Abstract
Anatomical proximity and functional correlations between the exocrine and endocrine pancreas warrant reciprocal effects between the two parts. Inflammatory diseases of the exocrine pancreas, such as acute or chronic pancreatitis, or the presence of cystic fibrosis disrupt endocrine function, resulting in diabetes of the exocrine pancreas. Although novel mechanisms are being increasingly identified, the intra- and intercellular pathways regulating exocrine–endocrine interactions are still not fully understood, making the development of new and more effective therapies difficult. Therefore, this review sought to accumulate current knowledge regarding the pathogenesis of diabetes in acute and chronic pancreatitis, as well as cystic fibrosis.
Highlights
The pancreas is a unique organ, having both the endocrine and exocrine functions
This study found that both the diabetes and CP groups had higher serum glucose levels after OGTT compared to controls and the serum glucagon level showed an initial increase in these groups, which is presumably due to the fact that postprandial glucagon release is not inhibited due to decreased endogenous insulin production
Regardless of species, it is generally accepted that exocrine inflammation in CF damages the entire pancreas to such an extent that the number of beta cells and insulin secretion are considerably reduced [162]. This hypothesis somewhat contradicts the fact that the remaining beta cells must produce enough insulin to prevent the development of diabetes, which suggests that CFTR intrinsically regulates insulin secretion and that the functional defect in residual beta cells causes the development of CF-related diabetes (CFRD)
Summary
The pancreas is a unique organ, having both the endocrine and exocrine functions. The exocrine pancreas is composed of acini, which are dome-shaped clusters of acinar cells that produce and secrete enzymes involved in the digestion of food. The number of functionally active beta cells decreases as the extent of necrosis increases, leading to altered insulin secretion. Experimental studies on rats have shown that sodium taurocholate-induced pancreatitis did not alter islet morphology or GLUT-2 expression but reduced insulin secretion in response to glucose stimulation, indicating functional deterioration of beta cells [63].
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