Insulin Receptors on Pancreatic Acinar Cells in Guinea Pigs*

Sjödin, Lars; Holmberg, K.; Lydén, Annika

doi:10.1210/endo-115-3-1102

Cited by 22 publications

(10 citation statements)

References 26 publications

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“…Insulin is believed to bind to its own receptor on the acinar cell (128,168,183,211), leading to stimulation and potentiation of amylase secretion by various mechanisms including regulation of amylase gene transcription (90); stimulation of DNA, RNA, and acinar protein synthesis (89,129,145); and increase in glucose uptake (209).…”

Section: Pancreatic Hormones and Neuropeptidesmentioning

confidence: 99%

The islet-acinar axis of the pancreas: more than just insulin

Barreto

Carati

Toouli³

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

103

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Although the role of the islets in the regulation of acinar cell function seemed a mystery to investigators who observed their dispersion among pancreatic acini, over time an appreciation for this intricate and unique structural arrangement has developed. The last three decades have witnessed a steadily growing understanding of the interrelationship of the endocrine and the exocrine pancreas. The islet innervation and vascular anatomy have been more fully characterized and provide an appropriate background for our current understanding. The interrelationship between the endocrine and exocrine pancreas is mediated by islet-derived hormones such as insulin and somatostatin, other humoral factors including pancreastatin and ghrelin, and also neurotransmitters (nitric oxide, peptide YY, substance P, and galanin) released by the nerves innervating the pancreas. Although considerable progress has been achieved, further work is required to fully delineate the complex interplay of the numerous mechanisms involved. This review aims to provide a comprehensive update of the current literature available, bringing together data gleaned from studies addressing the actions of individual hormones, humoral factors, and neurotransmitters on the regulation of amylase secretion from the acinar cell. This comprehensive view of the islet-acinar axis of the pancreas while acknowledging the dominant role played by insulin and somatostatin on exocrine secretion sheds light on the influence of the various neuropeptides on amylase secretion.

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Section: Pancreatic Hormones and Neuropeptidesmentioning

confidence: 99%

The islet-acinar axis of the pancreas: more than just insulin

Barreto

Carati

Toouli³

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

103

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“…It has been reported that insulin receptor exists in the membrane of the pancreatic acinar cells [4-6], and insulin directly enters to the acinar cells [7]. These findings suggest that insulin directly acts acinar cells and has important role to maintain exocrine secretion in the acinar cells.…”

mentioning

confidence: 96%

Age-associated changes in pancreatic exocrine secretion of the isolated perfused rat pancreas

Jiang

Chen

et al. 2013

Lab Anim Res

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Gut functions, such as gastrointestinal motility, gastric secretion and pancreatic secretion, were reduced with age. Glucose tolerance is impaired, and the release of insulin and β-cell's sensitivity on glucose are reduced with age. However, a lot of controversial data have been reported as insulin concentrations after glucose ingestion are either higher or no different in elderly and young subjects. Thus, this study was aimed to investigate whether aging could affect pancreatic exocrine secretion and its action mechanisms. An isolated perfused rat pancreatic model was used to exclude the effects of external nerves or hormones. Pancreatic secretion was increased by CCK under 5.6 mM glucose background in the isolated perfused pancreas of young (3 months), 12 months and 18 months aged rats. There was no significant difference between young and aged rats. In 3 months old rats, CCK-stimulated pancreatic secretion was potentiated under 18 mM glucose background. However, the potentiation effects of endogenous insulin and CCK were not observed in 12 and 18 months old rats. Exogenous insulin also potentiated CCK-stimulated pancreatic secretion in 3 months old rats. Similarly, exogenous insulin failed to potentiate CCK-stimulated pancreatic secretion as that of 3 months old rats. Wet weight of pancreas and amylase content in pancreatic tissue were not changed with age. These results indicate that pancreatic exocrine secretion is reduced with age and endogenous insulin secretion and/or action is involved in this phenomenon.

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“…

The secretion of the pancreatic acinar cells has for a long time been thought to be regulated by the islet hormones [7], but few detailed studies indicate hormonal regulation of the acinar cells.

…”

mentioning

confidence: 99%

A Reciprocal Regulation of Ca2+-Activated K+ Channel by Insulin and Somatostatin in Guinea-Pig Pancreatic Acinar Cells.

Yanagisawa¹,

Suzuki²

2001

JJP

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The pancreatic acini are in close contact with the surrounding islets, having no significant fibrous capsules, and receptors of insulin [1][2][3][4] and somatostatin [5,6] on the pancreatic acinar cell have been reported. Therefore, this might eventually enter into very close interrelation between the exocrine pancreas and the endocrine islet of Langerhans.The secretion of the pancreatic acinar cells has for a long time been thought to be regulated by the islet hormones [7], but few detailed studies indicate hormonal regulation of the acinar cells. In digestive enzyme secretion, for example, insulin potentiates acetylcholine-induced [8,9] and, cholecytokinin-induced amylase secretion [10]. In vivo, somatostatin inhibits both Ca 2ϩ -induced and cyclic AMP-induced amylase secretion [11][12][13][14], but in vitro, a few consistent effects on secretion have been described [13,15]. As for ionic fluid secretion from pancreatic acini, only one report concerns the effect of insulin on cation channel [16].Ca 2ϩ -activated K ϩ channels, which have been suggested to regulate the K ϩ permeability changes in plasma membrane during fluid secretion, have been identified on the basolateral membrane of Cl Ϫ -secreting pancreatic acinar cells in a variety of animal species [17][18][19][20]. It has been suggested that these K ϩ channels are important for Cl Ϫ uptake into cells [21]. Secretagogues evoking an increase in cytoplasmic Ca 2ϩ level activate K ϩ channels causing an increase in the local external K ϩ concentration. Na ϩ , K ϩ , and Cl Key words: insulin, somatostatin, potassium channels, pancreatic juice, cyclic AMP. Abstract:The effects of islet hormones, insulin and somatostatin, on the regulation of the opening of Ca 2ϩ -activated K ϩ channels in the basolateral plasma membrane of primary cultured pancreatic acinar cells of guinea-pig were studied by cell-attached single-channel recording technique. A single application of insulin or somatostatin did not influence the opening of K ϩ channel. The open-state probability (p) of K ϩ channel induced by the application of acetylcholine (ACh) to the bath solution was increased by insulin in the presence of ACh. The enhancement effect of insulin on the increased frequency of the channel opening was not seen when concomitantly applied with protein kinase A inhibitor, Rp-cAMPS triethylamine. Insulin increased the p value of K ϩ channel, which was reversed by an application of somatostatin (Tyr-somatostatin 28). The addition of ACh followed by forskolin or dibutyryl adenosine 3Ј,5Ј-cyclic monophosphate (dbcAMP) to the bath solution evoked an increase in the p value of K ϩ channel. After increasing the channel opening, the addition of somatostatin reduced the p value, but not with dbcAMP. Taken together, the results suggest that insulin and somatostatin reciprocally modify the ACh-induced opening of the Ca 2ϩ -activated K ϩ channel through a cyclic AMP-dependent signaling pathway.

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Insulin Receptors on Pancreatic Acinar Cells in Guinea Pigs*

Cited by 22 publications

References 26 publications

The islet-acinar axis of the pancreas: more than just insulin

The islet-acinar axis of the pancreas: more than just insulin

Age-associated changes in pancreatic exocrine secretion of the isolated perfused rat pancreas

A Reciprocal Regulation of Ca2+-Activated K+ Channel by Insulin and Somatostatin in Guinea-Pig Pancreatic Acinar Cells.

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