MD Anderson Cancer Center UTHealth
Graduate School of Biomedical Sciences

Work by GSBS, MD Anderson researchers links neuronal insulin signaling to diabetes-associated pain

May 15, 2018
Tracey Barnett

Research by The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences faculty member Michael Galko, Ph.D., and scientists at MD Anderson Cancer Center could eventually pave the way for potential new treatment strategies for diabetic neuropathy patients.

The underlying causes of diabetes-induced pain are largely unknown. Most studies have used vertebrate models such as mice to focus on how diabetes might affect the tissue surrounding sensory neurons, with a possible detrimental impact on neuron function. However, a wider investigation into whether other tissues could be linked to the development of disease-associated pain symptoms has yet to be attempted by the field. The current prevalent theory is that diabetes-associated pain is a secondary effect of vascular changes or the toxicity of high sugar levels to neurons.

New research published by the team at MD Anderson in the open access journal Disease Models & Mechanisms investigates the role of insulin receptor through use of a novel fly model; and finds that disrupted insulin signaling in pain sensory neurons could be the underlying cause of diabetes-associated pain. This suggests that targeting neuronal insulin signaling may be a reasonable strategy to alleviate diabetes-associated pain. Read the full report here

Galko is an associate professor in the Department of Genetics at MD Anderson and is affiliated with the GSBS Programs in Genetics and Epigenetics, and Neuroscience.

He has been a Graduate School faculty member since 2006.

Information for this story was provided by a media release here

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