Carbohydrate and lipid metabolism in multiple sclerosis: Clinical implications for etiology, pathogenesis, diagnosis, prognosis, and therapy

Pashaei, Somayeh; Mohammadi, Pantea; Yarani, Reza; Haghgoo, Seyyed Mortaza; Aleagha, Mohammad Sajad Emami

doi:10.1016/j.abb.2021.109030

Cited by 9 publications

(12 citation statements)

References 105 publications

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“…In particular, dysregulations in glycolysis, Krebs cycle, electron transport chain, pentose phosphate pathway, and glycogen metabolism were observed in pwMS. 50 Interestingly, while changes in glucose homeostasis typical of type 2 diabetes, such as hyperinsulinemia and decreased insulin sensitivity, were observed in pwMS, they seem unrelated to chronic inflammation or physical inactivity. 51 Furthermore, the levels of multiple plasma lipids and ketone bodies, the fatty acid oxidation pathway and involved enzymes, and the metabolism of eicosanoids, lipoproteins, and cholesterol were altered in MS, and, in part, correlated with its clinical aspects.…”

Section: Metabolic Disturbances In Msmentioning

confidence: 94%

“…51 Furthermore, the levels of multiple plasma lipids and ketone bodies, the fatty acid oxidation pathway and involved enzymes, and the metabolism of eicosanoids, lipoproteins, and cholesterol were altered in MS, and, in part, correlated with its clinical aspects. 50 Altered metabolic pathways of carbohydrates and lipids in pwMS may lead to further cellular damage, such as oxidative stress, which might be responsible for systemic complications. These metabolic abnormalities may be detected through altered levels of related metabolites in the blood and cerebrospinal fluid of MS patients.…”

Section: Metabolic Disturbances In Msmentioning

confidence: 99%

“…Notably, a hypothetical relationship between such metabolic changes and the immune system in patients with MS has been proposed. 50 Interestingly, cellular and whole-body inflammatory and metabolic processes are also under strong circadian control. 52,53 Therefore, their dysregulations might be, at least in part, induced by circadian disruption in MS.…”

Section: Metabolic Disturbances In Msmentioning

confidence: 99%

“…Overweight and obesity are associated with an increased risk of MS. 48,49 Further, pwMS often show other metabolic disturbances such as insulin resistance and changes in glucose and lipid homeostasis and the gut microbiome 20,[48][49][50] (Figure 1). In particular, dysregulations in glycolysis, Krebs cycle, electron transport chain, pentose phosphate pathway, and glycogen metabolism were observed in pwMS.…”

Section: Metabolic Disturbances In Msmentioning

confidence: 99%

“…74 pwMS show metabolic and immunological disturbances such as derailment of physiological T-and B-lymphocyte functions, alteration of innate immune responses, and in many cases, also changes in glucose and lipid homeostasis and gut microbiome. 20,[48][49][50] The circadian release of immune cells is controlled by hormones like melatonin and cortisol, which again are regulated by the suprachiasmatic nucleus. Indeed, an animal study showed that TH17 cell differentiation follows the circadian clock.…”

Section: Circadian Rhythms and Ms Riskmentioning

confidence: 99%

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Multiple sclerosis and circadian rhythms: Can diet act as a treatment?

2023

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Multiple sclerosis (MS) is an autoimmune inflammatory and neurodegenerative disease of the central nervous system (CNS) with increasing incidence and prevalence. MS is associated with inflammatory and metabolic disturbances that, as preliminary human and animal data suggest, might be mediated by disruption of circadian rhythmicity. Nutrition habits can influence the risk for MS, and dietary interventions may be effective in modulating MS disease course.Chronotherapeutic approaches such as time-restricted eating (TRE) may benefit people with MS by stabilizing the circadian clock and restoring immunological and metabolic rhythms, thus potentially counteracting disease progression. This review provides a summary of selected studies on dietary intervention in MS, circadian rhythms, and their disruption in MS, including clock gene variations, circadian hormones, and retino-hypothalamic tract changes. Furthermore, we present studies that reported diurnal variations in MS, which might result from circadian disruption. And lastly, we suggest how chrononutritive approaches like TRE might counteract MS disease activity.

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Section: Metabolic Disturbances In Msmentioning

confidence: 94%

Section: Metabolic Disturbances In Msmentioning

confidence: 99%

Section: Metabolic Disturbances In Msmentioning

confidence: 99%

Section: Metabolic Disturbances In Msmentioning

confidence: 99%

Section: Circadian Rhythms and Ms Riskmentioning

confidence: 99%

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Multiple sclerosis and circadian rhythms: Can diet act as a treatment?

2023

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The potential roles of amino acids and their major derivatives in the management of multiple sclerosis

et al. 2022

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Therapeutic Potential Effect of Glycogen Synthase Kinase 3 Beta (GSK-3β) Inhibitors in Parkinson Disease: Exploring an Overlooked Avenue

Turkistani,

Al-kuraishy,

Al-Gareeb

et al. 2024

Mol Neurobiol

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Parkinson’s disease (PD) is a progressive neurodegenerative disease of the brain due to degeneration of dopaminergic neurons in the substantia nigra (SN). Glycogen synthase kinase 3 beta (GSK-3β) is implicated in the pathogenesis of PD. Therefore, the purpose of the present review was to revise the mechanistic role of GSK-3β in PD neuropathology, and how GSK-3β inhibitors affect PD neuropathology. GSK-3 is a conserved threonine/serine kinase protein that is intricate in the regulation of cellular anabolic and catabolic pathways by modulating glycogen synthase. Over-expression of GSK-3β is also interconnected with the development of different neurodegenerative diseases. However, the underlying mechanism of GSK-3β in PD neuropathology is not fully clarified. Over-expression of GSK-3β induces the development of PD by triggering mitochondrial dysfunction and oxidative stress in the dopaminergic neurons of the SN. NF-κB and NLRP3 inflammasome are activated in response to dysregulated GSK-3β in PD leading to progressive neuronal injury. Higher expression of GSK-3β in the early stages of PD neuropathology might contribute to the reduction of neuroprotective brain-derived neurotrophic factor (BDNF). Thus, GSK-3β inhibitors may be effective in PD by reducing inflammatory and oxidative stress disorders which are associated with degeneration of dopaminergic in the SN.

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Carbohydrate and lipid metabolism in multiple sclerosis: Clinical implications for etiology, pathogenesis, diagnosis, prognosis, and therapy

Cited by 9 publications

References 105 publications

Multiple sclerosis and circadian rhythms: Can diet act as a treatment?

Multiple sclerosis and circadian rhythms: Can diet act as a treatment?

The potential roles of amino acids and their major derivatives in the management of multiple sclerosis

Therapeutic Potential Effect of Glycogen Synthase Kinase 3 Beta (GSK-3β) Inhibitors in Parkinson Disease: Exploring an Overlooked Avenue

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