Many of the pathophysiologic responses observed in chronic pancreatitis are related in part to disruption of the insulo-acinar axis, to destruction of islet cell mass, or to both. Each of the four types of hormone-secreting beta cells is affected by the destructive process of chronic pancreatitis. The insulin-secreting beta cells appear to be affected in both a qualitative and quantitative manner. Directly related to the changes in the beta cell are the physiologic responses of the glucagon-secreting alpha cells. Their physiologic response in chronic pancreatitis appears to be related to the residual beta cell function. Recently, pancreatic polypeptide has been implicated as a contributor to the abnormal glucose metabolism in pancreatogenic diabetes. The deficiency of this peptide appears to influence the expression of hepatocyte insulin receptors in chronic pancreatitis. There also appears to be a close correlation between the degree of PP secretion deficiency and pancreatic exocrine insufficiency. Although somatostatin appears to have an important role in the insulo-acinar axis, the effects of chronic pancreatitis on the function of somatostatin in the insulo-acinar axis are poorly understood. There is a need for further exploration of the interrelation of the endocrine and the exocrine pancreas to develop better treatment options for the alterations in glucose metabolism that occur in chronic pancreatitis.
|Original language||English (US)|
|Number of pages||10|
|Journal||Problems in General Surgery|
|State||Published - 1998|
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