Plasma beta-endorphin levels and glucose tolerance in patients with chronic renal failure

Barreca, T; Robaudo, Cristina; Cataldi, A.; Garibaldi, A; Cianciosi, P; Russo, Rodolfo; Rolandi, E; Franceschini, R.

doi:10.1016/0753-3322(96)82644-8

Cited by 4 publications

(3 citation statements)

References 25 publications

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“…The possibility that this hyperendorphinism might have a biologic importance at least as a contributory factor of impaired glucose tolerance in uremia might be suggested. 11 Beta-endorphin and other opioid peptides participate significantly in the development of uremic syndrome and its complications. On the other hand, hemodialysis treatment is an important factor influencing the concentration of most hormones.…”

Section: Effects Of Opioids On Renal Function In Pathological Statesmentioning

confidence: 99%

Opioids and renal function

Mercadante¹,

Arcuri²

2004

The Journal of Pain

128

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Section: Effects Of Opioids On Renal Function In Pathological Statesmentioning

confidence: 99%

Opioids and renal function

Mercadante¹,

Arcuri²

2004

The Journal of Pain

128

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“…Furthermore, β-endorphin also stimulates glucose uptake by the muscle and the sensitivity to β-endorphin is higher in contracted than non-contracted muscles [ 78 ]. Unlike hypoglycaemia, a rise in blood glucose levels (such as during an glucose tolerance test) did not increase plasma β-endorphin in most studies [ 112 – 116 ], or only mildly in some studies [ 117 – 119 ]. Thus, it appears that endogenous opioids are primarily released when there is an increased need for available glucose, such as during insulin-induced hypoglycaemia or during exercise, which is in line with the hyperglycaemic effects of opioid stimulation.…”

Section: Endogenous Opioid Release In Response To Changes In Glycaemiamentioning

confidence: 99%

The Clash of Two Epidemics: the Relationship Between Opioids and Glucose Metabolism

et al. 2022

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Purpose of Review We are currently in the midst of a global opioid epidemic. Opioids affect many physiological processes, but one side effect that is not often taken into consideration is the opioid-induced alteration in blood glucose levels. Recent Findings This review shows that the vast majority of studies report that opioid stimulation increases blood glucose levels. In addition, plasma levels of the endogenous opioid β-endorphin rise in response to low blood glucose. In contrast, in hyperglycaemic baseline conditions such as in patients with type 2 diabetes mellitus (T2DM), opioid stimulation lowers blood glucose levels. Furthermore, obesity itself alters sensitivity to opioids, changes opioid receptor expression and increases plasma β-endorphin levels. Summary Thus, opioid stimulation can have various side effects on glycaemia that should be taken into consideration upon prescribing opioid-based medication, and more research is needed to unravel the interaction between obesity, glycaemia and opioid use.

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“…β endorphin and other opioid peptides have been reported to participate in the development of uremic syndrome and its complications [10]. Furthermore, the elevated β endorphin levels in patients with chronic renal failure have also been documented [11]. Opioid exposure leads to both physiological and architectural renal changes [12].…”

Section: Introductionmentioning

confidence: 99%

Investigating the role of endogenous opioids and K_ATP channels in glycerol‐induced acute renal failure

Sauriyal

Jaggi

Singh³

et al. 2011

Fundamemntal Clinical Pharma

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The present study was designed to investigate the possible role of endogenous opioids and K(ATP) channels in glycerol-induced acute renal failure (ARF) in rats. The rats were subjected to rhabdomyolytic ARF by single intramuscular injection of hypertonic glycerol (50% v/v; 8 mL/kg), and the animals were sacrificed after 24 h of glycerol injection. The plasma creatinine, blood urea nitrogen, creatinine clearance, and histopathological studies were performed to assess the degree of renal injury. Naltrexone (2.5, 5.0 and 10.0 mg/kg s.c.), glibenclamide (5.0 and 10.0 mg/kg i.p.), and minoxidil (25 and 50 mg/kg) were employed to explore the role of endogenous opioids and K(ATP) channels in rhabdomyolysis-induced ARF. Pretreatment with naltrexone and glibenclamide attenuated hypertonic glycerol-induced renal dysfunction in a dose-dependent manner, suggesting the role of endogenous opioids and K(ATP) channels in the pathogenesis of myoglobuniric renal failure. However, the simultaneous pretreatment with naltrexone (10 mg/kg s.c.) and glibenclamide (10 mg/kg i.p.) did not enhance the reno-protective effects of individual drugs, suggesting that release of endogenous opioids and opening of K(ATP) channels constitute a single pathway in acute renal injury triggered by hypertonic glycerol-induced rhabdomyolysis. Furthermore, administration of minoxidil abolished the attenuating effects of naltrexone in glycerol-induced renal failure, suggesting that opening of K(ATP) channels is downstream to opioid receptor activation. It is concluded that hypertonic glycerol-induced rhabdomyolysis may involve release of endogenous opioids that in turn modulate K(ATP) channels to contribute in the pathogenesis of ARF.

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Plasma beta-endorphin levels and glucose tolerance in patients with chronic renal failure

Cited by 4 publications

References 25 publications

Opioids and renal function

Opioids and renal function

The Clash of Two Epidemics: the Relationship Between Opioids and Glucose Metabolism

Investigating the role of endogenous opioids and K_ATP channels in glycerol‐induced acute renal failure

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Plasma beta-endorphin levels and glucose tolerance in patients with chronic renal failure

Cited by 4 publications

References 25 publications

Opioids and renal function

Opioids and renal function

The Clash of Two Epidemics: the Relationship Between Opioids and Glucose Metabolism

Investigating the role of endogenous opioids and KATP channels in glycerol‐induced acute renal failure

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Product

Resources

About

Investigating the role of endogenous opioids and K_ATP channels in glycerol‐induced acute renal failure