Galanin was recently demonstrated to be a neuropeptide in intrapancreatic nerves. In this study, the effects of galanin on basal and stimulated insulin and glucagon secretion in the mouse were investigated. Galanin, injected intravenously at dose levels ranging from 0.53 to 8.5 nmol kg-1, markedly lowered basal plasma insulin levels and transiently increased basal plasma glucagon levels. Furthermore, galanin induced hyperglycaemia: plasma glucose levels were 11 +/- 0.2 mmol l-1 2 min after injection of galanin (4.25 nmol kg-1) compared with 9.3 +/- 0.3 mmol-1 in controls (P less than 0.001). Galanin also impaired the plasma insulin response to either glucose or the cholinergic agonist carbachol. Thus, galanin (4.25 nmol kg-1) inhibited the plasma insulin response to glucose by 65% (P less than 0.001), and that to carbachol by 85% (P less than 0.001). Moreover, glucose abolished the galanin-induced plasma glucagon response. Also, galanin and carbachol exerted additive stimulatory effects on glucagon levels. It is concluded from this study in mice that galanin inhibits basal and stimulated insulin secretion, stimulates glucagon secretion, and induces hyperglycaemia. It is suggested that the intrapancreatic neuropeptide galanin is of importance in the regulation of both insulin and glucagon secretion.

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Galanin-containing nerve fibers have previously been observed in the human, dog, and pig pancreas. Whether the mouse and rat pancreas also contain galanin nerve fibers has been a matter of debate. Therefore, we examined the distribution of galanin in the mouse and the rat pancreas. Further, the possible localization of galanin to adrenergic nerves was studied using sequential immunostaining for galanin and tyrosine hydroxylase (TH). In the mouse pancreas, numerous galanin-immunoreactive (GIR) nerve fibers occurred around blood vessels. They were less numerous in the exocrine parenchyma and in association with the islets. In contrast, in the rat pancreas, only a few GIR nerves were found. They were located around blood vessels and scattered in the exocrine parenchyma. Occasionally, GIR nerves were also observed in the islets. There was a dense distribution of TH-immunoreactive fibers in both the mouse and the rat pancreas. Sequential immunostaining revealed co-localization of galanin and TH immunoreactivity in nerve fibers in both the mouse and the rat pancreas. Following chemical sympathectomy using 6-hydroxydopamine (6-OHDA), not all GIR nerves disappeared. In the mouse pancreas a remaining population of galanin nerves was found around blood vessels, and occasionally in the islets. In the rat pancreas, a few GIR nerves were seen also after chemical sympathectomy. We conclude that intrapancreatic GIR nerves also occur in the mouse and the rat. These findings suggest that many of the GIR nerves are adrenergic but that non-adrenergic, possibly intrinsic or sensory GIR nerves exist as well in both the mouse and the rat pancreas.

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Background Laparoscopic fundoplication is an effective treatment for gastro‐oesophageal reflux disease (GERD). We aimed to assess quality of life (QoL), long‐term residual symptoms, patient satisfaction and use of acid‐suppression medication at 5, 10 and 20 years after surgery. Methods We identified a cohort of 100 patients who underwent laparoscopic fundoplication between 1993 and 1998. The validated QoL questionnaires Short Form health survey (SF‐36), and Quality‐of‐Life in Reflux and Dyspepsia (QOLRAD), as well as a specific questionnaire regarding post‐fundoplication symptoms, were sent to the patients at 5, 10 and 20 years after surgery. Furthermore, patients who reported using the acid‐suppression medication after 20 years were interviewed by telephone regarding their reason for taking it. Results Eighty‐eight percent of the patients responded at 5 and 10 years post‐surgery. Twenty years following fundoplication, 68 (84% of those still alive) patients completed the questionnaires. The patients had equivalent health‐related QoL scores in both the QOLRAD and SF‐36 questionnaires after 10 and 20 years, and those scores were in line with a Swedish age‐matched population. After 20 years, 87% were satisfied with the results, and 84% of the patients would recommend reflux surgery to a relative or a friend. At the telephone interview, 32% (22/68) confirmed using acid‐suppression medication, but only half (11/68) used it because of reflux symptoms. Conclusion The long‐term, satisfying outcomes in GERD symptoms and QoL 5 and 10 years after surgery were maintained at a 20‐year follow‐up. Half of the patients used acid‐suppression medication for reasons other than GERD symptoms.