Opioid antagonism alters blood glucose homeostasis during exercise in humans

Hickey, Matthew S.; Trappe, Susanne; Blostein, A. C.; Edwards, B. A.; Goodpaster, Bret H.; Craig, Bruce W.

doi:10.1152/jappl.1994.76.6.2452

Cited by 18 publications

(11 citation statements)

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“…In contrast, N infusion was reported to induce hyperglycemia at 90 min of exercise despite a signi®cant elevation of the level of plasma C-peptide (Hickey et al 1994). It is unclear why hyperglycemia occurred in this study.…”

Section: Introductioncontrasting

confidence: 69%

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Beta-endorphin infusion alters pancreatic hormone and glucose levels during exercise in rats

Fatouros

Goldfarb

Jamurtas

et al. 1997

European Journal of Applied Physiology

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beta-Endorphin (BE) infusion at rest can influence insulin and glucagon levels and thus may affect glucose availability during exercise. To clarify the effect of BE on levels of insulin, glucagon and glucose during exercise, 72 untrained male Sprague-Dawley rats were infused i.v. with either: (1) BE (bolus 0.05 mg.kg-1 + 0.05 mg.kg-1.h-1, n = 24); (2) naloxone (N, bolus 0.8 mg.kg-1 + 0.4 mg.kg-1, n = 24); or (3) volume-matched saline (S, n = 24). Six rats from each group were killed after 0, 60, 90 or 120 min of running at 22 m.min-1, at 0% gradient. BE infusion resulted in higher plasma glucose levels at 60 min [5.93 (0.32) mM] and 90 min [4,16 (0.29) mM] of exercise compared to S [4.62 (0.27) and 3.41 (0.26 mM] and N [4.97 (0.38) and 3.44 (0.25) mM]. Insulin levels decreased to a greater extent with BE [21.5 (0.9) and 18.3 (0.6) uIU.ml-1] at 60 and 90 min compared to S [24.5 (0.5) and 20.6 (0.6) uIU.ml-1] and N [24.5 (0.4) and 21.6 (0.7) uIU.ml-1] groups. Plasma C-peptide declined to a greater extent at 60 and 90 min of exercise with BE infusion compared to both S and N. BE infusion increased glucagon at all times during exercise compared to S and N. These data suggest that BE infusion during exercise influences plasma glucose by augmenting glucagon levels and attenuating insulin release.

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Section: Introductioncontrasting

confidence: 69%

“…The signi®cance of BE elevation during exercise remains unclear but BE has been implicated in the glucoregulatory response both at rest (Fatouros et al 1995;Feldman et al 1983;Giugliano et al 1987;Ipp et al 1978;Reid et al 1981) and during exercise (Hickey et al 1994).…”

Section: Introductionmentioning

confidence: 99%

Beta-endorphin infusion alters pancreatic hormone and glucose levels during exercise in rats

Fatouros

Goldfarb

Jamurtas

et al. 1997

European Journal of Applied Physiology

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“…Blockade of EA stimulation-induced increase of plasma insulin was also seen in rats receiving similar treatment with naloxone. Naloxone is often used as a tool in eliciting relations between b-endorphin and plasma glucose homeostasis [23,24]. In diabetic patients, b-endorphin stimulates insulin secretion [19].…”

Section: Discussionmentioning

confidence: 99%

An insulin-dependent hypoglycaemia induced by electroacupuncture at the Zhongwan (CV12) acupoint in diabetic rats

et al. 1999

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Diabetes mellitus ranks among the top ten causes of mortality throughout the world [1,2]. With the rapid advancement of medicine, treatments without side effect for the long-term control of this disorder becomes important. Alternative therapies have recently received attention. Physical exercise in the control of diabetes has been criticised because an increase in glucagon and adrenaline secretion could raise the plasma glucose [3]. Acupuncture has been used in traditional Chinese medicine to relieve symptoms of diabetes mellitus for many years [4].The Zhongwan acupoint is located on the abdominal wall associated with the pancreas [5]. This area contains muscle and adipose tissue, both of which are insulin sensitive tissues. Electroacupuncture (EA) is widely used in traditional Chinese medicine because it combines the effects achieved with traditional needle acupuncture with those of massage [4]. It causes a prolonged contraction of the abdominal muscle fibres and ATP expenditure in addition to an increase in blood circulation resulting in faster glu- Diabetologia (1999) Summary Acupuncture at the Zhongwan acupoint has been widely used in traditional Chinese medicine to relieve symptoms of diabetes mellitus. Our study investigated the effect on plasma glucose of electroacupuncture applied at the Zhongwan acupoint in rat diabetic models. Plasma concentrations of insulin, glucagon and b-endorphin were also determined using radioimmunoassay. A decrease in plasma glucose was observed in rats after electroacupuncture (15 Hz, 10 mA) for 30 min at the Zhongwan acupoint. This was observed in normal rats and rat models with Type II (non-insulin-dependent) diabetes mellitus. No significant effect on plasma glucose was observed in rat models with Type I (insulin-dependent) diabetes mellitus; neither the streptozotocin (STZ)-induced diabetic rats nor the genetic (BB/W) rats. Further, the hypoglycaemic action of electroacupuncture stimulation disappeared in rats with insulin-resistance induced by an injection of human long-acting insulin repeated daily to cause the loss of tolbutamide-induced hypoglycaemia. An insulin-related action can thus be hypothesised. This hypothesis is supported by an increase in plasma insulin-like immunoreactivity after electroacupuncture stimulation in normal rats. Participation of glucagon was ruled out because there was no change in plasma glucagonlike immunoreactivity resulting from electroacupuncture stimulation. In addition to an increase in plasma b-endorphin-like immunoreactivity, the plasma glucose lowering action of electroacupuncture stimulation at Zhongwan acupoint was abolished by naloxone in a sufficient dose to block opioid receptors. Thus we suggest that electroacupuncture stimulation at the Zhongwan acupoint induces secretion of endogenous b-endorphin which reduces plasma glucose concentration in an insulin-dependent manner. [Diabetologia (1999) 42: 250±255]

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“…Nevertheless, the first published work on the identification of endogenous opioids in the pancreas 22 gave rise to studies that focused on the ambiguous mechanisms involved in the endogenous opioid-mediated glucose and insulin homeostasis [23][24][25] . Green et al 24 first showed that morphine and met-enkephalin were able to stimulate glucose-induced insulin release in isolated pancreatic isles, an effect that was observed to develop rapidly, representing the first phase of pancreatic insulin release and which could be blocked by naloxone pre-treatment and therefore, showing an opioid-receptor mediated effect.…”

Section: Introductionmentioning

confidence: 99%

Opioid receptor-dependent modulation of insulin-release in pancreatic beta-cells

Paul¹,

Guven²,

Dietis

2014

PBJ

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In this study we aimed to look at the effects of opioid-receptor selective agonists and antagonists on insulin secretion in the pancreatic β-cell line RIN-5F. Cells were treated for 24 hours with 1μM of selective agonists (DAMGO for MOP, DPDPE for DOP, U50488 for KOP) in the presence or absence of 10μM of selective antagonists (CTOP for MOP, naltrindole for DOP, norBNI for KOP).An enzyme-based immunoassay was used to detect the amount of insulin in the supernatant, using a standard curve generated from known concentrations of rat insulin. A trypan blue viability assay was performed to assess the toxicity of each treatment and the secreted insulin was expressed as per 10 3 viable cells. Treatment with DAMGO or DPDPE caused an increase in secreted insulin by 94.2% and 76.3% respectively, compared to the non-treated controls. Cotreatment of DAMGO and CTOP was able to cancel out the agonists' effect. However, CTOP itself was able to increase insulin secretion by 72% when compared to control. These results suggest that opioid-induced insulin secretion may be based on G-protein independent mechanisms. In addition, none of the KOP-receptor selective ligands tested here were able to significantly affect insulin secretion compared to control, whereas naltrindole was highly toxic to pancreatic β-cells since it induced maximum cell death. Collectively, these findings suggest that MOP and DOP receptor-binding opioids might be more relevant in increasing insulin secretion from pancreatic β-cells than KOP receptor ligands.

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Opioid antagonism alters blood glucose homeostasis during exercise in humans

Cited by 18 publications

References 0 publications

Beta-endorphin infusion alters pancreatic hormone and glucose levels during exercise in rats

Beta-endorphin infusion alters pancreatic hormone and glucose levels during exercise in rats

An insulin-dependent hypoglycaemia induced by electroacupuncture at the Zhongwan (CV12) acupoint in diabetic rats

Opioid receptor-dependent modulation of insulin-release in pancreatic beta-cells

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