Effect of insulin deficiency on the rewarding properties of methamphetamine in streptozotocin-induced diabetic rats

Bayat, Amir‐Hossein; Haghparast, Abbas

doi:10.1016/j.pbb.2014.11.008

Cited by 10 publications

(6 citation statements)

References 56 publications

(75 reference statements)

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“…Radically, diabetes is a far-reaching pathophysiologic effect of ID [19,[21][22][23][24] , which may be caused by β-cells in the pancreas islet that do not produce enough insulin or cells of the body that do not correctly respond to secreted insulin [2,19,20] . In addition to the hypoglycemic effect, insulin has multiple effects on metabolism and cell growth.…”

Section: Igf-1r Blockade On Renal Function In Diabetic Ratsmentioning

confidence: 99%

Insulin deficiency induces rat renal mesangial cell dysfunction via activation of IGF-1/IGF-1R pathway

Kong

Shen

et al. 2016

Acta Pharmacol Sin

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Aim: Diabetic nephropathy is one of the major complications of diabetes and the major cause of end-stage renal disease. In this study we investigated the insulin deficiency (ID) induced changes in renal mesangial cells (MCs) and in the kidney of STZ-induced diabetic rats. Methods: Cultured rat renal MCs were incubated in ID media. Cell proliferation was analyzed using BrdU incorporation assay. The expression of insulin receptor (IR), insulin-like growth factor-1 receptor (IGF-1R), phosphorylated IGF-1R, fibronectin, and collagen IV was determined with Western blot analysis. STZ-induced diabetic rats were treated with an IGF-1R antagonist picropodophyllin (PPP, 20 mg·kg -1 ·d -1, po) for 8 weeks. After the rats were euthanized, plasma and kidneys were collected. IGF-1 levels in renal cortex were measured with RT-PCR or ELISA. The morphological changes in the kidneys were also examined. Results: Incubation in ID media significantly increased cell proliferation, the synthesis of fibronectin and collagen IV, and the expression of IGF-1 and IGF-1R and phosphorylated IGF-1R in renal MCs. Pretreatment of the cells with PPP (50 nmol/L) blocked ID-induced increases in cell proliferation and the synthesis of fibronectin and collagen IV; knockdown of IGF-1R showed a similar effect as PPP did. In contrast, treatment of the cells with IGF-1 (50 ng/mL) exacerbated ID-induced increases in cell proliferation. In the kidneys of diabetic rats, the expression of IGF-1, IGF-1R and phosphorylated IGF-1R were significantly elevated. Treatment of diabetic rats with PPP did not lower the blood glucose levels, but significantly suppressed the expression of TGF-β, fibronectin and collagen IV in the kidneys, the plasma levels of urinary nitrogen and creatinine, and the urinary protein excretion. Conclusion: Insulin deficiency increases the expression of IGF-1 and IGF-1R in renal MCs and the kidney of diabetic rats, which contributes to the development of diabetic nephropathy.

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Section: Igf-1r Blockade On Renal Function In Diabetic Ratsmentioning

confidence: 99%

Insulin deficiency induces rat renal mesangial cell dysfunction via activation of IGF-1/IGF-1R pathway

Kong

Shen

et al. 2016

Acta Pharmacol Sin

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“…Note that all methods described in this part were based on our prior studies (Bayat, Haghparast, 2015;Fatahi, Zibaii, Haghparast, 2017;Samandari et al, 2013).…”

Section: Methodsmentioning

confidence: 99%

“…On the other hand, chronic hyperglycemia in diabetes leads to long-term damage and malfunction of different organs especially the CNS (American-Diabetes-Association, 2014; Baluchnejadmojarad, Roghani, 2011). Hence, insulin cooperates in the regulation of neuronal function, especially in reward circuits (Bayat, Haghparast, 2015;Bruijnzeel et al, 2011;Davis, Choi, Benoit, 2010;Daws et al, 2011;O'Dell, Nazarian, 2016;Plum, Schubert, Brüning, 2005). Nevertheless, the concise role of these signals on the cerebral reward circuits still not well understood.…”

Section: Insulin Replacement Prevents the Acquisition But Not The Exp...mentioning

confidence: 99%

Insulin replacement prevents the acquisition but not the expression of morphine-induced conditioned place preference in streptozotocin-induced diabetic rats

Hassanpour

Chizari

Bayat

et al. 2022

Braz. J. Pharm. Sci.

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Insulin receptors have distributed in all brain regions, including the nucleus Accumbens (NAc), and where is implicated in the reward properties of drugs. It is well known that insulin signaling can regulate dopamine release. Therefore, in the present study, we tried to examine the effect of insulin replacement on the acquisition and expression of morphine-induced conditioned place preference (CPP) in diabetic rats. Forty-eight male Wistar rats were divided into two non-diabetic (Naïve) and diabetic groups rendered by a single injection of streptozotocin (STZ). These groups separately received insulin (10U/kg) or saline (1 ml/kg) one hour prior to morphine administration (5mg/kg;s.c.) during conditioning days (acquisition phase) or postconditioning day (expression phase) in the CPP paradigm. In this paradigm, conditioning score (CS) and locomotion activity were recorded by Ethovision. The STZ-induced diabetic rats displayed higher CS compared to naïve rats (P<0.05). This effect was abolished in all diabetic rats that received insulin during conditioning days but not the expression phase. This study has provided evidence that insulin plays a modulatory role in morphine-induced CPP, and insulin replacement during the acquisition phase could reduce the rewarding properties of morphine in diabetes conditions through a possible modulating effect on dopamine release in the NAc region.

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“…Only rats with blood glucose levels higher than 250 mg/dL were subjected to continuing the study as diabetic rats. Experimental diabetes also was determined by changing the behavior of animals through polyphagia, polydipsia, polyuria, and weight loss ( Bayat & Haghparast, 2015 ; Sadeghimahalli, Khaleghzadeh-Ahangar, & Baluchnejadmojarad, 2019 ).…”

Section: Methodsmentioning

confidence: 99%

“…STZ enters the pancreatic B cells via a glucose transporter (GLUT2) and causes alkylation of DNA which leads to DNA damage. As a result of the STZ action, pancreatic beta cells are destroyed ( Bayat & Haghparast, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Insulin Within the Arcuate Nucleus Has Paradoxical Effects on Nociception in Healthy and Diabetic Rats

Khaleghzadeh‐Ahangar

Sadeghimahalli

Khandan

et al. 2020

BCN

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Introduction: Broad neural circuits originate from the hypothalamic arcuate nucleus and project to many parts of the brain which are related to pain perception. Insulin receptors are found in the arcuate nucleus. Since nociception may be affected in type 1 diabetes, the present study aimed to investigate the intra-arcuate nucleus insulin role in pain perception in streptozotocin (STZ)-induced diabetic and healthy rats. Methods: Regular insulin was microinjected within the arcuate nucleus and the pain tolerance was measured using the hot plate and the tail-flick apparatus in diabetic rats. Results: The results showed that the arcuate nucleus suppression with lidocaine could increase thermal nociception in non-diabetic animals. Also, insulin within the arcuate nucleus decreased the acute thermal pain perception in these animals. STZ-induced diabetes produced hypoalgesia which the latency of these tests, progressively increased over time after induction of diabetes. Also, in the same animal group, intra-arcuate injection of insulin reduced the latency of nociception. Conclusion: Intra-arcuate insulin has paradoxical and controversial effects in healthy and diabetic rats’ nociception. These effects seem to be due to the insulin effect on releasing pro-opiomelanocortin and its deriv

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Effect of insulin deficiency on the rewarding properties of methamphetamine in streptozotocin-induced diabetic rats

Cited by 10 publications

References 56 publications

Insulin deficiency induces rat renal mesangial cell dysfunction via activation of IGF-1/IGF-1R pathway

Insulin deficiency induces rat renal mesangial cell dysfunction via activation of IGF-1/IGF-1R pathway

Insulin replacement prevents the acquisition but not the expression of morphine-induced conditioned place preference in streptozotocin-induced diabetic rats

Insulin Within the Arcuate Nucleus Has Paradoxical Effects on Nociception in Healthy and Diabetic Rats

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