High plasma choline has been associated with the metabolic syndrome and risk of chronic diseases, including cardiovascular disease. However, dietary choline is not correlated with choline plasma concentrations, and there are few studies and contradictory evidence regarding dietary choline and cardiovascular events. In addition, a recommended dietary allowance for choline has not been established and remains a point of contention. This study assessed the association between dietary choline, including choline forms, and risk of incident acute myocardial infarction (AMI) in patients with suspected stable angina pectoris (SAP). In total 1981 patients (80% men, median age 62) from the Western Norway B Vitamin Intervention Trial were included in this analysis. Information on dietary choline was obtained using a 169-item food frequency questionnaire. The Cardiovascular Disease in Norway project provided data on AMI. Risk associations were estimated using Cox-regression analysis using energy-adjusted choline intake. Median (25th, 75th percentile) total energy-adjusted choline intake was 288 (255, 326) mg/d. During a median (25th, 75th percentile) follow-up of 7.5 (6.3, 8.8) years, 312 (15.7%) patients experienced at least one AMI. Increased intakes of energy-adjusted choline (HR [95% CI] per 50 mg increase 1.11 [1.03, 1.20]), phosphatidylcholine (HR per 50 mg increase 1.24 [1.08, 1.42]) and sphingomyelin (HR per 5 mg increase 1.16 [1.02, 1.31]) were associated with higher AMI risk. In conclusion, higher dietary intakes of total choline, phosphatidylcholine and sphingomyelin were associated with increased risk of AMI in patients with SAP. Future studies are necessary to explore underlying mechanisms for this observation.
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http://dx.doi.org/10.1016/j.biochi.2019.11.001 | DOI Listing |
Biochim Biophys Acta Mol Basis Dis
January 2025
Department of Clinical Pharmacy, School of Pharmacy, Naval Medical University/Second Military Medical University, Shanghai 200433, China. Electronic address:
Orosomucoid (ORM) is an important hepatokine that regulates metabolism. Previous report showed that isoform ORM2 but not ORM1 could downregulate lipogenic genes and ameliorate hepatic steatosis in obese mice, thereby categorizing ORM2 as a promising candidate for therapeutic intervention in nonalcoholic fatty liver disease (NAFLD). However, our previous studies found that mice lacking ORM1 gradually developed an obese phenotype with severe hepatic steatosis at the age of 24 weeks.
View Article and Find Full Text PDFJ Lipid Res
January 2025
Institute of Endocrine and Metabolic Diseases, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230027, China. Electronic address:
Nonalcoholic fatty liver disease (NAFLD) is a progressive condition characterized by ectopic fat accumulation in the liver, for which no FAD-approved drugs currently exist. Emerging evidence highlights the role of liver kinase B1 (LKB1), a key metabolic regulator, has been proposed in NAFLD, particularly in response to excessive nutrient levels. However, few agents have been identified that can prevent the progression of nonalcoholic steatohepatitis (NASH) by targeting LKB1 deacetylation.
View Article and Find Full Text PDFWorld J Hepatol
December 2024
Graduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul, Porto Alegre 90035-007, Rio Grande do Sul, Brazil.
Background: Genetic and epigenetic alterations are related to metabolic dysfunction-associated steatotic liver disease (MASLD) pathogenesis.
Aim: To evaluate micro (mi)RNAs and lipophagy markers in an experimental model of metabolic dysfunction-associated steatohepatitis (MASH).
Methods: Adult male Sprague Dawley rats were randomized into two groups: Control group ( = 10) fed a standard diet; and intervention group ( = 10) fed a high-fat-choline-deficient diet for 16 weeks.
Free Radic Biol Med
December 2024
Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China; Department of Infectious Disease, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, China. Electronic address:
Phytomedicine
December 2024
Department of Pathology & Diagnosis Pathological Center, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian 350122, China. Electronic address:
Background And Purpose: Metabolic dysfunction-associated steatohepatitis (MASH) is an inflammatory lipotoxic disorder marked by hepatic steatosis, hepatocyte damage, inflammation, and varying stages of fibrosis. Sappanone A (SA), a flavonoid, exhibits anti-inflammatory and hepatoprotection activities. Nevertheless, the effects of SA on MASH remain ambiguous.
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