Objective: To explore the levels of serum GP73 in patients with fatty liver disease.
Methods: The sera GP73 were determined by ELISA in 178 patients with fatty liver disease and 100 healthy controls.
Results: Serum GP73 levels were significantly increased in patients with various fatty liver diseases(70.62 +/- 60.60 ng/ml), compared with those of control population (35.61 +/- 12.22 ng/ml). In patients with alcoholic fatty liver disease, acute liver injury, chronic hepatitis B, and non-alcoholic fatty liver disease, their serum GP73 concentration were 81.86 +/- 47.82 ng/ml, 82.77 +/- 77.73 ng/ml, 63.84 +/- 50.62 ng/ml, and 65.75 +/- 62.20 ng/ml, respectively. But no significant difference was found between these groups (P > 0.05). In 68 patients with F > or = 1.0 (71.46 +/- 66.48 ng/ml), 75 patients with F> or = 2.0 (69.58 +/- 62.31 ng/ml), and 34 patients with F3-F4 (71.65 +/- 43.89 ng/ml), there were also no marked differences was observed between these fatty groups (F = 0.02, P = 0.98).
Conclusion: Serum GP73 levels were increased in patients with different liver diseases, but its concentrations were seems not related with degree of fatty injury.
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J Complement Integr Med
January 2025
Department of Basic Medical Sciences, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka, India.
Background: Excessive fluoride exposure leads to increased oxidative stress and lipid peroxidation, causing harmful effects on the metabolic organs in the human body. Betanin, a pigment obtained from beetroot, is seen to have powerful anti-inflammatory and antioxidant. The study was conducted to determine the role of betanin in fluoride induced hepato-renal toxicity in Wistar rats.
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.
View Article and Find Full Text PDFBackground And Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) and its more severe subtype, metabolic dysfunction-associated steatohepatitis (MASH), are highly prevalent and strongly associated with obesity and type 2 diabetes (T2D). This study sought to identify challenges to the diagnosis, treatment and management of people living with MASLD and MASH and understand the key barriers to adopting relevant clinical guidelines.
Methods: A real-world, cross-sectional study (BARRIERS-MASLD) consisting of a quantitative survey and qualitative interviews of physicians in France, Germany, Italy, Spain and the United Kingdom was conducted from March to September 2023.
Alzheimers Dement
December 2024
University of California Davis Medical Center, Sacramento, CA, USA.
Background: Inflammation is crucial in Alzheimer's Disease (AD), where oxidized lipid derivatives of polyunsaturated fatty acids (PUFAs), i.e., oxylipins, are potent modulators.
View Article and Find Full Text PDFCardiol Rev
January 2025
From the First Department of Cardiology, School of Medicine, National and Kapodistrian University of Athens, Hippokration General Hospital, Athens, Greece.
Although metabolic dysfunction-associated steatotic liver disease (MASLD), previously termed nonalcoholic fatty liver disease, has become the most common chronic liver disorder, its complex pathophysiology has not been fully elucidated up to date. A correlation between elevated sympathetic activation and MASLD has been highlighted in recent preclinical and clinical studies. Furthermore, increased sympathetic activity has been associated with the main mechanisms involved in MASLD, such as lipid accumulation in the liver, insulin resistance, and metabolic dysregulation, while it has been also correlated with the progression of MASLD, leading to liver fibrosis.
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