summary: Research suggests that sugary diets, commonly associated with obesity, can cause insulin resistance in the brain and increase the risk of neurodegenerative diseases such as Alzheimer’s disease.
The study revealed that this insulin resistance impairs the ability of glial cells to clear neuronal debris, a key process for preventing neurodegeneration.
By studying Drosophila melanogaster, which shares physiological similarities with humans, the research team found that a sugar-rich diet reduced levels of the PI3k protein in glial cells and the Draper protein that coats glia, impeding their debris removal function. I discovered that.
Important facts:
- The high sugar diet associated with obesity can cause insulin resistance in the brain, which has been demonstrated to reduce the brain’s ability to clear nerve cell debris.
- The study found that this resistance reduced PI3k and Draper protein levels in glial cells, directly impacting the cells’ ability to clear debris.
- These findings link diet-induced insulin resistance to increased risk of neurodegenerative diseases and provide new insights into preventive therapies.
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Researchers led by Muloi Alasaf of the Fred Hutchinson Cancer Research Center in the US have discovered a link between obesity and neurodegenerative diseases such as Alzheimer’s disease.
The study in fruit flies showed that a high-sugar diet, a hallmark of obesity, causes the brain to become insulin resistant, which reduces the ability of nerve cells to clear debris and increases the risk of neurodegeneration. It was shown that
Published on November 7thth in open access journals PLOS Biology, This research will have implications for treatments designed to reduce the risk of developing neurodegenerative diseases.
Although it is known that obesity is a risk factor for neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease, how obesity leads to other diseases remains a mystery. A new study focused on answering this question by exploiting similarities between humans and fruit flies.
Having previously shown that a high-sugar diet causes insulin resistance in the peripheral organs of flies, the researchers now turned their attention to the fly’s brain. Specifically, the researchers examined glial cells, since microglial dysfunction is known to cause neurodegeneration.
Levels of the protein PI3k indicate how well a cell can respond to insulin. Researchers found that a high-sugar diet led to decreased PI3k levels in glial cells, indicating insulin resistance.
They also focused on the fly’s equivalent of microglia, called encapsulated glia, whose main function is to remove neural debris such as degenerated axons. They observed that these glia had low levels of Draper protein, indicating dysfunction.
Further studies revealed that artificially lowering PI3k levels caused both insulin resistance and reduced Draper levels in coated glia.
Finally, after actually damaging olfactory sensory neurons, Draper levels did not increase in flies fed a high-sugar diet, indicating that coated glia were unable to remove degenerating axons.
The authors go on to say, “Using Drosophila melanogaster, the authors demonstrated that a sugar-rich diet causes insulin resistance in glial cells, interfering with their ability to clear neuronal debris. “Providing insight into how inducing diets may contribute to increased risk of neurodegenerative diseases.”
About this diet, obesity, and neurodegeneration research news
author: Claire Turner
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contact: Claire Turner – PLOS
image: Image credited to Neuroscience News
Original research: Open access.
“Diet-induced glial insulin resistance impedes clearance of neuronal debris. Drosophila brain” written by Akira Rajan et al. PLOS Biology
abstract
Diet-induced glial insulin resistance impedes clearance of neuronal debris. Drosophila brain
Obesity significantly increases the risk of developing neurodegenerative diseases, but the exact mechanisms underlying this relationship remain unclear. Defective glial phagocytic function is an important feature of neurodegenerative diseases, as delayed clearance of neuronal debris can lead to inflammation, neuronal cell death, and impaired recovery of the nervous system.
Increasing evidence indicates that glial function can influence feeding behavior, body weight, and systemic metabolism, suggesting that diet may play a role in regulating glial function. Although it is understood that glial cells are insulin sensitive, it remains unclear whether an obesogenic diet induces glial insulin resistance and thereby impairs glial phagocytic function.
here, Drosophila Using this model, we show that a chronic obesogenic diet induces glial insulin resistance and impairs clearance of neuronal debris. Specifically, exposure to an obesogenic diet downregulates basal and injury-induced expression of Draper, a glial-associated phagocyte receptor.
Constitutive activation of systemic insulin release Drosophila Insulin-producing cells (IPCs) mimic the effects of diet-induced obesity on glial Draper expression. In contrast, genetically attenuating systemic insulin release from IPCs rescues diet-induced glial insulin resistance and Draper expression.
Importantly, we show that genetic stimulation of phosphoinositide 3-kinase (Pi3k), a downstream effector of insulin receptor (IR) signaling, rescues high sugar diet (HSD)-induced glial defects. showed that.
Therefore, we establish that an obesogenic diet impairs glial phagocytic function and slows clearance of neuronal debris.
