Since the isolation of
enkephalins 7 yr ago, there has been an
explosive increase in knowledge and an enormous interest in the action of both exogenous and
endogenous opiates. This review deals with the interaction of
opiates with the endocrine pancreas. The results of animal studies performed in vitro do not allow any conclusion to be drawn, because the effects of
opioid peptides on pancreatic
hormone release seem dependent on many variables, including the agent investigated, dose administered, concentration of
glucose in the medium, and experimental procedure used. The results of in vivo animal studies suggest that central administration of
opiates and
opioid peptides acts indirectly via the sympathetic nervous system to cause
hyperglycemia and impaired insulin secretion, while peripheral administration tends to stimulate
insulin and
glucagon secretion. This last statement seems also to be true for studies performed in human beings. The
narcotic addict offers a model to evaluate the hormonal and metabolic effects of a chronically administered agent that binds and activates endogenous receptors. In these subjects, it is possible to find increased concentrations of
glycosylated hemoglobin A1 and a marked reduction of the acute
insulin response to intravenous
glucose, but not to
arginine, which suggests a state of defective
glucose recognition by pancreatic beta-cells during
narcotic addiction. Thus, the
heroin addict, like patients with non-
insulin-dependent diabetes, does not respond appropriately to
glucose signals.(ABSTRACT TRUNCATED AT 250 WORDS)