ArticlePloS one2014
Non-alcoholic fatty pancreas disease pathogenesis: a role for developmental programming and altered circadian rhythms.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 45 citations in OpenAlex.
- Fatty Pancreas: Its Potential as a Risk Factor for Pancreatic Cancer and Clinical Implications.Cancers · 2025Review
- Adherence to the dietary approaches to stop hypertension (DASH) and risk of pancreatic steatosis.Journal of health, population, and nutrition · 2024Article
- Fatty Pancreas Is a Risk Factor for Pancreatic Cancer: A Systematic Review and Meta-Analysis of 2956 Patients.Cancers · 2023Review
- Uniting epidemiology and experimental models: pancreatic steatosis and pancreatic cancer.EBioMedicine · 2022Review
- Fatty Pancreas-Centered Metabolic Basis of Pancreatic Adenocarcinoma: From Obesity, Diabetes and Pancreatitis to Oncogenesis.Biomedicines · 2022Review
- Nonalcoholic Fatty Pancreas Disease: Role in Metabolic Syndrome, "Prediabetes," Diabetes and Atherosclerosis.Digestive diseases and sciences · 2022Review
- Nonalcoholic fatty pancreas disease: An emerging clinical challenge.World journal of clinical cases · 2021Review
- Perturbation of the circadian clock and pathogenesis of NAFLD.Metabolism: clinical and experimental · 2020Review
- Circadian Genes as Therapeutic Targets in Pancreatic Cancer.Frontiers in endocrinology · 2020Review
- MRI assessment of ectopic fat accumulation in pancreas, liver and skeletal muscle in patients with obesity, overweight and normal BMI in correlation with the presence of central obesity and metabolic syndrome.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019Article
- Prediabetes and Type 2 Diabetes are Independent Risk Factors for Computed Tomography-Estimated Nonalcoholic Fatty Pancreas Disease.Clinics (Sao Paulo, Brazil) · 2019Article
- Can pancreatic steatosis affect exocrine functions of pancreas?The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2018Article
- Diabetes Mellitus and Obesity as Risk Factors for Pancreatic Cancer.Journal of the Academy of Nutrition and Dietetics · 2018Review
- Article
- Maternal Macronutrient Consumption and the Developmental Origins of Metabolic Disease in the Offspring.International journal of molecular sciences · 2017Review
- Long-term consequences of obesity on female fertility and the health of the offspring.Current opinion in obstetrics & gynecology · 2017Review
- Article
- Non-Alcoholic Fatty Pancreatic Disease: A Review of Literature.Gastroenterology research · 2016Review
- Exploring the metabolic syndrome: Nonalcoholic fatty pancreas disease.World journal of gastroenterology · 2016Review
- Maternal obesity alters endoplasmic reticulum homeostasis in offspring pancreas.Journal of physiology and biochemistry · 2016Article
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 2 countries.
Funding
Abstract
objectivesEmerging evidence suggests that maternal obesity (MO) predisposes offspring to obesity and the recently described non-alcoholic fatty pancreas disease (NAFPD) but involved mechanisms remain unclear. Using a pathophysiologically relevant murine model, we here investigated a role for the biological clock--molecular core circadian genes (CCG) in the generation of NAFPD.
designFemale C57BL6 mice were fed an obesogenic diet (OD) or standard chow (SC) for 6 weeks, prior to pregnancy and throughout gestation and lactation: resulting offspring were subsequently weaned onto either OD (Ob_Ob and Con_Ob) or standard chow (Ob_Con and Con_Con) for 6 months. Biochemical, pro-inflammatory and pro-fibrogenic markers associated with NAFPD were then evaluated and CCG mRNA expression in the pancreas determined.
resultsOffspring of obese dams weaned on to OD (Ob_Ob) had significantly increased (p≤0.05): bodyweight, pancreatic triglycerides, macrovesicular pancreatic fatty-infiltration, and pancreatic mRNA expression of TNF-α, IL-6, α-SMA, TGF-β and increased collagen compared to offspring of control dams weaned on to control chow (Con_Con). Analyses of CCG expression demonstrated a phase shift in CLOCK (-4.818, p<0.01), REV-ERB-α (-1.4,p<0.05) and Per2 (3.27,p<0.05) in association with decreased amplitude in BMAL-1 (-0.914,p<0.05) and PER2 (1.18,p<0.005) in Ob_Ob compared to Con_Con. 2-way ANOVA revealed significant interaction between MO and post-weaning OD in expression of CLOCK (p<0.005), PER1 (p<0.005) and PER2 (p<0.05) whilst MO alone influenced the observed rhythmic variance in expression of all 5 measured CCG.
conclusionsFetal and neonatal exposure to a maternal obesogenic environment interacts with a post-natal hyper-calorific environment to induce offspring NAFPD through mechanisms involving perturbations in CCG expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.