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| http://dx.doi.org/10.1016/j.tvr.2023.200256 | DOI Listing |
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Lipid droplet targeting of the lipase co-activator ABHD5 and the fatty liver disease-causing variant PNPLA3 I148M is required to promote liver steatosis.
J Biol Chem
January 2025
Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, MI, 48202; Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA 48202. Electronic address:
The storage and release of triacylglycerol (TAG) in lipid droplets (LDs) is regulated by dynamic protein interactions. α/β hydrolase domain-containing protein 5 (ABHD5; also known as CGI-58) is a membrane/LD bound protein that functions as a co-activator of Patatin Like Phospholipase Domain Containing 2 (PNPLA2; also known as Adipose triglyceride lipase, ATGL) the rate-limiting enzyme for TAG hydrolysis. The dysregulation of TAG hydrolysis is involved in various metabolic diseases such as metabolic dysfunction-associated steatotic liver disease (MASLD).
View Article and Find Full Text PDFImpact of NAFLD-related SNPs on the carotid atherosclerosis development; a five-year prospective observational study.
Atheroscler Plus
March 2025
Cardiovascular Nutrition Laboratory, Human Nutrition Research Center on Aging at Tufts University, and Tufts University School of Medicine, Boston, MA, 711 Washington Street, 02111, USA.
Background And Aims: The prevalence of metabolic dysfunction associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD), has become a significant public health concern with an increased atherosclerotic cardiovascular disease risk. This study investigates the impact of NAFLD-related single nucleotide polymorphisms (SNPs) on carotid atherosclerosis development in a Japanese population without diabetes, dyslipidemia, and hypertension.
Methods: The prospective observational study, part of the Kyushu and Okinawa Population Study (KOPS), included 945 participants (median age 55 [47, 63]) without carotid atherosclerosis, increased alcohol intake, diabetes, dyslipidemia, hypertension, or chronic hepatitis at baseline.
A Very Low-Carbohydrate Program in Adults With Metabolic Dysfunction-Associated Steatotic Liver Disease and Phospholipase Domain-Containing Protein 3 Risk Genotype: Pre-Post Intervention Study.
JMIR Form Res
January 2025
Division of Gastroenterology, Department of Internal Medicine, University of Michigan Medical School, Medical Sciences Building II, Room 4741, Ann Arbor, MI, 48109, United States, 1 734-647-2964.
Background: Insulin resistance and the G allele of rs738409 interact to create a greater risk of metabolic dysfunction-associated steatotic liver disease.
Objective: This study aims to confirm that one promising way to reduce insulin resistance is by following a very low-carbohydrate (VLC) dietary pattern.
Methods: Adults with rs738409-GG or -CG with liver steatosis and elevated liver function tests, were taught an ad libitum VLC diet, positive affect and mindful eating skills, goal setting, and self-monitoring and given feedback and coaching for 4 months.
AZD2693, a PNPLA3 antisense oligonucleotide, for the treatment of MASH in 148M homozygous participants: two randomized phase I trials.
J Hepatol
January 2025
MASLD Research Center, Division of Gastroenterology and Hepatology, University of California at San Diego, La Jolla, CA, USA.
Background & Aims: A common genetic variant (rs738409) encoding isoleucine to methionine at position 148 in the PNPLA3 protein is a determinant of hepatic steatosis, inflammation, fibrosis, cirrhosis, and liver-related mortality. AZD2693 is a liver-targeted antisense oligonucleotide against PNPLA3 mRNA. We evaluated the safety, tolerability, pharmacokinetics, and pharmacodynamics in single ascending dose (SAD) and multiple ascending dose (MAD) studies.
View Article and Find Full Text PDFGenetic Risk Factors for Metabolic Dysfunction-Associated Steatotic Liver Disease.
Gut Liver
January 2025
Department of Gastroenterology and Hepatology, Singapore General Hospital, Singapore.
Metabolic dysfunction-associated steatotic liver disease (MASLD), is the most common cause of liver disease, and its burden on health systems worldwide continues to rise at an alarming rate. MASLD is a complex disease in which the interactions between susceptible genes and the environment influence the disease phenotype and severity. Advances in human genetics over the past few decades have provided new opportunities to improve our understanding of the multiple pathways involved in the pathogenesis of MASLD.
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