Centrally mediated drug-induced hyperglycemia in mice

Wannarka, Gerald L.; Fletcher, H. Patrick; Maickel, Roger P.

doi:10.1016/0028-3908(83)90250-2

Cited by 12 publications

(4 citation statements)

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“…Total ginsenosides have also been shown to modulate nitric oxide synthesis, the enhancement of which has been linked to ginseng' s effects (38). The former 3 systems affect glucose metabolism in vivo (39), and nitric oxide has been noticed to increase insulin-stimulated glucose uptake in rat skeletal muscles and adipose tissue (40) and to stimulate glucose-dependent secretion of insulin in rat islet cells (41). It is therefore possible that these ginsenosides contributed to the postprandial hypoglycemic effects we observed.…”

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confidence: 80%

Similar postprandial glycemic reductions with escalation of dose and administration time of American ginseng in type 2 diabetes.

et al. 2000

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OBJECTIVE -We previously demonstrated that 3 g American ginseng (AG) reduced postprandial glycemia (PPG) in type 2 diabetic individuals. We investigated whether further reductions can be achieved with escalation of dose and time of AG administration.RESEARCH DESIGN AND METHODS -Ten type 2 diabetic patients (6 men, 4 women; age 63 ± 2 years; BMI 27.7 ± 1.5 kg/m 2 ; HbA 1c 7.3 ± 0.3%) were randomly administered 0 g (placebo) or 3, 6, or 9 g ground AG root in capsules at 120, 80, 40, or 0 min before a 25-g oral glucose challenge. Capillary blood glucose was measured before ingestion of AG or placebo and at 0, 15, 30, 45, 60, 90, and 120 min from the start of the glucose challenge.RESULTS -Two-way analysis of variance (ANOVA) demonstrated that treatment (0, 3, 6, and 9 g AG) but not time of administration (120, 80, 40, or 0 min before the challenge) significantly affected PPG (P Ͻ 0.05), with significant (P = 0.037) interaction for area under the curve (AUC). Pairwise comparisons showed that compared with 0 g (placebo), 3, 6, or 9 g significantly (P Ͻ 0.05) reduced AUC (19.7, 15.3, and 15.9%, respectively) and incremental glycemia at 30 min (16.3, 18.4, and 18.4%, respectively), 45 min (12.5, 14.3, and 14.3%, respectively), and 120 min (59.1, 40.9, and 45.5%, respectively). However, pairwise comparisons showed no differences between the 3-, 6-, or 9-g doses and any of the times of administration.CONCLUSIONS -AG reduced PPG irrespective of dose and time of administration. No more than 3 g AG was required at any time in relation to the challenge to achieve reductions. Because these reductions included glycemia at the 2-h diagnostic end point, there may be implications for diabetes diagnosis and treatment.

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confidence: 80%

Interleukin-1 effect on glycemia in the non-obese diabetic mouse at the pre-diabetic stage

Amrani

Jafarian-Tehrani²,

Mormède³

et al. 1996

Journal of Endocrinology

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Cytokines, particularly interleukin 1 (IL-1) and tumor necrosis factor, are known to induce hypoglycemia in normal rodents or different experimental models of type II diabetes. We investigated, at the pre-diabetic stage, the effect of short-term administration of murine recombinant interleukin-1 alpha (mrIL-1 alpha) on the levels of glucose, insulin and corticosterone in the non-obese diabetic (NOD) mouse, a spontaneous model of type I diabetes. Two-month-old, pre-diabetic NOD mice of both sexes were insensitive to mrIL-1 alpha (12.5 and 50 micrograms/kg) 2 h after administration, the time at which the maximal decrease (around 50%) was observed in the C57BL/6 mouse strain. Kinetic studies however showed that mrIL-1 alpha lowered glycemia in both sexes of NOD mice, but the effect was limited and delayed. In the NOD and C57BL/6 strains, mrIL-1 alpha had no influence on insulin levels in females, but significantly increased them in males (P < 0.0001). Castration of NOD males abrogated the stimulatory effect of mrIL-1 alpha on insulin secretion. Corticosterone secretion was stimulated by mrIL-1 alpha in both sexes of NOD and C57BL/6 mice, and this effect was faster and greater in NOD females than in C57BL/6 females. The incomplete hypoglycemic response to mrIL-1 alpha in females may be attributed to the anti-insulin effect of glucocorticoids, an effect which can be demonstrated when mrIL-1 alpha is administered to adrenalectomized animals or when mrIL-1 alpha is administered together with the glucocorticoid antagonist RU38486. In NOD males, in contrast, glucocorticoids did not play a major role in the limited hypoglycemic response to mrIL-1 alpha, since RU38486 and adrenalectomy were not able to unmask a hypoglycemic effect. Moreover, NOD mice of both sexes were less sensitive than C57BL/6 mice to the hypoglycemic effect of insulin (2.5 U/kg), which suggests some degree of insulin-resistance in NOD mice. With regard to the effect of IL-1 on NOD mouse glycemia, therefore, these results suggest that glucocorticoids and/or androgens, according to the animal's sex, may induce a state of insulin-resistance.

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“…In future studies, we think that a method must be developed to reduce the burden of the oral glucose tolerance test. A variety of factors, including blockage of dopaminergic inhibitory neurons, increased adrenal medullary activity, and peripheral inhibitory actions on glucose utilization by tissues are being proposed for the mechanisms of antipsychotics concerning inhibition of blood glucose metabolism (Wannarka et al, 1983). If sympathetic neurons are stimulated or catecholamine is increased, insulin secretion reduces, and studies show that this inhibition of insulin secretion is mediated through 2 receptors (Steinberg, 1990;Van Kammen and Marder, 1995).…”

Section: Discussionmentioning

confidence: 96%

The effect of clozapine on blood glucose metabolism

Chae

Kang

2001

Human Psychopharmacology

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The aim of this prospective study was to examine the effect of clozapine on blood glucose metabolism compared with haloperidol. Oral glucose tolerance tests were taken every week for 8 weeks to assess the prevalence of diabetes mellitus, impaired glucose tolerance and glycemic peak delay in 19 patients of the clozapine group compared with 15 patients of the haloperidol group. There were two dropouts in the clozapine group and five in the haloperidol group. Finally 17 patients in the clozapine group and 10 patients in the haloperidol group participated in this study. In the clozapine group, six patients (35%) had impaired glucose tolerance, and seven patients (41%) had glycemic peak delay. In the haloperidol group, no patient (0%) had impaired glucose tolerance, and one patient (10%) had glycemic peak delay. None of either group developed diabetes mellitus. In conclusion, the clozapine group had more impaired glucose tolerance and glycemic peak delay than the haloperidol group. However, this difference did not achieve statistical significance (p = 0.056, p = 0.189). Copyright 2001 John Wiley & Sons, Ltd.

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Centrally mediated drug-induced hyperglycemia in mice

Cited by 12 publications

References 11 publications

Similar postprandial glycemic reductions with escalation of dose and administration time of American ginseng in type 2 diabetes.

Similar postprandial glycemic reductions with escalation of dose and administration time of American ginseng in type 2 diabetes.

Interleukin-1 effect on glycemia in the non-obese diabetic mouse at the pre-diabetic stage

The effect of clozapine on blood glucose metabolism

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