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Insulin resistance could be a link between diet and neurodegenerative diseases
Neurons like it tidy. Brain cells called glia help neurons perform at their best by cleaning up toxic cellular debris. But a diet high in sugar makes glia insulin resistant — which turns them into apathetic housekeepers that let damaging debris pile up, according to new work from Fred Hutchinson Cancer Center scientists, published in the journal PLOS Biology. The findings in fruit flies could help explain how diet influences risk of neurodegenerative disorders like Alzheimer’s disease.
“These findings show how eating processed food doesn’t just affect weight gain, it affects cognitive function. It affects a deep functioning of your body,” said Fred Hutch obesity researcher and senior author Akhila Rajan, PhD. “Our study provided missing evidence that glial insulin resistance has consequences to glia’s debris-clearing role.”
The high levels of insulin induced by excess dietary sugar causes glial dysfunction, which prevents glial cells from cleaning up damaging cellular debris.
“Obesity is an independent risk factor for dementia, but the causative mechanism underlying that connection is largely unknown,” Alassaf said.
What is known is that malfunctioning of glial cells, which tidy up debris and influence neuron function by “pruning” nerve cells, can contribute to neurodegeneration. Studies have shown that changes in glial cell function can alter animals’ weight, metabolism and feeding behaviors. Whether glia can become insulin resistant, and whether this could cause changes in their function, was also unknown.
“What happens in these conditions is that glia become less efficient in clearing up these cytotoxic [cell-damaging] debris,” Alassaf said. “Leaving that debris behind induces inflammation, it induces secondary cell death — so clearing it up is a pretty crucial step in remedying damage.”
As over-sugared flies’ insulin jumps, they also store the excess energy as fat, which can communicate with brain cells. To untangle the influence insulin and fat on glia, Alassaf genetically engineered flies to release extra insulin even when she kept the sugar in their diets at a normal level. This mimicked the insulin levels of flies eating a high-sugar diet — without the sugar. Alassaf showed that glia in these genetically manipulated flies turned down Draper. When she genetically manipulated fruit flies to keep their insulin levels low even when they ate excess sugar, their glia remained insulin sensitive, and Draper levels remained normal.
This shows that flies’ diet-induced glial dysfunction resulted from their insulin response, not their fat stores, she said.
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