alzheimer’s disease, while polymorphisms in the gene have been linked to congenital anomalies such as nonsyndromic cleft lip and palate and are proposed to impact global DNA methylation. Further associations extend to reproductive outcomes—including effects on sperm quality, intrauterine fetal death, and preterm birth—as well as to metabolic and hemodynamic traits, such as type 2 diabetes risk and blood pressure regulation in adolescents. Collectively, these findings underscore the broad clinical relevance of PEMT, spanning from its canonical biochemical role to emerging impacts on human development and disease."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "29"}]}, {"type": "t", "text": ""}]}]}]}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "David J Shields, Richard Lehner, Luis B Agellon, et al. 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