Reduced epidermal thickness, nerve degeneration and increased pain-related behavior in rats with diabetes type 1 and 2

Borić, Matija; Škopljanac, Ivan; Ferhatović, Lejla; Kadić, Antonia Jeličić; Banožić, Adriana; Puljak, Livia

doi:10.1016/j.jchemneu.2013.10.001

Cited by 25 publications

(24 citation statements)

References 36 publications

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“…The significant decrease in nerve fibre lengths and IENF density between ZDF and ZL rats at 35 weeks suggested the existence of a neuropathy in the ZDF group, as previously reported (Hirai et al, 2000;Pittenger et al, 2004;Beiswenger et al, 2008;Brussee et al, 2008;Malik et al, 2011;Boric et al, 2013;Jelicic Kadic et al, 2014;Wang et al, 2015). However, all strains used in our study showed a decreased IENF density at age 35 weeks compared to baseline values.…”

Section: Discussionsupporting

confidence: 84%

Behavioural, morphological and electrophysiological assessment of the effects of type 2 diabetes mellitus on large and small nerve fibres in Zucker diabetic fatty, Zucker lean and Wistar rats

García‐Pérez¹,

Schönberger

Sumalla³

et al. 2018

European Journal of Pain

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ZDF rats presented a diabetic neuropathy involving large and small nerve fibres; additionally, ZL and WH rats also showed early small abnormalities in C-fibres, clearly detected by microneurography SIGNIFICANCE: This study provides a functional description of large and small nerve fibre function in a diabetic model that recapitulates many of the findings observed in patients suffering from type 2 diabetes mellitus.

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Section: Discussionsupporting

confidence: 84%

Behavioural, morphological and electrophysiological assessment of the effects of type 2 diabetes mellitus on large and small nerve fibres in Zucker diabetic fatty, Zucker lean and Wistar rats

García‐Pérez¹,

Schönberger

Sumalla³

et al. 2018

European Journal of Pain

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“…Cutaneous changes, including reduced epidermal thickness can be used as an outcome measure for predegenerative markers of DN. 30 Reduction of muscle fiber diameter is also seen with STZ diabetic rats. 31 In the current research, we adopted a potential approach to study the possible molecular mechanism of ibuprofen and L arginine in protecting against DN through combining in silico data and functional validation.…”

Section: Discussionmentioning

confidence: 92%

Prophylactic L-arginine and ibuprofen delay the development of tactile allodynia and suppress spinal miR-155 in a rat model of diabetic neuropathy

El-Lithy

El-Bakly

Matboli

et al. 2016

Translational Research

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“…Our results stress the functional importance of AMPK and FOXO3 working in concert with insulin to maintain proliferation in the epidermis. This could be of physiological importance since diabetes is a condition in which insulin signaling is impaired, and it is accompanied by epidermal thinning in experimental rat models in vivo [ 69 , 70 ]. Proliferative dysfunction in keratinocytes delays epidermal turnover and is associated with decreased epidermal thickness [ 11 , 71 , 72 ].…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Prevents Oxidative Stress-Induced Senescence and Proliferative Dysfunction by Activating the AMPK-FOXO3 Cascade in Cultured Primary Human Keratinocytes

et al. 2015

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The aging process is perceived as resulting from a combination of intrinsic factors such as changes in intracellular signaling and extrinsic factors, most notably environmental stressors. In skin, the relationship between intrinsic changes and keratinocyte function is not clearly understood. Previously, we found that increasing the activity of AMP-activated protein kinase (AMPK) suppressed senescence in hydrogen peroxide (H2O2)-treated human primary keratinocytes, a model of oxidative stress-induced cellular aging. Using this model in the present study, we observed that resveratrol, an agent that increases the activities of both AMPK and sirtuins, ameliorated two age-associated phenotypes: cellular senescence and proliferative dysfunction. In addition, we found that treatment of keratinocytes with Ex527, a specific inhibitor of sirtuin 1 (SIRT1), attenuated the ability of resveratrol to suppress senescence. In keeping with the latter observation, we noted that compared to non-senescent keratinocytes, senescent cells lacked SIRT1. In addition to these effects on H2O2-induced senescence, resveratrol also prevented the H2O2-induced decrease in proliferation (as indicated by 3H-thymidine incorporation) in the presence of insulin. This effect was abrogated by inhibition of AMPK but not SIRT1. Compared to endothelium, we found that human keratinocytes expressed relatively high levels of Forkhead box O3 (FOXO3), a downstream target of both AMPK and SIRT1. Treatment of keratinocytes with resveratrol transactivated FOXO3 and increased the expression of its target genes including catalase. Resveratrol’s effects on both senescence and proliferation disappeared when FOXO3 was knocked down. Finally, we performed an exploratory study which showed that skin from humans over 50 years old had lower AMPK activity than skin from individuals under age 20. Collectively, these findings suggest that the effects of resveratrol on keratinocyte senescence and proliferation are regulated by the AMPK-FOXO3 pathway and in some situations, but not all, by SIRT1.

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Reduced epidermal thickness, nerve degeneration and increased pain-related behavior in rats with diabetes type 1 and 2

Cited by 25 publications

References 36 publications

Behavioural, morphological and electrophysiological assessment of the effects of type 2 diabetes mellitus on large and small nerve fibres in Zucker diabetic fatty, Zucker lean and Wistar rats

Behavioural, morphological and electrophysiological assessment of the effects of type 2 diabetes mellitus on large and small nerve fibres in Zucker diabetic fatty, Zucker lean and Wistar rats

Prophylactic L-arginine and ibuprofen delay the development of tactile allodynia and suppress spinal miR-155 in a rat model of diabetic neuropathy

Resveratrol Prevents Oxidative Stress-Induced Senescence and Proliferative Dysfunction by Activating the AMPK-FOXO3 Cascade in Cultured Primary Human Keratinocytes

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