Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of oral bromocriptine in acromegaly have been studied. A dose of 5 mg six-hourly suppressed circulating growth hormone (GH) levels in nine out of 11 patients treated for seven to 11 weeks. This was associated with considerable clinical improvement in all patients, with abolition of excessive sweating, reduction in soft-tissue thichening, loosening of rings, decrease in shoe size, improvement in facial features, and loosening of dentures. Metabolic changes included improvement in glucose tolerance and reduction in hydroxyproline excretion. Unlike the actions of growth hormone release inhibiting hormone the suppression of GH was not accompanied by a reduction in insulin or glucagon secretion, though prolactin levels were suppressed. Side effects other than mild constipation were not seen when the full dose regimen was reached by slowly increasing the dose from 2-5 mg once daily. Bromocriptine holds promise as a safe and orally effective medical treatment to augment surgical or radiotherapeutic measures directed at the pituitary tumour. Its efficacy during longterm administration remains to be established.
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PMID:Bromocriptine treatment of acromegaly. 111 90

Plasma levels of prolactin, growth hormone, glucagon insulin and glucose were measured in non-treated control rats, bromocriptine-treated control rats and GH3-cell-tumor-bearing rats with and without bromocriptine treatment. Bromocriptine treatment increased plasma levels of glucagon, insulin and glucose in control rats. Tumor-bearing rats had increased body weight and increased plasma levels of prolactin, growth hormone, glucagon, insulin and glucose. Bromocriptine treatment reduced body weight and decreased the plasma levels of prolactin, glucagon and insulin, as compared to non-treated tumor-bearing rats. The drug had no effect on plasma levels of growth hormone and glucose. These results indicate that, in GH3-cell-tumor-bearing rats, prolactin, glucagon and insulin are more sensitive to the action of bromocriptine than growth hormone.
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PMID:Effects of hypersecretion of growth hormone and prolactin on plasma levels of glucagon and insulin in GH3-cell-tumor-bearing rats, and the influence of bromocriptine treatment. 352 70

A 31-year old female presented with recurrent episodes of post-prandial hypoglycaemic symptoms. Basal serum levels of ACTH, cortisol, GH, insulin and glucagon were normal. An adrenaline test demonstrated a normal peripheral response. An exercise test failed to produce ACTH, cortisol or FFA responses. Insulin (0.1 u/kg)-induced-hypoglycaemia failed to elevate serum ACTH, cortisol or GH. Metyrapone and ACTH tests were normal, demonstrating adequate hypophyseal and adrenal function. These findings suggested that the patient suffered from hypothalamic dysfunction. Bromocriptine (Parlodel, 7.5 mg/d for 5 weeks) resulted in an improved general condition, accompanied by a decrease in sugar consumption. Following treatment, FFA, ACTH and cortisol responses to exercise test were normal, as were ACTH, cortisol and GH responses to insulin-induced hypoglycaemia. It is concluded that bromocriptine may be useful in the treatment of post-prandial hypoglycaemic symptoms associated with hypothalamic dysfunction.
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PMID:Correction by bromocriptine of hypothalamic dysfunction and post-prandial hypoglycaemic symptoms in a 31-year-old woman. 662

Blood glucose, plasma GH, insulin and glucagon levels during oral glucose tolerance test before and after treatment with bromocriptine (5-20 mg daily for 2-9 months) were investigated in eleven acromegalic patients with glucose intolerance. Nine out of 11 patients showed improvement or normalization in glucose tolerance after bromocriptine therapy. Basal levels of plasma GH were markedly decreased in 7 of 11 patients treated, although the improved glucose tolerance was not always associated with a drop of basal plasma GH levels. In contrast, basal plasma glucagon level showed a distinct fall in all the patients whose glucose tolerance was improved, but unchanged in whom glucose tolerance was not ameliorated. The mean values of plasma GH and glucagon after oral glucose load were significantly lower during bromocriptine therapy than those before the treatment, respectively. Basal levels of plasma insulin and its response to glucose load did not change after bromocriptine treatment. Bromocriptine thus appears to be a good alternative in the treatment of glucose intolerance in acromegalic patients and the improvement of glucose tolerance by bromocriptine may be related to the reduction in plasma glucagon levels. The possibility, however, is not excluded that a decrease by bromocriptine in the total daily GH secretion is a cause of the improved glucose tolerance.
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PMID:Effect of long term bromocriptine treatment on glucose intolerance in acromegaly. 704 Jan 91

The effects of bromocriptine (10 mg/kg), known to inhibit prolactin secretion and lower autoimmune processes, were studied on glucose homeostasis in non-fasted non-obese diabetic mice, a spontaneous model of type 1 diabetes. Hyperglycemia was observed 120 and 240 min after i.p. but not s.c. injection. Bromocriptine administration i.p. led to rapid and marked hyperglycemia characterized by sexual dimorphism with males having higher glycemia than females. Bromocriptine induced a rapid but transient decrease in insulinemia in males only and biphasic increases in glucagon levels and a sustained stimulatory effect on circulating corticosterone in both sexes. Bromocriptine-induced hyperglycemia involved D2-dopaminergic receptors, as demonstrated by the inhibitory effect of the D2-dopamine antagonist, metoclopramide (10 mg/kg). Simultaneous injection of bromocriptine and metoclopramide also blocked the rise in blood corticosterone. In conclusion, by inducing hyperglycemia, i.p. bromocriptine administration to prediabetic autoimmune mice may counteract its beneficial anti-immunostimulatory effects.
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PMID:Bromocriptine-induced hyperglycemia in nonobese diabetic mice: kinetics and mechanisms of action. 1808 76