Lithium effect on plasma glucagon, liver phosphorylase-a and liver glycogen in rats

Mellerup, Erling T.; Thomsen, Hans; Plenge, Per; Rafaelsen, Ole J.

doi:10.1016/0022-3956(70)90014-2

Cited by 19 publications

(6 citation statements)

References 13 publications

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“…The present study confirms previously findings that, in the intact rat, lithium administration in¬ duces a rise in blood glucose during the first hour after injection (Bhattacharya 1964;Mellerup et al 1970;Plenge et al 1970). In contrast to our ob¬ servations, Shah & Pishdad (1980) found no effect of lithium on the basal serum level of glucose.…”

Section: Discussionsupporting

confidence: 93%

Blocking effect of naloxone, dihydroergotamine and adrenalectomy in lithium-induced hyperglycaemia and glucose intolerance in the rat

Fontela¹,

Hermida²,

Gómez-Acebo³

1986

Acta Endocrinologica

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The direct effect of lithium administration on plasma glucose levels and glucose-induced insulin release, and the role of opioid and amine systems in these effects were examined in rats. Naloxone, an opiate antagonist, and dihydroergotamine, an alpha-adrenergic blocking agent, reversed the hyperglycaemia as well as the inhibition of glucose-stimulated insulin release induced by lithium. In adrenalectomized rats, administration of lithium induced hypoglycaemia and not hyperglycaemia as in the intact rats. The results suggest that the interaction of secreted endorphins with the sympathetic nervous system is the likely cause of the hyperglycaemia and the inhibition of the glucose-stimulated insulin release induced by lithium.

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Section: Discussionsupporting

confidence: 93%

Blocking effect of naloxone, dihydroergotamine and adrenalectomy in lithium-induced hyperglycaemia and glucose intolerance in the rat

Fontela¹,

Hermida²,

Gómez-Acebo³

1986

Acta Endocrinologica

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“…The effect of lithium relevant to the present study is the induction of marked hyperglycaemia with inappropriately low plasma IRI levels and impaired glucose tolerance (Bhattacharya, 1964;Plenge et al, 1970;Mellerup et al, 1970;Fontela et al, 1986). In addition, lithium impairs IRI secretion in vitro, glucose-induced IRI being partially inhibited by lithium (Anderson & Blackard, 1978;Fontela et al, 1987).…”

Section: Discussionmentioning

confidence: 92%

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

Fontela

Hermida

Gómez-Acebo

1990

British J Pharmacology

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1 Pretreatment of rats with the non-selective a-adrenoceptor antagonist dihydroergotamine counteracts the inhibition of glucose-induced insulin secretion caused by lithium both in vitro and in vivo. The present study was therefore carried out to specify further which type of adrenoceptor is involved in lithiuminduced hyperglycaemia and inhibition of insulin secretion. 2 The lithium-induced effects were reversibly blocked by pretreatment of rats with the a2-adrenoceptor antagonist yohimbine or a combination of yohimbine and the non-selectivefl-receptor antagonist propranolol, whereas the a,-receptor antagonist prazosin and propranolol alone were ineffective in blocking these effects. 3 These findings suggest that the effects of lithium on plasma glucose and insulin levels are mediated mainly by the stimulation of a2-adrenoceptors.

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“…The existence of a glucagon response to lithium, previously suggested by Mellerup et al (1970), has, as far as we know, not hitherto been substantiated by more recent work. In the present state of knowledge, it may be regarded as a consequence of activation of the sympatho-adrenal system.…”

Section: Effect Of Lithium On Plasma Glucagonmentioning

confidence: 84%

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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Lithium effect on plasma glucagon, liver phosphorylase-a and liver glycogen in rats

Cited by 19 publications

References 13 publications

Blocking effect of naloxone, dihydroergotamine and adrenalectomy in lithium-induced hyperglycaemia and glucose intolerance in the rat

Blocking effect of naloxone, dihydroergotamine and adrenalectomy in lithium-induced hyperglycaemia and glucose intolerance in the rat

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

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

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