White Matter Abnormalities in the Corpus Callosum in Acute and Recovered Anorexia Nervosa Patients—A Diffusion Tensor Imaging Study

Nickel, Kathrin; Elst, Ludger Tebartz van; Holovics, Lukas; Feige, Bernd; Glauche, Volkmar; Fortenbacher, Tina; Endres, Dominique; Zeeck, Almut; Tüscher, Oliver; Joos, Andreas; Maier, Simon

doi:10.3389/fpsyt.2019.00490

Cited by 18 publications

(28 citation statements)

References 61 publications

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“…Also, oligodendrocyte-specific knockout of Glut1, limiting glucose uptake, leads to a reduction in myelin thickness in vivo. In addition, MRI scans of patients suffering from anorexia nervosa show a loss of white matter, indicating that severe nutrient restriction in humans can also cause oligodendrocytes to metabolize lipids stored in the myelin sheath, to maintain cerebral energy homeostasis 36,37 .…”

Section: Discussionmentioning

confidence: 99%

Glycolytically impaired glial cells fuel neural metabolism via β-oxidation

Schirmeier

Hertenstein

McMullen³

et al. 2021

Preprint

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Neuronal function is highly energy demanding and thus requires efficient and constant metabolite delivery. Like their mammalian counterparts Drosophila glia are highly glycolytic and provide lactate to fuel neuronal metabolism. However, flies are able to survive for several weeks in the absence of glial glycolysis1. Here, we study how glial cells maintain sufficient nutrient supply to neurons under conditions of carbohydrate restriction. We show that glycolytically impaired glia switch to fatty acid breakdown via β-oxidation and provide ketone bodies as an alternate neuronal fuel. Moreover, flies also rely on glial β-oxidation under starvation conditions with glial loss of β-oxidation increasing susceptibility to starvation. Further, we show that glial cells act as a metabolic sensor in the brain and can induce mobilization of peripheral energy stores to ensure brain metabolic homeostasis. In summary, our study gives pioneering evidence on the importance of glial β-oxidation and ketogenesis for brain function, and survival, under adverse conditions, like malnutrition. The glial capacity to utilize lipids as an energy source seems to be conserved from flies to humans.

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Section: Discussionmentioning

confidence: 99%

Glycolytically impaired glial cells fuel neural metabolism via β-oxidation

Schirmeier

Hertenstein

McMullen³

et al. 2021

Preprint

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“…If nutritional stress becomes prolonged, myelin energy reserves will also reach a limit. We note reports of MRI-detectable white matter lesions in patients with diabetic hypoglycemic coma 41 or severe anorexia nervosa 42,43 , which was mechanistically unexplained. Individuals with obesity that underwent gastric bypass (bariatric) surgery have developed encephalopathy and peripheral neuropathy 44 .…”

Section: Discussionmentioning

confidence: 77%

Myelin lipids as nervous system energy reserves

Asadollahi¹,

Trevisiol

Saab

et al. 2022

Preprint

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Neuronal functions and impulse propagation depend on the continuous supply of glucose1,2. Surprisingly, the mammalian brain has no obvious energy stores, except for astroglial glycogen granules3. Oligodendrocytes make myelin for rapid axonal impulse conduction4 and also support axons metabolically with lactate5-7. Here, we show that myelin itself, a lipid-rich membrane compartment, becomes a local energy reserve when glucose is lacking. In the mouse optic nerve, a model white matter tract, oligodendrocytes survive glucose deprivation far better than astrocytes, by utilizing myelin lipids which requires oxygen and fatty acid beta-oxidation. Importantly, fatty acid oxidation also contributes to axonal ATP and basic conductivity. This metabolic support by fatty acids is an oligodendrocyte function, involving mitochondria and myelin-associated peroxisomes, as shown with mice lacking Mfp2. To study reduced glucose availability in vivo without physically starving mice, we deleted the Slc2a1 gene from mature oligodendrocytes. This caused a significant decline of the glucose transporter GLUT1 from the myelin compartment leading to myelin sheath thinning. We suggest a model in which myelin turnover under low glucose conditions can transiently buffer axonal energy metabolism. This model may explain the gradual loss of myelin in a range of neurodegenerative diseases8 with underlying hypometabolism9.

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“…This study was part of a multimodal MRI study, which assessed structural, metabolic and other functional data [see, e.g., (31)(32)(33)(34)(35)(36)]. We replicated the aforementioned food paradigm with 31 AN and 27 NP.…”

Section: Methodsmentioning

confidence: 99%

A Neglected Topic in Neuroscience: Replicability of fMRI Results With Specific Reference to ANOREXIA NERVOSA

et al. 2020

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Functional magnetic resonance imaging (fMRI) studies report impaired functional correlates of cognition and emotion in mental disorders. The validity of preexisting studies needs to be confirmed through replication studies, which there is a lack of. So far, most replication studies have been conducted on non-patients (NP) and primarily investigated cognitive and motor tasks. To fill this gap, we conducted the first fMRI replication study to investigate brain function using disease-related food stimuli in patients with anorexia nervosa (AN). Using fMRI, we investigated 31 AN patients and 27 NP for increased amygdala and reduced midcingulate activation when viewing food and nonfood stimuli, as reported by the original study (11AN, 11NP; Joos et al., 2011). Similar to the previous study, we observed in the within group comparisons (food>non-food) a frontoinsular activation for both groups. Although in AN the recorded activation clustered more prominently and extended into the cingulate cortex. In the between-group comparisons, the increased amygdala and reduced midcingulate activation could not be replicated. Instead, AN showed a higher activation of the cingulate cortices, the pre-/ postcentral gyrus and the inferior parietal lobe. Unlike in the initial study, no significant differences between NP>AN could be observed. The inconsistency of results and the nonreplication of the study could have several reasons, such as high inter-individual variance of functional correlates of emotion processing, as well as intra-individual variances and the smaller group size of the initial study. These results underline the importance of replication for assessing the reliability and validity of results from fMRI research.

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White Matter Abnormalities in the Corpus Callosum in Acute and Recovered Anorexia Nervosa Patients—A Diffusion Tensor Imaging Study

Cited by 18 publications

References 61 publications

Glycolytically impaired glial cells fuel neural metabolism via β-oxidation

Glycolytically impaired glial cells fuel neural metabolism via β-oxidation

Myelin lipids as nervous system energy reserves

A Neglected Topic in Neuroscience: Replicability of fMRI Results With Specific Reference to ANOREXIA NERVOSA

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