Diminished inhibitory effect of noradrenaline on insulin release from mouse islets transplanted to kidney

Shi, Chun-Liang; Täljedal, Inge‐Bert

doi:10.1007/bf00569569

Cited by 11 publications

(6 citation statements)

References 17 publications

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“…As previously shown (6), the attenuation of the inhibitory response to NA in islet grafts requires about 6 weeks to develop. However, the effect does not reflect 124.7 ± 6.9 84.4 + 5.1 42.9 ± 3.9*" -15.1 ± 6.8*** Rates of insulin release are given for fresh, cultured, or cultured and transplanted islets perifused with glucose alone or in combination with UK-14,304.…”

Section: Discussionmentioning

confidence: 86%

“…In previous experiments, graft insulin secretory responses have been found to be quite stable from about 6 weeks up to at least one year when challenged by glucose, NA or acetylcholine in vitro (6,11,12). Most experiments in the present study were therefore performed with grafts 30-40 weeks old.…”

Section: Perifusion Of Isolated Graftsmentioning

confidence: 95%

“…Based on previous experiences (6,11,12), a selfcontrol experimental design was used. After 40 min of preliminary perifusion with 2.8 mmol/1 D-glucose, islet grafts were stimulated by 16.7 mmol/1 D-glucose for 20 or 25 min, allowed to rest during perifusion with 2.8 mmol/1 D-glucose for 20 min, and again stimulated with 16.7mmol/I D-glucose for 20 or 25 min.…”

Section: Perifusion Of Isolated Graftsmentioning

confidence: 99%

“…Noradrenaline (NA) typically inhibits insulin secretion by its dominating action on the a2 adrenoceptors (2)(3)(4)(5). In syngeneic islet grafts under the kidney capsule of C57BL/6J mice, this inhibitory effect of NA was clearly diminished 6, but not 1-3, weeks after transplantation (6). In contrast to NA, which affects both and ß receptors, the adrenoceptor agonist, UK-14,3 04 has a high specificity for a2 receptors in inhibiting insulin release (7,8).…”

mentioning

confidence: 96%

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Effects of UK-14,304, noradrenaline, and propranolol on insulin release from transplanted mouse islets

Shi

Sehlin²,

Täljedal³

1996

European Journal of Endocrinology

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To elucidate the adrenergic responsiveness of transplanted pancreatic islets, normal BALB/c mice received 150 syngeneic islets under the left kidney capsule. After 12-40 weeks, the grafts were removed and compared with untransplanted islets by an in vitro perifusion technique. Noradrenaline (NA), 3 mumol/l, completely inhibited glucose-stimulated insulin release from untransplanted islets but not from grafts, whether or not the beta adrenergic blocker, L-propranolol, was present. UK-14,304, an alpha 2-specific adrenergic agonist, inhibited glucose-induced insulin secretion from untransplanted islets by 80-92% at 0.1 or 1 mumol/l, and by 35-56% at 5-10 nmol/l. Insulin secretion from islet grafts was also markedly inhibited by 0.1 or 1 mumol/l, but not by 5 or 10 nmol/l, UK-14,304. It is suggested that the diminished adrenergic inhibition of insulin release from islet grafts reflects an altered function of the alpha 2 adrenoceptors on the beta-cells.

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Section: Discussionmentioning

confidence: 86%

Section: Perifusion Of Isolated Graftsmentioning

confidence: 95%

Section: Perifusion Of Isolated Graftsmentioning

confidence: 99%

mentioning

confidence: 96%

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Effects of UK-14,304, noradrenaline, and propranolol on insulin release from transplanted mouse islets

Shi

Sehlin²,

Täljedal³

1996

European Journal of Endocrinology

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“…Mouse islets that are transplanted to the kidney lose their responsiveness to the neurotransmitters acetylcholine and noradrenaline ( Shi & Täljedal 1995a, b, Shi et al , 1996 ). In an effort to understand how islets may be affected by changes in microenvironment, we studied the insulin secretion and the muscarinic acetylcholine receptor messenger RNA (mAChR mRNA) expression of islets kept in culture for 1–7 days.…”

Section: Introductionmentioning

confidence: 99%

Effect of carbachol on regulation of the mACh receptor mRNA expression ADN insulin secretion in mouse pancreatic islets

Shi¹,

Täljedal²,

Mattsson³

1999

Acta Physiologica Scandinavica

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Introduction. Mouse islets that are transplanted to the kidney lose their responsiveness to the neurotransmitters acetylcholine and noradrenaline (Shi & Ta Èljedal 1995a,b, Shi et al, 1996. In an effort to understand how islets may be affected by changes in microenvironment, we studied the insulin secretion and the muscarinic acetylcholine receptor messenger RNA (mAChR mRNA) expression of islets kept in culture for 1±7 days.Methods. Islets were isolated from BALB/c or ob/ob mice. The effects of glucose and carbachol on islets insulin secretion were studied by static incubation or dynamic perifusion methods; insulin content extracted by acid ethanol and ultrasonication; and mACh-RmRNA level were investigated by the RT-PCR method.Results. Islet insulin content was not affected by the glucose concentration in culture medium, nor by the addition of carbachol into the culture medium (average about 62 ng per lg islets dry weight). However, the insulin secretion in response to glucose was markedly decreased when islets were cultured in medium containing 2 mmol/l glucose, in comparison to islets cultured in medium containing 11.2 mmol/l (0.07 0.0 vs 2.56 0.4 ng per hr per 3 islets). The glucose-induced insulin secretions was also decreased when islets were cultured in medium containing cholinergic agaonist carbachol in comparison with islets cultured without carbachol (26.1 5.1 vs 55.9 3.5 ng per 25 min per 50 islets). Acetylcholine potentiated glucose-induced insulin secretion in fresh islets and cultured islets. This potentiating effect was diminished when islets were cultured with carbachol (5.53 + 0.7 vs 1.99 0.1 ng per 60 min per 3 islets). When measured by RT-PCR method, the expression of mAChR mRNA in pancreatic islets was up-regulated after 3-days in vitro culture. The up-regulation of mAChR mRNA was not affected by adding carbachol in culture medium, neither by culture islets in 2 mmol/l glucose.Conclusions. 1. The mAChR mRNA was up-regulated when pancreatic islets were isolated and kept in culture.The mechanism is not known, but seems to be related to the denervation states of islets, and not related to glucose concentration in the culture medium. 2. Persistent activation of mAChR by agonist carbachol decreased glucose-induced insulin secretion and diminished the potentiating efffect of acetylcholine.

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Factors influencing Islet of Langerhans graft function and monitoring

Pileggi

Ricordi

Alessiani

et al. 2001

Clinica Chimica Acta

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Diminished inhibitory effect of noradrenaline on insulin release from mouse islets transplanted to kidney

Cited by 11 publications

References 17 publications

Effects of UK-14,304, noradrenaline, and propranolol on insulin release from transplanted mouse islets

Effects of UK-14,304, noradrenaline, and propranolol on insulin release from transplanted mouse islets

Effect of carbachol on regulation of the mACh receptor mRNA expression ADN insulin secretion in mouse pancreatic islets

Factors influencing Islet of Langerhans graft function and monitoring

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