Disability in patients with multiple sclerosis: Influence of insulin resistance, adiposity, and oxidative stress

Oliveira, Sayonara Rangel; Simão, Andréa Name Colado; Kallaur, Ana Paula; Almeida, Elaine Regina Delicato de; Morimoto, Helena Kaminami; Lopes, Josiane; Dichi, Isaías; Kaimen-Maciel, Damacio Ramón; Reiche, Edna Maria Vissoci

doi:10.1016/j.nut.2013.08.001

Cited by 94 publications

(98 citation statements)

References 40 publications

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“…An earlier study reported that glucose tolerance is not impaired in MS patients [10]. On the contrary, Wens et al demonstrated that MS patients are at increased risk to develop impaired glucose tolerance [39].…”

Section: Discussionmentioning

confidence: 95%

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Association of sex hormones and glucose metabolism with the severity of multiple sclerosis

Triantafyllou

Thoda

Armeni

et al. 2015

International Journal of Neuroscience

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Section: Discussionmentioning

confidence: 95%

“…It has been postulated that MS may be associated with metabolic derangement, leading to obesity [9]. Moreover, insulin resistance may be associated with the extent of disability, as estimated by the Expanded Disability Status Scale (EDSS) [10].…”

Section: Introductionmentioning

confidence: 99%

Association of sex hormones and glucose metabolism with the severity of multiple sclerosis

Triantafyllou

Thoda

Armeni

et al. 2015

International Journal of Neuroscience

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“…Recently, increased prevalence of insulin resistance and impaired glucose tolerance in MS patients was reported (Oliveira et al, 2014; Penesova et al, 2015; Wens et al, 2013). In previous studies, IL-17A inhibited adipogenesis and moderated adipose tissue accumulation in vitro and IL-17a −/− mice showed increased bodyweight, glucose tolerance and insulin sensitivity (Ahmed and Gaffen, 2010; Ahmed and Gaffen, 2013; Straus, 2013; Winer et al, 2009; Zuniga et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Intracranial delivery of interleukin-17A via adeno-associated virus fails to induce physical and learning disabilities and neuroinflammation in mice but improves glucose metabolism through AKT signaling pathway

Yang

Kou

Lim

et al. 2016

Brain, Behavior, and Immunity

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Interleukin-17A (IL-17A) is generally considered as one of the pathogenic factors involved in multiple sclerosis (MS). Indirect evidence for this is that IL-17A-producing T helper 17 (Th17) cells preferentially accumulate in lesions of MS and experimental autoimmune encephalomyelitis (EAE). However, a direct involvement of IL-17A in MS pathogenesis is still an open question. In this study, we overexpressed IL-17A in the brains of mice (IL-17A-in-Brain mice) via recombinant adeno-associated virus serotype 5 (rAAV5)-mediated gene delivery. In spite of high levels of IL-17A expression in the brain and blood, IL-17A-in-Brain mice exhibit no inflammatory responses and no abnormalities in motor coordination and spatial orientation. Unexpectedly, IL-17A-in-Brain mice show decreases in body weight and adipose tissue mass and an improvement in glucose tolerance and insulin sensitivity. IL-17A enhances glucose uptake in PC12 cells by activation of AKT. Our results provide direct evidence for the first time that IL-17A overexpression in the central nervous system does not cause physical and learning disabilities and neuroinflammation and suggest that IL-17A may regulate glucose metabolism through the AKT signaling pathway.

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“…The compounds that can readily cross the BBB include:simvastatin, atorvastatin, cerivastatin, pravastatin and rosuvastatin (87). Exendin-4 and GLP-1 have been shown to reduce inflammation, demyelination and cytokine release in various animal models of MS (88). Most glucagon-like peptide-1 (GLP-1) mimetics such as exendin-4, liraglutide, and lixisenatide cross the BBB and show neuroprotective effects in many studies.…”

Section: New Possibilities In the Treatment Of Ms-neuroprotectionmentioning

confidence: 99%

Novel Approaches of Oxidative Stress Mechanisms in the Multiple Sclerosis Pathophysiology and Therapy

Adamczyk

Niedziela

Adamczyk-Sowa

2017

Multiple Sclerosis: Perspectives in Treatment and Pathogenesis

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Abstract:It is suspected that the development of multiple sclerosis (MS) can be affected by oxidative stress (OS). In the acute phase of the disease, OS is responsible for initiating inflammation, whereas in the chronic phase it sustains neurodegenerative process. Redox processes in MS are related to dysregulation of axonal bioenergetics, cerebral iron accumulation, mitochondrial dysfunction, impaired oxidant/antioxidant balance, and OS memory. This chapter gives an overview of the role of OS in MS.

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Disability in patients with multiple sclerosis: Influence of insulin resistance, adiposity, and oxidative stress

Cited by 94 publications

References 40 publications

Association of sex hormones and glucose metabolism with the severity of multiple sclerosis

Association of sex hormones and glucose metabolism with the severity of multiple sclerosis

Intracranial delivery of interleukin-17A via adeno-associated virus fails to induce physical and learning disabilities and neuroinflammation in mice but improves glucose metabolism through AKT signaling pathway

Novel Approaches of Oxidative Stress Mechanisms in the Multiple Sclerosis Pathophysiology and Therapy

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