Testosterone promotes glucose intolerance, lipid disorder and oxidative stress in type 1 diabetic rats

Morakinyo, Ayodele Olufemi; Adekunbi, Daniel; Dada, Kayode; Adegoke, OA

doi:10.1515/jbcpp-2012-0072

Cited by 11 publications

(6 citation statements)

References 12 publications

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“…In addition, DM has been reported to lead to a decrease in enzymatic antioxidants, such as superoxide dismutase (SOD), glutathione peroxidase, and glutathione reductase, and non‐enzymatic antioxidants, such as glutathione, vitamins C and E, and total antioxidant capacity 10 . The present results showing that alloxan‐induced type 1 DM leads to an increase in serum TOS and OSI levels and a decrease in TAS level support the results of previous animal studies 35 , 36 …”

Section: Discussionsupporting

confidence: 90%

Effects of Melatonin on Oxidative Stress Index and Alveolar Bone Loss in Diabetic Rats With Periodontitis

Köse

Arabacı

Kara

et al. 2016

Journal of Periodontology

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Section: Discussionsupporting

confidence: 90%

Effects of Melatonin on Oxidative Stress Index and Alveolar Bone Loss in Diabetic Rats With Periodontitis

Köse

Arabacı

Kara

et al. 2016

Journal of Periodontology

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“…), but testosterone also evokes oxidative stress, depending on the conditions (Morakinyo et al . ; Victor et al . ).…”

mentioning

confidence: 99%

“…Furthermore, testosterone is converted into estradiol, a potent form of estrogen, by aromatase in brain tissues (Michael et al 1986). Some experimental studies have described antioxidant effects for testosterone in the brain under pathogenic conditions (Chisu et al 2006;Fanaei et al 2014), but testosterone also evokes oxidative stress, depending on the conditions (Morakinyo et al 2014;Victor et al 2014). Unlike estrogen, however, testosterone has not yet been well characterized in terms of how it affects the brain, especially under psychological stress.…”

mentioning

confidence: 99%

Testosterone depletion increases the susceptibility of brain tissue to oxidative damage in a restraint stress mouse model

Son

Lee

Kim

et al. 2015

Journal of Neurochemistry

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Among sex hormones, estrogen is particularly well known to act as neuroprotective agent. Unlike estrogen, testosterone has not been well investigated in regard to its effects on the brain, especially under psychological stress. To investigate the role of testosterone in oxidative brain injuries under psychological stress, we adapted an orchiectomy and restraint stress model. BALB/c mice were subjected to either an orchiectomy or sham operation. After allowing 15 days for recovery, mice were re-divided into four groups according to exposure of restraint stress: sham, sham plus stress, orchiectomy, and orchiectomy plus stress. Serum testosterone was undetectable in orchiectomized groups and restraint-induced stress significantly reduced testosterone levels in sham plus stress group. The serum levels of corticosterone and adrenaline were notably elevated by restraint stress, and these elevated hormones were markedly augmented by orchiectomy. Two oxidative stressors and biomarkers for lipid and protein peroxidation were significantly increased in the cerebral cortex and hippocampus by restraint stress, while the reverse pattern was observed in antioxidant enzymes. These results were supported by histopathological findings, with 4-hydroxynonenal staining for oxidative injury and Fluoro-Jade B staining showing the degenerating neurons. The aforementioned patterns of oxidative injury were accelerated by orchiectomy. These findings strongly suggest the conclusion that testosterone exerts a protective effect against oxidative brain damage, especially under stressed conditions.

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“…Consistent with the previous results with DHEA, utamide did not inhibit the synaptogenic effects of DHT. Also Leydig cell had been previously linked to male hypogonadism which in agreement with hypogodanism (Bhasin, 2010;Morakinyo, 2014;Beattie, 2015;Grossmann, 2021;Kinoshita, 2022). Upon analysis the characterization of cellular changes occurring in the cortico-hippocampal regions in models of androgen deprived insulin-resistant adult male rats was determined.…”

Section: Resultsmentioning

confidence: 78%

Characterization of Hippocampal Synaptic Plasticity in Orchidectomized Insulin-resistant Rats

Akinbampe

Abayomi

Opuwari

et al. 2022

Preprint

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BackgroundAndrogen deprivation can be achieved through testosterone antagonists (chemical castration) with or without orchidectomy. There is this hypothesis that stipulates that testesterone exerts supreme effects on synaptic plasticity, however low testosterone has been linked to type- 2 diabetics mellitus, insulin resistance and Alzheimer’s disease. The aim of the study was to investigate the cellular changes that occur from bilateral orchidectomy and examine the effects of androgen deprivation, orchidectomy and flutamide administration on the histoarchitectural organization of the hippocampus in male Wistar rats. MethodologyThirty-six (36) adult male Wistar rats were randomly divided into into six (6) groups: Control group (distilled water),orchidectomy group (bilateral orchidectomy), flutamide group (oral 10mg,20mg), orchidectomy+flutamide. Animals were sacrificed at 30 days respectively. ResultsThe total plasma; testesterone, insulin levels, fasting blood glucose, and nitric oxide were assayed; the homeostasis model for insulin resistance was also calculated. Histological examinations by Hematoxylin and Eosin(H&E) and Cresyl fast violet (CFV), while immunohistochemical analysis of astrocytes were performed using Glial fibrillary acidic protein (GFAP). Results of study show that androgen deprived insulin-resistance state primarily affects fasting blood glucose and lead to increases in the level of serum insulin, glucose and nitric oxide and caused a decrease in serum testosterone levels. The hippocampal response to flutamide was unaffected by blockade of intracerebral estrogen biosynthesis. In comparison flutamide alone increased CA1 spine synapse density also whereas in combination the effects of flutamide+orchidectomy were additive rather than inhibitory. ConclusionHistopathological results showed that flutamide significantly restored the histological damage of rat brain in flutamide treatment+ orchidectomy.

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Testosterone promotes glucose intolerance, lipid disorder and oxidative stress in type 1 diabetic rats

Abstract: These data indicate that TD attenuates glucose intolerance under diabetic conditions and is equally associated with a considerable reduction in oxidative stress, which implies that testosterone may be a pro-oxidant.

Cited by 11 publications

References 12 publications

Effects of Melatonin on Oxidative Stress Index and Alveolar Bone Loss in Diabetic Rats With Periodontitis

Effects of Melatonin on Oxidative Stress Index and Alveolar Bone Loss in Diabetic Rats With Periodontitis

Testosterone depletion increases the susceptibility of brain tissue to oxidative damage in a restraint stress mouse model

Characterization of Hippocampal Synaptic Plasticity in Orchidectomized Insulin-resistant Rats

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