The activity of the rectal gland of the North Pacific spiny dogfish Squalus suckleyi is glucose dependent and stimulated by glucagon-like peptide-1.

CA Deck, WG Anderson, JM Conlon, PJ Walsh

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Elasmobranchs possess a specialised organ, the rectal gland, which is responsible for excreting sodium chloride via the posterior intestine. Previous work has indicated that the gland may be activated by a number of hormones, some of which are likely related to the salt or volume loads associated with feeding. Furthermore, evidence exists for the gland being glucose dependent which is atypical for an elasmobranch tissue. In this study, the presence of sodium-glucose co-transporters (SGLTs) in the rectal gland and their regulation by feeding were investigated. In addition, the hypothesis of glucose dependence was examined through the use of glucose transporter (GLUT and SGLT) inhibitors, phlorizin, Indinavir, and STF-31 and their effect on secretion by the rectal gland. Finally, the effects on rectal gland activity of insulin, glucagon, and glucagon-like peptide-1, hormones typically involved in glucoregulation, were examined. The results showed that sglt1 mRNA is present in the gland, and there was a significant reduction in sglt1 transcript abundance 24 h post-feeding. An almost complete suppression of chloride secretion was observed when glucose uptake was inhibited, confirming the organ's glucose dependence. Finally, perfusion with dogfish GLP-1 (10 nmol L-1), but not dogfish glucagon, was shown to markedly stimulate the activity of the gland, increasing chloride secretion rates above baseline by approximately 16-fold (p <0.001). As GLP-1 is released from the intestine upon feeding, we propose that this may be the primary signal for activation of the rectal gland post-feeding.
LanguageEnglish
Pages1155-1161
JournalJournal of Comparative Physiology B
Volume187
Issue number8
Early online date25 Apr 2017
DOIs
Publication statusE-pub ahead of print - 25 Apr 2017

Fingerprint

Squalus
glucagon-like peptide 1
Squalus acanthias
glucose
symporters
glucagon
secretion
glucoregulation
chlorides
intestines
hormones
sodium
glucose transporters
sodium chloride
insulin
salts
uptake mechanisms

Keywords

  • Rectal gland
  • Glucose transporter
  • Glucagon-like peptide
  • Elasmobranchs
  • Dogfish

Cite this

@article{a05f4f0047494181a72892cfe8c982f9,
title = "The activity of the rectal gland of the North Pacific spiny dogfish Squalus suckleyi is glucose dependent and stimulated by glucagon-like peptide-1.",
abstract = "Elasmobranchs possess a specialised organ, the rectal gland, which is responsible for excreting sodium chloride via the posterior intestine. Previous work has indicated that the gland may be activated by a number of hormones, some of which are likely related to the salt or volume loads associated with feeding. Furthermore, evidence exists for the gland being glucose dependent which is atypical for an elasmobranch tissue. In this study, the presence of sodium-glucose co-transporters (SGLTs) in the rectal gland and their regulation by feeding were investigated. In addition, the hypothesis of glucose dependence was examined through the use of glucose transporter (GLUT and SGLT) inhibitors, phlorizin, Indinavir, and STF-31 and their effect on secretion by the rectal gland. Finally, the effects on rectal gland activity of insulin, glucagon, and glucagon-like peptide-1, hormones typically involved in glucoregulation, were examined. The results showed that sglt1 mRNA is present in the gland, and there was a significant reduction in sglt1 transcript abundance 24 h post-feeding. An almost complete suppression of chloride secretion was observed when glucose uptake was inhibited, confirming the organ's glucose dependence. Finally, perfusion with dogfish GLP-1 (10 nmol L-1), but not dogfish glucagon, was shown to markedly stimulate the activity of the gland, increasing chloride secretion rates above baseline by approximately 16-fold (p <0.001). As GLP-1 is released from the intestine upon feeding, we propose that this may be the primary signal for activation of the rectal gland post-feeding.",
keywords = "Rectal gland, Glucose transporter, Glucagon-like peptide, Elasmobranchs, Dogfish",
author = "CA Deck and WG Anderson and JM Conlon and PJ Walsh",
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The activity of the rectal gland of the North Pacific spiny dogfish Squalus suckleyi is glucose dependent and stimulated by glucagon-like peptide-1. / Deck, CA; Anderson, WG; Conlon, JM; Walsh, PJ.

In: Journal of Comparative Physiology B, Vol. 187, No. 8, 25.04.2017, p. 1155-1161.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The activity of the rectal gland of the North Pacific spiny dogfish Squalus suckleyi is glucose dependent and stimulated by glucagon-like peptide-1.

AU - Deck, CA

AU - Anderson, WG

AU - Conlon, JM

AU - Walsh, PJ

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N2 - Elasmobranchs possess a specialised organ, the rectal gland, which is responsible for excreting sodium chloride via the posterior intestine. Previous work has indicated that the gland may be activated by a number of hormones, some of which are likely related to the salt or volume loads associated with feeding. Furthermore, evidence exists for the gland being glucose dependent which is atypical for an elasmobranch tissue. In this study, the presence of sodium-glucose co-transporters (SGLTs) in the rectal gland and their regulation by feeding were investigated. In addition, the hypothesis of glucose dependence was examined through the use of glucose transporter (GLUT and SGLT) inhibitors, phlorizin, Indinavir, and STF-31 and their effect on secretion by the rectal gland. Finally, the effects on rectal gland activity of insulin, glucagon, and glucagon-like peptide-1, hormones typically involved in glucoregulation, were examined. The results showed that sglt1 mRNA is present in the gland, and there was a significant reduction in sglt1 transcript abundance 24 h post-feeding. An almost complete suppression of chloride secretion was observed when glucose uptake was inhibited, confirming the organ's glucose dependence. Finally, perfusion with dogfish GLP-1 (10 nmol L-1), but not dogfish glucagon, was shown to markedly stimulate the activity of the gland, increasing chloride secretion rates above baseline by approximately 16-fold (p <0.001). As GLP-1 is released from the intestine upon feeding, we propose that this may be the primary signal for activation of the rectal gland post-feeding.

AB - Elasmobranchs possess a specialised organ, the rectal gland, which is responsible for excreting sodium chloride via the posterior intestine. Previous work has indicated that the gland may be activated by a number of hormones, some of which are likely related to the salt or volume loads associated with feeding. Furthermore, evidence exists for the gland being glucose dependent which is atypical for an elasmobranch tissue. In this study, the presence of sodium-glucose co-transporters (SGLTs) in the rectal gland and their regulation by feeding were investigated. In addition, the hypothesis of glucose dependence was examined through the use of glucose transporter (GLUT and SGLT) inhibitors, phlorizin, Indinavir, and STF-31 and their effect on secretion by the rectal gland. Finally, the effects on rectal gland activity of insulin, glucagon, and glucagon-like peptide-1, hormones typically involved in glucoregulation, were examined. The results showed that sglt1 mRNA is present in the gland, and there was a significant reduction in sglt1 transcript abundance 24 h post-feeding. An almost complete suppression of chloride secretion was observed when glucose uptake was inhibited, confirming the organ's glucose dependence. Finally, perfusion with dogfish GLP-1 (10 nmol L-1), but not dogfish glucagon, was shown to markedly stimulate the activity of the gland, increasing chloride secretion rates above baseline by approximately 16-fold (p <0.001). As GLP-1 is released from the intestine upon feeding, we propose that this may be the primary signal for activation of the rectal gland post-feeding.

KW - Rectal gland

KW - Glucose transporter

KW - Glucagon-like peptide

KW - Elasmobranchs

KW - Dogfish

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T2 - Journal of Comparative Physiology B

JF - Journal of Comparative Physiology B

SN - 0174-1578

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ER -