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Med Hypotheses. 2008 Sep;71(3):399-403. doi: 10.1016/j.mehy.2008.04.006. Epub 2008 Jul 14.

Invivo insulin deficiency as a potential etiology for demyelinating disease.

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  • 1Medical College, Tsinghua University, Beijing, China.


Demyelinating disease is pathologically characterized by the death of mature oligodendrocytes that normally synthesize myelin to perform insulating functions. Moreover, demyelinating disease also results in the failure of remyelination process in which oligodendrocyte progenitor cells reactivate and differentiate into new oligodendrocytes. Thus, this disease reflects decreased nerve conduction velocity and eventually dysfunction of the nervous system. A notable fact in the clinic is that demyelination is one of the most common diabetes-induced complications, implying that demyelinating disease may be relevant to insulin deficiency in vivo. However, the explicit pathological relationship between demyelination and diabetes remains unclear. Mainstream theories posit that demyelinating disease is an autoimmune disease arising from abnormal immunological reactions, but this perspective is limited when applied to the clinic. Olig1 is a vital transcription factor involved in oligodendrogenesis and is essential for the survival and maturation of oligodendrocyte progenitor cells. Furthermore, Olig1 is required for the onset of remyelination in adults. In the present study, we serendipitously found by means of protein immunoblot that the expression of nuclear Olig1 was inhibited when mouse oligodendrocyte progenitor cells were cultured in the absence of insulin. Combining this finding with the clinical relevance of demyelination and diabetes, we hypothesize that in vivo insulin deficiency impairs the reactivation and differentiation of oligodendrocyte progenitor cells through downregulation of nuclear Olig1 expression and therefore hinders the remyelination, which is an important process required for functional recovery in demyelinating disease. This hypothesis implies that in vivo insulin deficiency may be a novel etiological cause of demyelinating disease and thus contribute to improved the clinical therapies for remyelination repair. We suggest that sustaining normal insulin levels and stable nuclear Olig1 expression in vivo can be new therapeutic targets for remyelination repair and diabetic neuropathy. In addition, with respect to the clinical transplantation of oligodendrocyte progenitor cells for remyelination repair, supplementing cell suspensions that are to be transplanted with appropriate doses of insulin potentially may facilitate adaptation of the transplanted progenitor cells to the heterogeneous and pathological environment in vivo and eventually improve the efficacy of the cellular transplantation.

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