Pancreastatin (PST) is a chromogranin A (CGA)-derived peptide that was first isolated from the porcine pancreas. In fact, PST was the first known biologically active peptide to be derived from CGA. Although the physiological role of PST has yet to be fully established, a multitude of effects have implicated PST in the modulation of secretion and the control of energy metabolism, with a consequence which is generally counter-regulatory to that of insulin. Thus, PST has a glycogenolytic effect in the liver and a lipolytic effect in the adipocyte. Besides, PST inhibits leptin and increases UCP-2 expression in isolated adipocytes. In liver and adipose tissue, specific PST receptors and PST-induced signal transduction have been characterized, involving a Gq-PLCb-calcium-PKC pathway, providing a basis for the molecular mechanisms of the metabolic effects of PST, and the cross-talk to the insulin receptor signalling. Our current hypothesis is that PST plays a role in the physiology of stress, by regulating the supply of energy to the body. In this line, PST could play a role potentiating the metabolic effects of catecholamines, and further maintaining these effects after the short life of the amines. Besides, PST could also play a role not only in the physiology of stress, but also in pathophysiological conditions such as insulin-resistant states. In support of this, increased levels of PST, which correlate with those of catecholamines, have been found in insulin resistance states, such as gestational diabetes, and essential hypertension. In conclusion PST is a regulatory peptide derived from CGA and, therefore, may be regarded as part of the functional axis controlled by this protein, after the release from secretory granules.
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