Carbohydrate metabolism in motor neurone disease.

Saffer, D; Morley, J. E.; Bill, Pedrini

doi:10.1136/jnnp.40.6.533

Cited by 31 publications

(23 citation statements)

References 11 publications

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“…In ALS patients, studies examining insulin and glucose responses, using a compound that stimulates the secretion of insulin, indicate impaired synthesis or release of insulin from the pancreas [110,111]. Strikingly, recent findings in ALS patients provide further evidence to support altered insulin release and function in ALS [67].…”

Section: Meeting Energy Needs In Alsmentioning

confidence: 98%

“…Since the 1960s, there have been reports of impaired glucose tolerance and insulin resistance in ALS [9,11,109,110,111,112,113]. The possibility of impaired function of insulin is of particular interest in ALS because reduced glucose availability could exacerbate neuronal dysfunction, particularly in the CNS, which relies predominantly on glucose as fuel.…”

Section: Meeting Energy Needs In Alsmentioning

confidence: 99%

“…Congruent with this, muscle wasting is correlated with abnormal glucose tolerance in some ALS patients [10,11]. However, this correlation is not universal [115], and controlling for muscle wasting does not affect the occurrence of impaired glucose handling [111]. Thus, muscle wasting, while a possible contributor, is unlikely to be the sole explanation for abnormal glucose handling in all ALS cases.…”

Section: Meeting Energy Needs In Alsmentioning

confidence: 99%

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Altered Metabolic Homeostasis in Amyotrophic Lateral Sclerosis: Mechanisms of Energy Imbalance and Contribution to Disease Progression

et al. 2016

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the death of motor neurones, which leads to paralysis and death in an average of 3 years following diagnosis. The cause of ALS is unknown, but there is substantial evidence that metabolic factors, including nutritional state and body weight, affect disease progression and survival. This review provides an overview of the characteristics of metabolic dysregulation in ALS focusing on mechanisms that lead to disrupted energy supply (at a whole-body and cellular level) and altered energy expenditure. We discuss how a decrease in energy supply occurs in parallel with an increase in energy demand and leads to a state of chronic energy deficit which has a negative impact on disease outcome in ALS. We conclude by presenting potential and tested strategies to compensate for, or correct this energy imbalance, and speculate on promising areas for further research.

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Section: Meeting Energy Needs In Alsmentioning

confidence: 98%

Section: Meeting Energy Needs In Alsmentioning

confidence: 99%

Section: Meeting Energy Needs In Alsmentioning

confidence: 99%

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Altered Metabolic Homeostasis in Amyotrophic Lateral Sclerosis: Mechanisms of Energy Imbalance and Contribution to Disease Progression

et al. 2016

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“…Since the 1960s, there have been reports of impaired glucose tolerance and insulin resistance in ALS (Cumings, 1962, Ionasescu and Luca, 1964, Steinke and Tyler, 1964, Saffer et al, 1977, Gotoh et al, 1972, Reyes et al, 1984, Pradat et al, 2010.…”

Section: Impaired Glucose Handlingmentioning

confidence: 99%

“…Thus, muscle wasting in ALS could affect glucose handling by altering insulin-mediated translocation to the muscle membrane of the glucose transporter type 4 (GLUT4), which is critical in regulating cellular glucose uptake and whole body glucose homeostasis (Henriksen et al, 1991). Congruent with this, muscle wasting is correlated with abnormal glucose tolerance in some ALS patients (Collis andEngel, 1968, Gotoh et al, 1972), however this correlation is not universal (Mueller and Quick, 1970) and controlling for muscle wasting does not affect the occurrence of impaired glucose handling (Saffer et al, 1977). Thus, muscle wasting, while a possible contributor, is unlikely to be the sole explanation for abnormal glucose handling in all ALS cases.…”

Section: Impaired Glucose Handlingmentioning

confidence: 99%

Energy metabolism in amyotrophic lateral sclerosis: assessment of body composition and energy expenditure

Ioannides¹

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Amyotrophic leteral sclerosis: Part 2. Etiopathogenesis

Tandan

Bradley

1985

Annals of Neurology

139

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The pathogenesis of the motor neuronal degeneration in amyotrophic lateral sclerosis (ALS) is unclear, though several possible etiological factors are currently being investigated. A unifying hypothesis will have to explain the diverse geographical occurrence, clinical features, and selective vulnerability and relative resistance of different neuronal populations in the disease. It is possible that different biochemical defects underlie this diversity, or alternatively that the many factors incriminated in the etiology may act upon an underlying genetic-biochemical abnormality to trigger premature neuronal death. Viruses, metals, endogenous toxins, immune dysfunction, endocrine abnormalities, impaired DNA repair, altered axonal transport, and trauma have all been etiologically linked with ALS, but convincing research evidence of a causative role for any of these factors is yet to be demonstrated.

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Carbohydrate metabolism in motor neurone disease.

Cited by 31 publications

References 11 publications

Altered Metabolic Homeostasis in Amyotrophic Lateral Sclerosis: Mechanisms of Energy Imbalance and Contribution to Disease Progression

Altered Metabolic Homeostasis in Amyotrophic Lateral Sclerosis: Mechanisms of Energy Imbalance and Contribution to Disease Progression

Energy metabolism in amyotrophic lateral sclerosis: assessment of body composition and energy expenditure

Amyotrophic leteral sclerosis: Part 2. Etiopathogenesis

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