The effect of chronic prolactin administration upon the blood sugar, insulin and free fatty acid response to a glucose load in the dog

Renauld, A; Sverdlik, Rita C.; Andrade, L

doi:10.1007/bf02590715

Cited by 9 publications

(6 citation statements)

References 18 publications

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“…In hypophysectomized and adrenalectomized dogs or in partially depancreatized animals ovine PRL produced overt diabetes [13]. However, in arecent study Renauld et al [14] were not able to demonstrate any significant "anti-insulin" effects of chronic PRL administration in the normal dog. A similar finding was made in hypophysectomized rats treated with ovine PRL [15].…”

Section: Discussionmentioning

confidence: 94%

Prolactin: A diabetogenic hormone

Landgraf

Mm²,

Weißmann³

et al. 1977

Diabetologia

174

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Summary. During an oral glucose tolerance test (OGTT) glucose and insulin levels were measured in 26 patients with prolactin-producing pituitary tumours without growth hormone excess. Basal glucose and insulin levels did not differ from the values of an age-matched control group. After glucose load the hyperprolactinaemic patients showed a decrease in glucose tolerance and a hyperinsulinaemia. Bromocriptine (CB 154), which suppressed PRL, improved glucose tolerance and decreased insulin towards normal in a second OGTT. -Human PRL or CB 154 had no significant influence on insulin release due to glucose in the perfused rat pancreas. -These findings suggest a diabetogenic effect of PRL. CB 154 might be a useful drug in improving glucose utilization in hormone-active pituitary tumours.Key words: Prolactin, insulin release, glucose tolerance, pituitary tumours, pancreas perfusions, bromocriptine.Acute administration of ovine prolactin (PRL) has been shown to influence glucose metabolism in animals [1,2], to impair glucose tolerance in hypopituitary dwarfs and in hypophysectomized juvenile-type diabetics [3], and to stimulate lipid metabolism [4]. In order to study the long term effects of endogenous PRL on glucose tolerance and glucose-induced insulin secretion, patients with hyperprolactinaemia were investigated. In vitro experiments with the isolated perfused rat pancreas were undertaken to elucidate the direct effect of hPRL on insulin release. * Presented in part at the 11 th Annual Meeting of the European Association for the Study of Diabetes (EASD), Munich, September 4-6, 1975, and published in abstract form in Diabetologia 11, 357 (1975) Material aud Methods a. In vivo-StudyFifteen female and 11 male patients with hyperprolactinaemia were studied (Tab. 1). Twenty-four patients had a pituitary tumour, one had a craniopharyngioma and one had anormal sella turcica. A galactorrhoeaamenorrhoea syndrome was observed in 9 women.The average body weight was 13 ± 4 % above the ideal body weight and the average age was 34 ± 2 years (mean ± SEM). None of the patients had elevated plasma growth hormone concentrations. Eighteen patients had blunted hGH-secretion after insulin-induced hypoglycaemia. In six subjects TSH levels before and after TRH stimulation were below the lower limit of detection; six patients showed TSH values which were subnormal and two suffered from primary hypothyroidism. Thirteen had secondary hypogonadism, eleven had a latent or manifest secondary adrenal insufficiency and three had diabetes insipidus. The mean basal PRL level (x ± SEM) measured by radioimmunoassay [5] was 2422 ± 800 ng/ml ranging from 47 to 18 860 ng/ml. Our normal range for men is 8.5 to 25 ng/ml and for women up to 37.5 ng/ml. Fourteen patients were on appropriate hormone replacement therapy at the time of the study. Hypothyroidism was treated in all cases except two (Tab. 1) in order to avoid effects of low thyroid hormone levels on glucose tolerance.Fifteen patients (nine females and six males) were treated with bromocripti...

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Section: Discussionmentioning

confidence: 94%

Prolactin: A diabetogenic hormone

Landgraf

Mm²,

Weißmann³

et al. 1977

Diabetologia

174

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“…These findings are in line with the deep fall in the serum FFA during the IVGTT in the bitches "in season" shown here, thereby suggesting that the whole "season" is connected with a good lipogenic response to combined hyperglycemia/hyperinsulinemia. The impaired return of BS to base line and the intense rebound of FFA during the subsequent test period, both in line with a high basal serum FFA value, suggest the existence of an intense insulin antagonism and/or the participation of prolactin (Renauld, Sverdlik, Andrade and Rodriguez 1973). Nevertheless, these observations disagree with the lack of serum FFA response to insulin-induced hypoglycemia, which are certainly difficult to explain.…”

Section: Discussionmentioning

confidence: 95%

“…Progesterone was reported to increase the percentage of islets of Langerhans in rat pancreas, to promote the insulinemic response to hyperglycemia in this species without affecting their BS profile and to increase the cAMP content in the pancreatic beta cells (Bottiglioni and Flamigni 1963;Costrini and Kalkhoff 1971;Ashby, Shirling and Baird 1978). As for prolactin, it neither affects glucose tolerance nor modifies the insulin response to hyperglycemia in dogs, but it promotes lipogenesis during combined hyperglycemia/hyperinsulinemia actions (Renauld et al 1973). Nevertheless, it is difficult to select a particular hormones and/or mechanisms tightly depending upon them as responsible for the findings reported in this paper because their actions at physiological level is a still unsettled topic.…”

Section: Discussionmentioning

confidence: 99%

Serum Insulin, Free Fatty Acids and Blood Sugar during the Estrous Cycle of Dogs

Renauld¹,

Sverdlik²,

Agüero³

et al. 1982

Horm Metab Res

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Changes in blood sugar and both serum, immunoreactive insulin and free fatty acid responses to glucose-induced hyperglycemia and insulin-induced hypoglycemia in normal bitches over different phases of their spontaneous estrous cycles were studied. The phases were carfully checked through series of vaginal smears, taken over several months.The "sex seasons" did not affect both mean, basal blood sugar and serum immunoreactive insulin levels in these animals, while they increased their mean, basal circulating free fatty acids. Mean blood sugar during the intravenous glucose tolerance test was higher (34-37%) in the bitches "in season" than that in anestrous; no differences at every phase of the cycle were found. Mean glucose space was smaller (22%) in the former, and glucose "k" value was not affected by the season. Mean blood sugar during the insulin tolerance test in the bitches in anestrous, proestrous and estrous coincided, but it was slightly higher in those in metadiestrous. Mean serum immunoreactive insulin after exogenous insulin administration was similar in the bitches in anestrous (42 µU/ml) and proestrous (49 µU/ml), it significantly grew during estrous (81 µU/ml) and fell over metadiestrous (57 µU/ml), still above the anestrous value. Insulin space, 73% of body weight during anestrous, significantly fell just over estrous to 46%. Insulin "k" constants per group were not affected by the "season". Mean endogenous insulin response to hyperglycemia in bitches in anestrous was weak and nonsignificant; it was hardly more intense but significant at estrous and metadiestrous, and was the highest in those at proestrous. Therefore, the mean pancreatic insulin release was increased at proestrous and metadiestrous, but the hyperinsulinemia following glucose load over estrous was chiefly mediated by a reduction in the insulin space. The mean serum free fatty acid curve in the bitches at anestrous during the intravenous glucose tolerance test was definitely flat. while a mean intense initial fall and a mean following rebound in those "in season" was observed. During the insulin tolerance test, positively flat mean serum free fatty acid curves at the mean basal level in all groups were found.The present paper shows that "sex seasons" in bitches do develop several major alterations in the three parameters studied by us, which are obviously due to the activation of the hypothalamic-pituitary-ovarian axis whose metabolic, combined actions at physiological level still remain unknown. IntroductionFemale dogs' spontaneous ovulators under reflex control {Hafez 1970), show quite an unusually long sex cycle pattern among mammals. Their cycles, consisting of proestrous (P), estrous (E), by one week each, and metadiestrous (MD), 15 days-3 months are followed by prolonged periods of sex inactivity referred to as anestrous (A) {Christie, Bell, Horth and Palmer 1971). Although some observations in women {Curtis-Prior, NicolaBrewster, Temple, Ross and Field 1974; and many others) and in female rats (Bailey and Matty 1971) appear t...

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“…1 A). Eight patients did not fulfil the criteria of impaired glucose tolerance [11], whereas two patients (nos. 2 and 6) had slightly elevated blood glucose concentrations after 120 min (8.0mmol/1 and 8.2 mmol/1 respectively).…”

Section: Oral Glucose Tolerance and Intravenous Glucose Tolerance Testmentioning

confidence: 95%

“…In these studies, impaired glucose tolerance was noted in some but not all patients. By contrast, other investigators could not demonstrate a diabetogenic effect of prolactin either in man [7][8][9] or in animals [10,11]. Furthermore, the underlying mechanisms involved in prolactin-induced changes in insulin release and glucose homeostasis are unknown.…”

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confidence: 97%

Severe hyperprolactinaemia is associated with decreased insulin binding in vitro and insulin resistance in vivo

et al. 1985

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We studied insulin receptor binding and carbohydrate metabolism in 10patients with severe hyperprolactinaemia and compared the findings with those obtained in 20 healthy control subjects. Insulin binding to monocytes and erythrocytes was significantly decreased in the patients with an excess of prolactin. Scatchard analysis of binding data indicated that a decrease in the number of receptors rather than in receptor affinity seems to be the prevailing cause of lowered binding in hyperprolactinaemic patients. Furthermore, patients with severe hyperprolactinaemia demonstrated significantly elevated blood glucose levels following oral or intravenous glucose load despite having significantly increased insulin levels after glucose administration. The infusion of insulin induced a delayed hypoglycaemic effect and a decreased inhibition of endogenous insulin secretion, as indicated by the suppression of C-peptide in the hyperprolactinaemic patients. The present data indicate that severe hyperprolactinaemia is associated with an insulin-resistant state, which seems to be caused, at least in part, by a down-regulation of insulin receptors.

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The effect of chronic prolactin administration upon the blood sugar, insulin and free fatty acid response to a glucose load in the dog

Cited by 9 publications

References 18 publications

Prolactin: A diabetogenic hormone

Prolactin: A diabetogenic hormone

Serum Insulin, Free Fatty Acids and Blood Sugar during the Estrous Cycle of Dogs

Severe hyperprolactinaemia is associated with decreased insulin binding in vitro and insulin resistance in vivo

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