Altered metabolic function has many detrimental effects on the body that can manifest as cardiovascular and liver diseases. Traditional approaches to understanding and treating metabolic dysfunction-associated disorders have been organ-centered, leading to silo-type disease care. However, given the broad impact that systemic metabolic dysfunction has on the human body, approaches that simultaneously involve multiple medical specialists need to be developed and encouraged to optimize patient outcomes. In this review, we highlight how several of the treatments developed for cardiac care may have a beneficial effect on the liver and vice versa, suggesting that there is a need to target the disease process, rather than specifically target the cardiovascular or liver specific sequelae of metabolic dysfunction.
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http://dx.doi.org/10.1016/j.atherosclerosis.2024.117523 | DOI Listing |
BMC Gastroenterol
January 2025
Department of Gastroenterology and Hepatology, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, No. 55 Zhenhai Road, Xiamen, 361003, China.
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) has become the most common chronic liver disease worldwide. The pan-immune-inflammation value (PIV) has been proposed as a biomarker for assessing immune status and inflammation. There is currently no evidence regarding the effect of PIV on the risk of MASLD.
View Article and Find Full Text PDFCurr Obes Rep
January 2025
Department of Endocrinology and Metabolism, Zhuhai People's Hospital (The Affiliated Hospital of Beijing Institute of Technology, Zhuhai Clinical Medical College of Jinan University), Zhuhai, China.
Purpose Of Review: Review the latest data regarding the intersection of adipose tissue (AT) and iron to meet the needs of AT metabolism and the progression of related diseases.
Recent Findings: Iron is involved in fundamental biological metabolic processes and is precisely fine-tuned within the body to maintain cellular, tissue and even systemic iron homeostasis. AT not only serves as an energy storage depot but also represents the largest endocrine organ in the human body, maintaining systemic metabolic homeostasis.
Prostaglandins Leukot Essent Fatty Acids
December 2024
Department of Medicine III, Division of Endocrinology and Metabolism, Medical University of Vienna, Austria; Department of Medicine III and Karl Landsteiner Institute for Metabolic Diseases and Nephrology, Clinic Hietzing, Vienna, Austria. Electronic address:
Background And Aims: Obesity is associated with a higher risk of severe diseases such as atherosclerotic cardiovascular disease, type 2 diabetes mellitus (T2DM), and metabolic dysfunction-associated steatotic liver disease (MASLD). Polyunsaturated fatty acids, of the omega-3 family (n-3 PUFA), have been shown to reduce adipose tissue inflammation in obesity, as well as to have lipid-lowering effects and improve insulin sensitivity. However, direct effects on liver transcriptome in humans have not been described.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Department of Endocrinology, Second Hospital of Shanxi Medical University, Taiyuan 030000, China. Electronic address:
Tirzepatide is a dual agonist of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptors and is a promising therapeutic option for type 2 diabetes mellitus (T2DM). Nevertheless, its effect and underlying mechanism on hepatic steatosis remain ambiguous. Herein, we explored the impact of tirzepatide on improving hepatic steatosis in diabetic mice, with a particular focus on the gut microbiota and bile acids (BAs) using animal models.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Laboratory of Obesity and Aging Research, Cardiovascular Branch, National Heart Lung and Blood Institute, NIH, Bethesda, MD 20892.
Mitochondrial endonuclease G (EndoG) contributes to chromosomal degradation when it is released from mitochondria during apoptosis. It is presumed to also have a mitochondrial function because EndoG deficiency causes mitochondrial dysfunction. However, the mechanism by which EndoG regulates mitochondrial function is not known.
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