Circadian rhythm disruption is linked to various pancreatic diseases, including type 2 diabetes and pancreatic cancer.
In type 2 diabetes, reduced clock gene expression in pancreatic islets correlates with impaired insulin secretion.
Type 1 diabetes is associated with increased immune activation due to circadian dysregulation, potentially accelerating disease progression.
In chronic pancreatitis, loss of core clock components exacerbates pancreatic cell activation, fibrosis, and inflammation.
Circadian disruption may contribute to pancreatic tumor development by affecting inflammation and tissue remodeling.
Simplified
BACKGROUND: , governed by core , are essential for maintaining metabolic, endocrine, and immune homeostasis. Disruption of these rhythms has been increasingly implicated in the pathogenesis of various pancreatic diseases.
OBJECTIVE: This review summarizes current evidence on the role of circadian rhythm disruption in pancreatic diseases, including type 2 diabetes (T2D), type 1 diabetes (T1D), pancreatitis, and pancreatic cancer (PC), with a focus on underlying mechanisms involving clock gene dysregulation.
RECENT FINDINGS: In T2D, dampened oscillations of clock gene expression in pancreatic islets are associated with impaired insulin secretion and loss of cellular synchrony. In T1D, circadian dysregulation enhances immune activation and reduces β-cell tolerance, accelerating disease progression. In pancreatitis, especially in chronic forms, loss of core clock components such as Bmal1 exacerbates pancreatic stellate cell activation, fibrosis, and inflammatory cytokine release. Additionally, circadian disruption has been linked to pancreatic tumorigenesis, suggesting a potential role of clock genes in early cancer development through modulation of the inflammatory microenvironment and stromal remodeling.
CONCLUSION: Circadian clock genes play a multifaceted role in pancreatic disease pathophysiology, extending beyond metabolic regulation to influence immune responses, inflammation, and tumorigenesis. Understanding these mechanisms may inform the development of novel circadian-based therapeutic strategies for pancreatic disorders.
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