Objective: The aim of this study was to determine the association of the pancreatic steatosis with obesity, chronic pancreatitis (CP), and type 2 diabetes mellitus.
Methods: Patients (n = 118) were retrospectively identified and categorized into no CP (n = 60), mild (n = 21), moderate (n = 27), and severe CP (n = 10) groups based on clinical history and magnetic resonance cholangiopancreatography using the Cambridge classification as the diagnostic standard. Visceral and subcutaneous compartments were manually segmented, and fat tissue was quantitatively measured on axial magnetic resonance imaging.
Results: Pancreatic fat fraction showed a direct correlation with fat within the visceral compartment (r = 0.54). Patients with CP showed higher visceral fat (P = 0.01) and pancreatic fat fraction (P < 0.001): mild, 24%; moderate, 23%; severe CP, 21%; no CP group, 15%. Patients with type 2 diabetes mellitus showed higher pancreatic steatosis (P = 0.03) and higher visceral (P = 0.007) and subcutaneous fat (P = 0.004). Interobserver variability of measuring fat by magnetic resonance imaging was excellent (r ≥ 0.90-0.99).
Conclusions: Increased visceral adipose tissue has a moderate direct correlation with pancreatic fat fraction. Chronic pancreatitis is associated with higher pancreatic fat fraction and visceral fat. Type 2 diabetes mellitus is associated with higher pancreatic fat fraction and visceral and subcutaneous adiposity.
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http://dx.doi.org/10.1097/MPA.0000000000001252 | DOI Listing |
Nutrients
December 2024
Department of Cardiology, University Medical Centre Groningen, University of Groningen, 9713 GZ Groningen, The Netherlands.
Background: Micronutrient deficiencies are common and play a significant role in the prognosis of many chronic diseases, including heart failure (HF), but their prevalence in HF is not well known. As studies have traditionally focused on causes originating within the intestines, exocrine pancreatic insufficiency (EPI) has been overlooked as a potential contributor. The exocrine pancreas enables the absorption of various (fat-soluble) micronutrients and may be insufficient in HF.
View Article and Find Full Text PDFRev Esp Enferm Dig
January 2025
Gastroenterología. Unidad de Endoscopia, Hospital Universitario Donostia.
The pancreatitis, panniculitis, polyarthritis (PPP) syndrome involves the association of pancreatic pathology, panniculitis of pancreatic origin, and polyarthritis secondary to intra-articular fat necrosis. The incidence is unknown, and the mortality rate is as high as 24%. Treatment targets the underlying pancreatic pathology.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Internal Medicine, Erasmus Medical Center (Erasmus MC), Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.
Consuming a "modern" Western diet and overnutrition may increase insulin secretion. Additionally, nutrition-mediated hyperinsulinemia is a major driver of ectopic fat deposition. The global prevalence of metabolic syndrome is high and growing.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
Department of Psychology, University of Miami, Coral Gables, FL, United States.
The neuropeptide oxytocin (OXT) and its receptor (OXTR) have been shown to play an important role in glucose metabolism, and pancreatic islets express this ligand and receptor. In the current study, OXTR expression was identified in α-, β-, and δ-cells of the pancreatic islet by RNA hybridization, and OXT protein expression was observed only in β-cells. In order to examine the contribution of islet OXT/OXTR in glycemic control and islet β-cell heath, we developed a β-cell specific OXTR knock-out (β-KO) mouse.
View Article and Find Full Text PDFbioRxiv
December 2024
Brenden-Colson Center for Pancreatic Care, Oregon Health & Science University, Portland, OR.
Background: Cachexia is defined by chronic loss of fat and muscle, is a frequent complication of pancreatic ductal adenocarcinoma (PDAC), and negatively impacts patient outcomes. Nutritional supplementation cannot fully reverse tissue wasting, and the mechanisms underlying this phenotype are unclear. This work aims to define the relative contributions of catabolism and anabolism to adipose wasting in PDAC-bearing mice.
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