Interaction of Amino Acids and Cyclic AMP on the Release of Insulin and Glucagon by Newborn Rat Pancreas

Jarrousse, C.; Rosselin, G

doi:10.1210/endo-96-1-168

Cited by 34 publications

(20 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus arginine appeared to protect the A-cells against the inhibitory effect of cyclic AMP and only the early stimulatory effect was seen. This agrees with the report by Jarrousse and Rosselin [36] that dibutyryl cyclic AMP and theophylline enhanced amino acid induced glucagon release, but is at variance with the findings of Marco et a1. [54], who observed an inhibitory effect of aminophylline on arginine-induced glucagon release in vivo.…”

Section: Discussionsupporting

confidence: 92%

“…This has been shown with cyclic AMP [33,34,35], dibutyryl cyclic AMP [32,35,36], and by raising intracellular cyclic AMP levels with theophylline [24,32,35,36,37,38]. By contrast, our own data [39] showed consistent inhibition of glucagon release with cyclic AMP or theophylline in monolayer cultures of newborn rat pancreas.…”

Section: Introductionmentioning

confidence: 64%

“…Firstly, the inhibitory effects were seen with rather lengthy incubations of four hours. Secondly, the Ca ++ concentration of the media was higher (2.5 mM) than in studies reporting stimulation by cyclic AMP [32,36] or the effective, free Ca ++ concentration in the latter was in effect lowered by higher albumin concentrations in the media [25,38]. Consequently, the studies reported here were performed to document fully the inhibitory effects of cyclic AMP and to investigate the time course of the response.…”

Section: Introductionmentioning

confidence: 90%

See 2 more Smart Citations

Stimulatory and inhibitory effects of cyclic AMP on pancreatic glucagon release from monolayer cultures and the controlling role of calcium

et al. 1976

View full text Add to dashboard Cite

Summary. When glucagon release from monolayer cultures of newborn rat pancreas was measured over four hours in media containing 2.5 mM Ca + +, a significant cyclic AMP-related inhibition of release was observed. This was noted whether intracellular cyclic AMP levels were raised by the addition of exogenous cyclic AMP or dibutyryl cyclic AMP, by phosphodiesterase inhibition with theophylline, or by the stimulation of adenylate cyclase with cholera toxin. The inhibition was concentration dependent for cyclic AMP and could not be reproduced by the addition of AMP, ADP or ATP. Adenosine also inhibited glucagon release while ATP was stimulatory. From time course studies it appeared that the inhibitory effects of cyclic AMP and cholera toxin were progressive after two hours of incubation. With cholera toxin an early stimulation of glucagon release was observed. The effects of cyclic AMP and cholera toxin on argininestimulated glucagon release were to stimulate further the glucagon release during the first hour of the incubation. Thus, the effects of raising intracellular cyclic AMP levels were biphasic in that both an early stimulation and a late inhibition of glucagon release were observed. In examining the nature of these responses a remarkable controlling role for Ca ++ was uncovered: at Ca + + concentrations of 0.3 mM and lower no effect of cyclic AMP on glucagon release was found. With 1 mM Ca ++ in the medium cyclic AMP stimulated glucagon release early (30 min) and thereafter had no further effect. In the presence of 2.5 mM Ca + + cyclic AMP did not stimulate early but did cause the delayed inhibition of release. It is concluded that the effect of cyclic AMP on glucagon release can be either stimulatory or inhibitory depending upon the Ca + + concentration of the medium and the duration of exposure to raised cyclic AMP levels.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 64%

Section: Introductionmentioning

confidence: 90%

See 1 more Smart Citation

Stimulatory and inhibitory effects of cyclic AMP on pancreatic glucagon release from monolayer cultures and the controlling role of calcium

et al. 1976

View full text Add to dashboard Cite

show abstract

“…The present investigation, showing a similar low threshold for insulin biosynthesis and release in the control group of neonatal offspring, is at variance with previous studies in both adult [9] and neonatal [3] rat islets in vitro. In those studies it was found that the glucose threshold of insulin biosynthesis was lower than that of insulin secretion, and that the half maximal response for glucose-stimulated insulin release was found in the glucose concentration range 7-8 mmol/1 in islets from neonatal animals, compared with 4.1 mmol/1 glucose in the control group in the present study.…”

Section: Discussionsupporting

confidence: 60%

The effect of maternal caffeine ingestion on pancreatic function in the neonatal rat

1982

View full text Add to dashboard Cite

Summary. Pancreatic function was investigated in neonatal suckling offspring of caffeine-ingesting dams, with or without maternal sucrose supplementation, throughout pregnancy and lactation. In offspring of rats ingesting caffeine without sucrose supplementation, there was initial hyperinsulinaemia, followed by a progressive fall of plasma insulin to subnormal levels. This fall in plasma insulin coincided with depletion of pancreatic insulin stores. Both the fall in plasma insulin and depletion of pancreatic insulin stores were prevented by sucrose supplementation of caffeine-ingesting dams. Offspring of dams fed sucrose alone and control offspring also maintained pancreatic insulin stores and circulating insulin levels over the first 14 days of postnatal life. Pancreases from offspring of caffeine-exposed animals tested in vitro showed enhanced sensitivity of the insulin release process to glucose. This was reflected in the glucose concentration required to elicit half-maximal insulin release (2.4 ___ 0.2 mmol/1 for caffeine offspring, 2.3 + 0.2 mmol/1 for caffeine with sucrose, 3.8 _+ 0.3 mmol/1 for sucrose and 4.1 + 0.3 mmol/1 for control offspring, mean +_ SEM). In contrast, offspring of sucrose-supplemented (with or without caffeine) dams showed increased sensitivity of the proinsulin biosynthetic process to glucose, whereas offspring of dams ingesting caffeine alone showed no significant enhancement of the biosynthetic process compared with control offspring. Thus enhanced sensitivity of the insulin secretory process to glucose without a change in the sensitivity of the biosynthetic process in the offspring of the caffeine ingesting (nonsucrose supplemented) dams could explain the progressive depletion of pancreatic insulin stores and eventual hypoinsulinaemia seen in this group.

show abstract

“…Coughlin, unpublished observations). GPRC6A may be activated by arginine and lysine (42), basic amino acids that can stimulate β cell insulin secretion (43), by a mechanism as yet incompletely understood. Might insulin secretion in response to basic amino acids be mediated by GPRC6A?…”

Section: Figurementioning

confidence: 99%

Probing cell type–specific functions of Gi in vivo identifies GPCR regulators of insulin secretion

Regard¹,

Kataoka²,

Cano³

et al. 2007

J. Clin. Invest.

167

242

View full text Add to dashboard Cite

The in vivo roles of the hundreds of mammalian G protein-coupled receptors (GPCRs) are incompletely understood. To explore these roles, we generated mice expressing the S1 subunit of pertussis toxin, a known inhibitor of G i/o signaling, under the control of the ROSA26 locus in a Cre recombinase-dependent manner (ROSA26 PTX ). Crossing ROSA26 PTX mice to mice expressing Cre in pancreatic β cells produced offspring with constitutive hyperinsulinemia, increased insulin secretion in response to glucose, and resistance to dietinduced hyperglycemia. This phenotype underscored the known importance of G i/o and hence of GPCRs for regulating insulin secretion. Accordingly, we quantified mRNA for each of the approximately 373 nonodorant GPCRs in mouse to identify receptors highly expressed in islets and examined the role of several. We report that 3-iodothyronamine, a thyroid hormone metabolite, could negatively and positively regulate insulin secretion via the G i -coupled α 2A -adrenergic receptor and the G s -coupled receptor Taar1, respectively, and proteaseactivated receptor-2 could negatively regulate insulin secretion and may contribute to physiological regulation of glucose metabolism. The ROSA26 PTX system used in this study represents a new genetic tool to achieve tissue-specific signaling pathway modulation in vivo that can be applied to investigate the role of G i/o -coupled GPCRs in multiple cell types and processes.

show abstract

Interaction of Amino Acids and Cyclic AMP on the Release of Insulin and Glucagon by Newborn Rat Pancreas

Cited by 34 publications

References 0 publications

Stimulatory and inhibitory effects of cyclic AMP on pancreatic glucagon release from monolayer cultures and the controlling role of calcium

Stimulatory and inhibitory effects of cyclic AMP on pancreatic glucagon release from monolayer cultures and the controlling role of calcium

The effect of maternal caffeine ingestion on pancreatic function in the neonatal rat

Probing cell type–specific functions of Gi in vivo identifies GPCR regulators of insulin secretion

Contact Info

Product

Resources

About