NDLI: Alcohol promotes CPT1A-induced lipid metabolism disorder to sentinel-regulate acute pancreatitis

Content Provider	Springer Nature : BioMed Central
Author	Li, Zenghui Li, Xinghui Jiang, Hui Li, Jingdong Xiao, Bin Chen, Yong Jian, Shunhai Zeng, Mei Zhang, Xiaoming
Abstract	Background and aims Previous studies have confirmed that alcohol can increase the sensitivity of the pancreas to stressors and exacerbate the severity of pancreatitis when excessive alcohol intake is combined with other causes. In the current work, this study attempted to explore how does alcohol regulate cerulein-induced acute pancreatitis, especially before inflammation occurs. Methods Proteomics was performed to analyze the differentially expressed proteins in pancreatic tissues from a rat model of pancreatitis. The metabolite levels in the pancreatic tissue, serum of rats and serum of persons with a history of alcohol consumption were detected by LC‒MS/MS. In the present study the impact of etomoxir (a carnitine palmitoyl-transferase 1A-specific inhibitor) treatment on AR42J cells treated with alcohol and the effect of etomoxir injection on the inflammatory response in an alcohol + cerulein-induced AAP rat model was evaluated. Results When treated with the same amount of cerulein, the rats that ingested alcohol presented with more severe pancreatitis. The proteomics results revealed that the fatty acid degradation pathway was closely related to the development of alcoholic acute pancreatitis, and CPT1A exhibited the greatest increase (approximately twofold increase). The products (acylcarnitines) of CPT1A were changed in the serum of persons with a history of alcohol consumption. Etomoxir treatment mitigates the influence of alcohol stimulation on the aberrant expression of proteins associated with oxidative stress, increased ROS production, mitochondrial ultrastructural alterations and mitochondrial dysfunction in AR42J cells. Etomoxir injection reduced the inflammatory response in the AAP rat model. Conclusion Alcohol upregulates CPT1A protein expression in pancreatic tissue, resulting in abnormal lipid metabolism. The products of lipid metabolism, ROS, contribute to mitochondrial ultrastructural alterations and mitochondrial dysfunction. These changes act as sentinel events that regulate acute pancreatitis.
Related Links	https://eurjmedres.biomedcentral.com/counter/pdf/10.1186/s40001-024-02213-8.pdf
Ending Page	17
Page Count	17
Starting Page	1
File Format	HTM / HTML
DOI	10.1186/s40001-024-02213-8
Journal	European Journal of Medical Research
Issue Number	1
Volume Number	30
Language	English
Publisher	BioMed Central
Publisher Date	2025-01-17
Access Restriction	Open
Subject Keyword	Medicine Public Health Infectious Diseases Internal Medicine Surgery Oncology Biomedicine Acute pancreatitis Proteomics Mitochondrial dysfunction Lipid metabolism Medicine/Public Health
Content Type	Text
Resource Type	Article
Subject	Medicine
Journal Impact Factor	2.8/2023
5-Year Journal Impact Factor	2.9/2023

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

ACACA reduces lipid accumulation through dual regulation of lipid metabolism and mitochondrial function via AMPK- PPARα- CPT1A axis

Efficacy analysis of pancreatic duct stenting in treating severe acute pancreatitis: a retrospective study

Clinical characteristics and short-term outcomes of acute pancreatitis among patients with COVID-19

Establishment and validation of a prediction model for acute kidney injury in moderate severe and severe acute pancreatitis patients

Stellate ganglion block relieves acute lung injury induced by severe acute pancreatitis via the miR-155-5p/SOCS5/JAK2/STAT3 axis

TFR1 knockdown alleviates iron overload and mitochondrial dysfunction during neural differentiation of Alzheimer’s disease-derived induced pluripotent stem cells by interacting with GSK3B

Bioinformatics insights into mitochondrial and immune gene regulation in Alzheimer's disease

Cortical lipid metabolic pathway alteration of early Alzheimer’s disease and candidate drugs screen

Retraction Note: Triptolide ameliorates lipopolysaccharide-induced acute lung injury in rats

Alcohol promotes CPT1A-induced lipid metabolism disorder to sentinel-regulate acute pancreatitis

Similar Documents

ACACA reduces lipid accumulation through dual regulation of lipid metabolism and mitochondrial function via AMPK- PPARα- CPT1A axis

Efficacy analysis of pancreatic duct stenting in treating severe acute pancreatitis: a retrospective study

Clinical characteristics and short-term outcomes of acute pancreatitis among patients with COVID-19

Establishment and validation of a prediction model for acute kidney injury in moderate severe and severe acute pancreatitis patients

Stellate ganglion block relieves acute lung injury induced by severe acute pancreatitis via the miR-155-5p/SOCS5/JAK2/STAT3 axis

TFR1 knockdown alleviates iron overload and mitochondrial dysfunction during neural differentiation of Alzheimer’s disease-derived induced pluripotent stem cells by interacting with GSK3B

Bioinformatics insights into mitochondrial and immune gene regulation in Alzheimer's disease

Cortical lipid metabolic pathway alteration of early Alzheimer’s disease and candidate drugs screen

Retraction Note: Triptolide ameliorates lipopolysaccharide-induced acute lung injury in rats

Alcohol promotes CPT1A-induced lipid metabolism disorder to sentinel-regulate acute pancreatitis