Schwann cells contribute to demyelinating diabetic neuropathy and nerve terminal structures in white adipose tissue

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Peripheral neuropathy, which can include axonal degeneration and/or demyelination, impacts adipose tissues with obesity, diabetes, and aging. However, the presence of demyelinating neuropathy had not yet been explored in adipose. Both demyelinating neuropathies and axonopathies implicate Schwann cells (SCs), a glial support cell that myelinates axons and contributes to nerve regeneration after injury. We performed a comprehensive assessment of SCs and myelination patterns of subcutaneous white adipose tissue (scWAT) nerves, and changes across altered energy balance states. We found that mouse scWAT contains both myelinated and unmyelinated nerves and is populated by SCs, including SCs that were associated with synaptic vesicle-containing nerve terminals. BTBR ob/ob mice, a model of diabetic peripheral neuropathy, exhibited small fiber demyelinating neuropathy and alterations in SC marker gene expression in adipose that were similar to obese human adipose. These data indicate that adipose SCs regulate the plasticity of tissue nerves and become dysregulated in diabetes.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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