Nonalcoholic fatty pancreatic disease (NAFPD) integrates the spectrum of chronic clinical and morphological pancreatic changes: steatosis and nonalcoholic steatopancreatitis. NAFPD prevalence in USA was 27.8%, in China--12.9-16%. According to our data, 51.8% of patients with chronic pancreatitis was diagnosed MS. Association NAFPD with MS has been confirmed in most studies, the presence of any components of MS increases the prevalence NAFPD by 37 %. In the NAFPD pathogenesis is important not only excessive intake of free fatty acids (FFA), which leads to the pancreatic parenchyma inflammation and fibrosis, but also "glucolipotoxicity" (i.e., the combined toxicity of hyperglycemia and increased FFA level) for β-cells. It is shown that NAFPD is an initial index ofectopic fat deposition, and the earlier manifestation of MS than NAFLD. Most likely, a stage (or degree) of the MS is usefully to determine as the pancreatic status--its exo- and endocrine functions, and fat deposition. This approach will allow us to develop new therapeutic approaches not only to treatment but also to the primary prevention of metabolic syndrome.
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Endocrinology
January 2025
Department of Pediatrics, Divisions of Neonatology & Developmental Biology and Endocrinology, Neonatal Research Center of the UCLA Children's Discovery & Innovation Institute at the David Geffen School of Medicine at UCLA, Los Angeles, California 90095-1752.
To determine the basis for perinatal nutritional mismatch causing metabolic dysfunction associated steatotic liver disease (MASLD) and diabetes mellitus, we examined adult phenotype, hepatic transcriptome, and pancreatic β-islet function. In prenatal caloric restricted rat with intrauterine growth restriction (IUGR) and postnatal exposure to high fat with fructose (HFhf) or high carbohydrate (RC), we investigated male and female IUGR-Hfhf and IUGR-RC, versus HFhf and CON offspring. Males more than females displayed adiposity, glucose intolerance, insulin resistance, hyperlipidemia, hepatomegaly with hepatic steatosis.
View Article and Find Full Text PDFEur J Med Res
January 2025
Medical Imaging Key Laboratory of Sichuan Province, Department of Radiology, Affiliated Hospital of North Sichuan Medical College, 1# South Maoyuan Street, Nanchong, 637001, Sichuan, China.
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.
World J Gastrointest Oncol
January 2025
Faculty of Medicine, Carol Davila University of Medicine and Pharmacy, Bucharest 050474, Romania.
Background: Pancreatic ductal adenocarcinoma (PDAC) is an aggressive lethal malignancy with limited options for treatment and a 5-year survival rate of 11% in the United States. As for other types of tumors, such as colorectal cancer, aberrant lipid synthesis and reprogrammed lipid metabolism have been suggested to be associated with PDAC development and progression.
Aim: To identify the possible involvement of lipid metabolism in PDAC by analyzing in tumoral and non-tumoral tissues the expression level of the most relevant genes involved in the long-chain fatty acid (FA) import into cell.
Sisli Etfal Hastan Tip Bul
December 2024
Department of Gastroenterology, Antalya Training and Research Hospital, Antalya, Türkiye.
Objectives: Inflammatory bowel diseases (IBD) are chronic, immune-mediated disorders of the gastrointestinal system. Pancreas can be affected in IBD patients with a wide array of clinical conditions including acu-te pancreatitis, abnormalities of pancreatic duct and pancreatic insufficiency. Pancreatic steatosis (PS) is an important but often overlooked pathology of pancreas.
View Article and Find Full Text PDFJ Biol Chem
January 2025
Laboratory of Immunogenetics, Pennington Biomedical Research Center, Baton Rouge, LA, 70808, USA; Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803, USA. Electronic address:
Pancreatic islet β-cells express the Cpt1a gene, which encodes the enzyme carnitine palmitoyltransferase 1A (CPT1A), an enzyme that facilitates entry of long chain fatty acids into the mitochondria. Because fatty acids are required for glucose-stimulated insulin secretion, we tested the hypothesis that CPT1A is essential to support islet β-cell function and mass. In this study, we describe genetic deletion of Cpt1a in pancreatic tissue (Cpt1a) using C57BL/6J mice.
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