Non-Alcoholic Fatty Pancreas Disease Pathogenesis: A Role for Developmental Programming and Altered Circadian Rhythms

Rebeca Carter, Angelina Mouralidarane, Junpei Soeda, Shuvra Ray, Joaquim Pombo, Ruma Saraswati, Marco Novelli, Giuseppe Fusai, Francesca Rappa, Chiara Saracino, Valerio Pazienza, Lucilla Poston, Paul D Taylor, Manlio Vinciguerra and Jude A Oben

PLOS ONE, 2014, vol. 9, issue 3, 1-12

Abstract: Objectives: Emerging 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. Design: Female 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. Results: Offspring 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

Date: 2014
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Persistent link: https://EconPapers.repec.org/RePEc:plo:pone00:0089505

DOI: 10.1371/journal.pone.0089505

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