Role of receptors in mediating trophic stimuli in the pancreas.

Pancreatic acinar cells synthesise and secrete a variety of digestive enzymes as well as a NaCI-rich pancreatic juice. Acinar cells are able to adapt to the changing needs of the organism both by regulating the total pancreatic mass as well as by altering the synthesis of specific molecules. Adaptive regulation occurs with the onset of oral feeding at birth, the regrowth that follows surgical resection or destruction of the gland during pancreatitis, and as a change in content of specific digestive enzymes following a shift from one diet to another.' Although not totally established, it is generally assumed that these adaptive responses are mediated by hormones or other regulatory molecules. Early work has focused on secretagogues such as cholecystokinin (CCK), acetylcholine and secretin. Cholecystokinin when injected into rats has been repeatedly shown to increase the mass and DNA and protein content of the gland.' This makes teleological sense in that a secretory stimulus should enhance the synthesis of replacement digestive enzymes. Recently other regulatory molecules with more subtle or no secretory effects such as insulin, EGF, IGF, and corticosteroids have been shown to induce adaptive changes. While the different regulatory agents and mechanism of action involved in mediating growth are not well established these effectors are certain to interact with cellular receptors, therefore, it is clearly relevant to consider the properties of pancreatic receptors and how they could be involved in the initiation of a trophic response. Consideration of second messengers mediating intracellular responses will be mentioned when relevant but treated in less detail as they are covered elsewhere2 as well as in this volume.