About this Research Topic
Pancreatogenic diabetes is a distinct form of diabetes mellitus, recently categorized as Type3c. It differs in clinical and laboratory features from Type1 and Type 2 and is caused by a variety of exocrine pancreatic diseases. The most common cause being chronic pancreatitis and pancreatic ductal adenocarcinoma with varying mechanisms of hyperglycemia. Although Type3c diabetes can be treated by oral hypoglycemics/exogenous insulin, glycemic control in Type3C is difficult because of the complex metabolic alterations. Pancreatognic diabetes is brittle in nature, underdiagnosed and lacks management guidelines due to knowledge gaps in the pathogenesis. Comprehensive understanding of the cellular and molecular mechanisms would enable development of measures either to delay or arrest progression of glucose intolerance to clinical diabetes, so that quality of life and productivity can be improved.
The goal of this Research Topic is to create general awareness among professionals that the pathogenesis of Type3c diabetes is not the same as other forms of diabetes and is an unmet need. Published literature to date, points to the involvement of inflammation in pancreatogenic diabetes. However, the pathophysiology of development of Type3c diabetes mellitus is unclear, despite the differences observed among the diabetes entities. Therefore, there is an urgent need to understand the pathogenesis, so that suitable, therapeutic strategies could be developed for this form of diabetes.
The overall purpose of this Research Topic is to understand the pathophysiology of Type3c Diabetes. The topics to cover include:
1. Is there a Genetic basis for Pancreatogenic diabetes associated with exocrine diseases?
2. Is inflammation solely responsible for impaired glycemia in exocrine dysfunction?
3. Does the cellular cross talk in the pancreatic inflammatory milieu regulate islet gene expression and related signaling events, contributing to β-cell dysfunction?
4. Omics in understanding development of pancreatogenic diabetes.
5. Progression of β cell dysfunction to overt clinical diabetes.
Keywords: Type3c Diabetes, Exocrine disease, inflammation, islet dysfunction, clinical diabetes
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