Glucagon Induces a Rapid and Sustained Phosphorylation of the Human Glucagon Receptor in Chinese Hamster Ovary Cells

Heurich, Rainer O.; Buggy, Joseph J.; Vandenberg, Mark; Rossomando, Anthony

doi:10.1006/bbrc.1996.0504

Cited by 14 publications

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“…Specific signaling of the GR may be dispensable for GR endocytosis since the peptide antagonist des-His 1 -[Glu 9 ]glucaA C H T U N G T R E N N U N G gon induces a detectable internalization of the GR, albeit less pronounced compared to that induced by wild-type glucagon [151]. These in vivo studies are in accordance with the in vitro experiments of Heurich et al [153] in which a rapid, time-and concentration-dependent phosphorylation of GR on Ser residues induced by glucagon was demonstrated using 32 P labeling of a chinese hamster ovary (CHO) cell line expressing the human GR. Interestingly, neither forskolin nor phorbol ester increased glucagon-induced GR phosphorylation, suggesting that neither PKA nor PKC catalyze this phosphorylation event in vivo [153].…”

supporting

confidence: 88%

“…These in vivo studies are in accordance with the in vitro experiments of Heurich et al [153] in which a rapid, time-and concentration-dependent phosphorylation of GR on Ser residues induced by glucagon was demonstrated using 32 P labeling of a chinese hamster ovary (CHO) cell line expressing the human GR. Interestingly, neither forskolin nor phorbol ester increased glucagon-induced GR phosphorylation, suggesting that neither PKA nor PKC catalyze this phosphorylation event in vivo [153]. On the other hand, in vitro phosphorylation studies have recently shown that PKCa, PKCz, and to a lesser extent, PKCd, phosphorylate the GR in vitro, and that certain bile acids, such as chenodeoxycholic acid, might stimulate phosphorylation and heterologous desensitization of GR via a potential PKCa activation [154].…”

supporting

confidence: 86%

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Glucagon receptors

Authier

Desbuquois

2008

Cell. Mol. Life Sci.

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Glucagon is a pancreatic peptide hormone that, as a counterregulatory hormone for insulin, stimulates glucose release by the liver and maintains glucose homeostasis. First described as a glucagon binding entity functionally linked to adenylyl cyclase, the glucagon receptor is a member of the family B receptors within the G protein coupled superfamily of seven transmembrane-spanning receptors. During the past decade, considerable progress has been made in the identification of the molecular determinants of the glucagon receptor that are important for ligand binding and signal transduction, in the development of glucagon analogs and of nonpeptide small molecules acting as receptor antagonists, and in the characterization of the mechanisms involved in the regulation of expression of the glucagon receptor gene. In the present review, the current knowledge of glucagon receptor structure, function and expression is described, with emphasis on the metabolic fate of glucagon and on the endocytosis and cell itinerary of both ligand and receptor.

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supporting

confidence: 88%

supporting

confidence: 86%

Glucagon receptors

Authier

Desbuquois

2008

Cell. Mol. Life Sci.

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“…3), indicating that follicular fluid glucagon concentration increased in R and S groups in follicles O2.5 mm in diameter. The glucagon receptor has been reported in mammalian ovaries (Hansen et al 1995, Heurich et al 1996, Cascieri et al 1999, Wang et al 2008. Glucagon might have a novel physiological function in regulating folliculogenesis.…”

Section: Parametersmentioning

confidence: 99%

“…LDH activity tended to be increased in atretic follicles or smaller follicles. Glucagon, released from pancreatic a cells, is the principal counterregulatory hormone that opposes the action of insulin by promoting hepatic glycogenolysis, gluconeogenesis, and ketogenesis and its receptor was present in ovary (Hansen et al 1995, Heurich et al 1996, Cascieri et al 1999, Wang et al 2008. It might improve reproductive performance indirectly by increasing concentrations of plasma glucose and insulin (Bobe et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Effect of different levels of short-term feed intake on folliculogenesis and follicular fluid and plasma concentrations of lactate dehydrogenase, glucose, and hormones in Hu sheep during the luteal phase

Ying¹,

Wang²,

Wang³

et al. 2011

Reproduction

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This study investigated the effects of short-term food restriction or supplementation on folliculogenesis and plasma and intrafollicular metabolite and hormone concentrations. Ewes were randomly assigned to three groups: the control group received a maintenance diet (M) while the supplemented group and restricted group received 1.5!M and 0.5!M respectively on days 6-12 of their estrous cycle. Estrus was synchronized by intravaginal progestogen sponges for 12 days. On days 7-12, blood samples were taken. After slaughter, the ovarian follicles were classified and the follicular fluid was collected. Compared with restriction, supplementation shortened the estrous cycle length, decreased the number of follicles 2.5-3.5 mm and follicular fluid estradiol (E 2 ) concentration, increased the number of follicles O3.5 mm and plasma glucose, insulin and glucagon concentrations, and augmented the volume of follicles O2.5 mm. Restricted ewes had higher intrafollicular insulin concentration, but it was similar to that of supplemented ewes. Compared with follicles %2.5 mm, the intrafollicular glucose and E 2 concentrations were increased and the testosterone, insulin, and glucagon concentrations and lactate dehydrogenase (LDH) activity were decreased in follicles O2.5 mm. Only in restricted ewes were intrafollicular LDH and testosterone concentrations in follicles %2.5 mm not different from those in follicles %2.5 mm. In conclusion, the mechanism by which short-term dietary restriction inhibits folliculogenesis may involve responses to intrafollicular increased E 2 , testosterone, and LDH levels in late-stage follicles. This may not be due to the variation of intrafollicular insulin level but rather due to decreased circulating levels of glucose, insulin, and glucagon.

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“…Many G protein-coupled receptors become phosphorylated in response to agonist stimulation (Palmer et al, 1995;Pals-Rylaarsdam et al, 1995;Pippig et al, 1995;Heurich et al, 1996), and this modification has been linked to the functional desensitization of the receptor (Pippig et al, 1995;Garland et al, 1996). Furthermore, subsequent dephosphorylation of the receptor by protein phosphatases may play a role in receptor resensitization (Krueger et al, 1997).…”

Section: Role Of Receptor Dephosphorylation In Resensitizationmentioning

confidence: 99%

Involvement of Receptor Cycling and Receptor Reserve in Resensitization of Muscarinic Responses in SH‐SY5Y Human Neuroblastoma Cells

Szekeres¹,

Koenig²,

Edwardson³

1998

Journal of Neurochemistry

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Preexposure of SH-SY5Y cells to the muscarinic agonist carbachol caused a rapid desensitization of subsequent carbachol-stimulated intracellular Ca 2~re-sponses and a slower decrease in the number of receptors at the plasma membrane. Desensitization (to 30% of the control response) was maximal after 1 min of exposure to agonist, whereas the number of cell surface receptors reached a minimum (33% of control) only after 5 min. Following agonist washout, the recovery of response was complete within 12 mm, whereas the recovery of surface receptor number reached a plateau at 65% of control after 30 min. Treatment with inhibitors of endocytosis (concanavalin A) or recycling (nigericin) did not affect rapid desensitization but did decrease resensitization, suggesting that receptor cycling is involved in resensitization. Experiments with the irreversible antagonist propylbenzilylcholine mustard demonstrated that the receptor reserve for the Ca2~response to 1 mM carbachol is -..50%. Removal of this receptor reserve led to a decrease in the rate of resensitization. We propose that the existence of a receptor reserve might explain The poor correlation between functional response and surface receptor number, and that one of its roles might be to permit rapid resensitization after a significant agonist-induced decrease in surface receptor number. The purpose of receptor cycling might be to allow dephosphorylation (and reactivation) of receptors that have become phosphorylated (and inactivated) in response to agonist stimulation, because the protein phosphatase inhibitor calyculin A significantly reduced resensitization.

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Glucagon Induces a Rapid and Sustained Phosphorylation of the Human Glucagon Receptor in Chinese Hamster Ovary Cells

Cited by 14 publications

References 0 publications

Glucagon receptors

Glucagon receptors

Effect of different levels of short-term feed intake on folliculogenesis and follicular fluid and plasma concentrations of lactate dehydrogenase, glucose, and hormones in Hu sheep during the luteal phase

Involvement of Receptor Cycling and Receptor Reserve in Resensitization of Muscarinic Responses in SH‐SY5Y Human Neuroblastoma Cells

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