Role of adrenoceptors <i>in vitro</i> and <i>in vivo</i> in the effects of lithium on blood glucose levels and insulin secretion in the rat

Fontela, Tomás; Hermida, O. García; Gómez-Acebo, J.

doi:10.1111/j.1476-5381.1990.tb15796.x

Cited by 9 publications

(10 citation statements)

References 18 publications

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“…Glucose-stimulated insulin release is inhibited both in vivo and in vitro (Anderson & Blackard, 1978;Shah & Pishdad, 1980;Fontela et al, 1986;1987), and these effects appear to be mediated by central opiate and by neural and endocrine catecholamine pathways, the latter acting on the pancreatic P cell through its a2-adrenoceptors (Fontela et al, 1990; GarciaHermida et al, 1991). The aim of the present study was to investigate how this 'diabetogenic' effect of lithium in rats interacts with pre-existing diabetes mellitus, using streptozotocin-induced diabetes as the experimental model.…”

Section: Introduction Methodsmentioning

confidence: 99%

“…Male Wistar rats (160-220 g) were kept under standard conditions previously described (Fontela et al, 1990). Randomly chosen rats were injected i.p.…”

Section: Animalsmentioning

confidence: 99%

“…Animals were anaesthetized with pentobarbitone sodium, 60 mg kg-', i.p., and the previously described experimental protocol was followed (Fontela et al, 1990). Venous blood samples (0.5 ml) were collected before and at 5, 30, 60, 90 and thod.…”

Section: Experimental Protocolmentioning

confidence: 99%

“…On this response, lithium treatment superimposed a rise in glucagon of the same magnitude and time-course as that seen in the non-diabetic rats, reaching a maximum of 14pmollh' at 60min (P<0.02, n=8). (I) Activation of the sympatho-adrenal system rhis involves both neural and humoral catecholamine path-;vays, as shown by the partial reversal of the effects of ithium on plasma glucose and glucose-stimulated insulin ;ecretion by bilateral adrenalectomy (Fontela et al, 1986), -he elevation of plasma adrenaline and noradrenaline in res-?onse to lithium , and the reversal by idrenoceptor antagonists (specifically by the X2-selective antagonist, yohimbine) of the inhibitory effect of lithium on the ;econd phase of glucose-stimulated insulin secretion from solated islets (Fontela et al, 1987;1990). The rise in plasma :lucose may thus be attributed to the stimulatory effect of adrenaline and noradrenaline on glycogenolysis, combined Avith an inhibition of insulin secretion mediated by M2-adreioceptors of the pancreatic B cell.…”

Section: Effect Of Lithium On Plasma Glucagonmentioning

confidence: 99%

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Effect of lithium on plasma glucose, insulin and glucagon in normal and streptozotocin‐diabetic rats: role of glucagon in the hyperglycaemic response

Hermida

Fontela

Ghiglione

et al. 1994

British J Pharmacology

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1 Lithium salts, used in the treatment of affective disorders, may have adverse effects on glucose tolerance in man, and suppress glucose-stimulated insulin secretion in rats. 2 To study the interaction of these effects with pre-existing diabetes mellitus, plasma glucose and insulin responses to lithium chloride were measured in male Wistar rats made diabetic with intraperitoneal streptozotocin, and in normal controls. 3 In both normal and diabetic anaesthetized rats, intravenous lithium (4 mEq kg-') caused a rise in plasma glucose. In absolute terms, the rise was greater in diabetic (5.2 mmol l ) than in normal rats (2.3 mmol I`).4 Plasma insulin concentrations were reduced by lithium in normal rats, but the low insulin concentrations measured in the diabetic rats were not significantly changed. 5 After intravenous glucose (0.5 g kg-'), lithium-treated diabetic rats showed a second rise in plasma glucose at 60-90 min without any insulin response, while normal rats showed typically reduced insulin responses and initial glucose disappearance rates. 6 Intravenous glucose reduced plasma glucagon concentrations to a greater extent in normal than in diabetic rats, but lithium induced an equal rise in plasma glucagon in both groups, with a time-course similar to that of the hyperglycaemic effect. 7 The hyperglycaemic action of lithium is greater in the hypoinsulinaemic diabetic rats and appears to involve a stimulation of glucagon secretion in both normal and diabetic animals.

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Section: Introduction Methodsmentioning

confidence: 99%

“…Male Wistar rats (160-220 g) were kept under standard conditions previously described (Fontela et al, 1990). Randomly chosen rats were injected i.p.…”

Section: Animalsmentioning

confidence: 99%

Section: Experimental Protocolmentioning

confidence: 99%

Section: Effect Of Lithium On Plasma Glucagonmentioning

confidence: 99%

See 2 more Smart Citations

Effect of lithium on plasma glucose, insulin and glucagon in normal and streptozotocin‐diabetic rats: role of glucagon in the hyperglycaemic response

Hermida

Fontela

Ghiglione

et al. 1994

British J Pharmacology

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“…Correspondingly it has been shown that glucose-stimulated insulin release is inhibited by lithium, both in vivo and in vitro (Anderson & Blackard, 1978;Shah & Pishdad, 1980). These effects are blocked by pretreatment of rats with the non-selective a-adrenoceptor antagonist, dihydroergotamine (Fontela et al, 1986;1987) and the selective CX2-adrenoceptor antagonist, yohimbine (Fontela et al, 1990). It has therefore been suggested that this action of lithium is mediated via catecholaminergic stimulation, acting predominantly on the a2-adrenoceptors of the pancreatic I cell.…”

Section: Introductionmentioning

confidence: 99%

Effect of pertussis pretreatment on plasma glucose and insulin responses to lithium in rats

Hermida

Fontela

Ghiglione

et al. 1991

British J Pharmacology

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1 Administration of lithium to rats causes a rise in plasma glucose and suppresses glucose-stimulated insulin secretion. These effects are blocked by the X2-adrenoceptor antagonist, yohimbine. 2 Pretreatment of rats with Bordetella pertussis toxin resulted in a reversal of the usual plasma glucose and insulin responses to intravenously administered lithium (4 mEq kg-1). There was a slow fall in plasma glucose, while plasma insulin rose to 267 + 42% (±s.e.mean) of control values at 30 min. The effect of lithium on glucose-stimulated insulin secretion was also reversed; there was a marked increase in the insulin response which contrasted with the suppression seen in normal controls. 3 In perifused islets of Langerhans isolated from pertussis pretreated rats, the previously described inhibition by lithium of the second phase of glucose-stimulated insulin secretion from normal islets was almost completely abolished. 4 The results are consistent with the hypothesis that these effects of lithium are mediated by the influence of catecholamines on the islets. When the inhibitory effect of a2-adrenoceptors is abolished by pertussis treatment, which blocks the action of the inhibitory guanine nucleotide-binding protein G., effects of fl-adrenoceptor stimulation predominate, leading to an increased secretion of insulin.

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Lithium‐induced gene expression of inducible cyclic adenosine monophosphate early repressor in the rat adrenal gland

Spencer

Jahng

Ryu

et al. 2005

J of Neuroscience Research

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Lithium has acute and chronic effects on the hypothalamic-pituitary-adrenal gland (HPA) axis that are important for both therapeutic (e.g., treatment of mood disorders) and experimental (e.g., as the toxin in conditioned taste aversion studies) applications. We visualized lithium-induced activation of the HPA axis in rats by the adrenal expression of inducible cAMP early repressor (ICER), which is activated by elevated intracellular cAMP. We have shown that 1) intraperitoneal lithium chloride (LiCl) induces transient expression of ICER and c-fos mRNAs in the rat adrenal cortex and increases plasma level of corticosterone; 2) the cortical expression of ICER mRNA by LiCl occurs in a dose-dependent manner; 3) adrenal induction of ICER expression is delayed compared with c-fos expression; 4) dexamethasone pretreatment (4 mg/kg) blocks corticosterone release and adrenocortical ICER induction either by systemic LiCl (76 mg/kg) or by restraint stress; and 5) intracerebroventricular LiCl (127 microg/5 microl) is sufficient for adrenocortical, but not medullary, ICER induction. These results suggest that adrenocortical ICER expression could serve as a reliable marker for lithium-induced activation of the HPA axis. Understanding the activation of immediate-early genes such as c-fos or ICER in response to a single LiCl injection is an important first step in understanding the long-term changes in gene expression elicited by lithium that are involved in its therapeutic and toxic effect. The pattern and mechanism by which lithium stimulates ICER transcription in the adrenal gland would serve as a useful model system in future studies of lithium.

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Role of adrenoceptors in vitro and in vivo in the effects of lithium on blood glucose levels and insulin secretion in the rat

Cited by 9 publications

References 18 publications

Effect of lithium on plasma glucose, insulin and glucagon in normal and streptozotocin‐diabetic rats: role of glucagon in the hyperglycaemic response

Effect of lithium on plasma glucose, insulin and glucagon in normal and streptozotocin‐diabetic rats: role of glucagon in the hyperglycaemic response

Effect of pertussis pretreatment on plasma glucose and insulin responses to lithium in rats

Lithium‐induced gene expression of inducible cyclic adenosine monophosphate early repressor in the rat adrenal gland

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