summary: Researchers at Ohio State University took a closer look at how a high-fat diet affects memory. This study identified the omega-3 fatty acid DHA as a potential protector against fat-induced brain inflammation.
Furthermore, in aging mice, high-fat diets were found to alter cell signaling and impede the generation of new memories. Their previous research on aging rats established a link between a diet of processed foods, brain inflammation, and signs of memory loss.
Important facts:
- The omega-3 fatty acid DHA suppresses brain inflammation caused by high-fat diets.
- A high-fat diet in aging mice has been shown to disrupt signaling in certain brain cells and prevent the formation of new memories.
- The study focused on microglia and hippocampal neurons and found that palmitic acid, found in high-fat foods, induced increased inflammation in both neurons.
sauce: ohio state university
A new study suggests several ways that fatty foods affect brain cells, and this finding could help explain the link between high-fat diets and memory problems, especially as we age. may be helpful.
A cell culture study at Ohio State University found that the omega-3 fatty acid DHA may protect the brain from the effects of an unhealthy diet by suppressing fat-induced inflammation at cellular sources.
Other experiments using brain tissue from older mice showed that a high-fat diet can cause certain brain cells to over-manage cell signals, preventing them from creating new memories.
The lab has previously shown that eating highly processed foods triggers a strong inflammatory response in the brain accompanied by behavioral signs of memory loss, and that DHA supplementation We have discovered that these problems can be prevented.
“What’s great about this paper is that for the first time, we’re starting to really understand these things for each cell type,” said lead author Ruth Barrientos, a researcher and associate professor of psychiatry at the Ohio State Institute for Behavioral Medicine. he says. In medical school, I majored in behavioral health and neuroscience.
“Our lab and others have frequently looked at the entire tissue of the hippocampus to observe the brain’s memory-related responses to high-fat meals. But we have no idea which cell types We are interested in whether these are more or less affected by saturated fats, and this is our first effort to determine that.”
This study was recently published in the journal Frontiers of cellular neuroscience.
In this study, the researchers focused on microglia, cells in the brain that promote inflammation, and hippocampal neurons, which are important for learning and memory. They used immortalized cells. These are copies of cells taken from animal tissue that have been modified to divide continuously and respond only to lab-based stimuli. This means that their behavior may not exactly match that of primary cells of the same type.
The researchers exposed these model microglia and neurons to palmitic acid, a saturated fatty acid most abundant in high-fat foods such as lard, shortening, meat, and dairy products, which led to increased gene activation in the cells and mitochondria. We observed how it affects the function and structure of. Inside cells whose main metabolic role is to produce energy.
The results showed that palmitic acid promoted gene expression changes associated with increased inflammation in both microglia and neurons, but microglia were affected by a wider range of inflammatory genes.
Pre-treating these cells with DHA, one of the two omega-3 fatty acids found in fish and other seafood and available in supplement form, results in a potent response to increased inflammation in both cell types. A protective effect was obtained.
“Previous studies have shown that DHA protects the brain and palmitate is harmful to brain cells, but we investigated how DHA could directly protect against the effects of palmitate on microglia. “This is the first time we’ve seen a strong protective effect,” said Michael Butler, lead author of the study and a researcher in the Barrientos lab.
However, regarding mitochondria, DHA did not prevent the loss of function associated with palmitate exposure.
“In this context, the protective effects of DHA may be limited to its effects on gene expression associated with pro-inflammatory responses, as opposed to saturated fat-induced metabolic abnormalities,” Butler said. Ta.
In another series of experiments, the researchers investigated how a diet high in saturated fat affects signaling in the brains of older mice by looking at another microglial function called synaptic pruning. Examined. Microglia monitor signal transmission between neurons and keep communication at ideal levels by gradually removing excess synaptic spines, the connection sites between axons and dendrites.
Microglia were exposed to mouse brain tissue containing both presynaptic and postsynaptic material from animals fed a high-fat diet or a normal diet for 3 days.
Microglia ate synapses in old mice fed a high-fat diet at a faster rate than they ate synapses in mice fed a normal diet. Butler said this suggests that high-fat diets have some effect on those synapses, giving microglia a reason to eat them.
“When we talk about necessary pruning and refinement, it’s like Goldilocks: You have to optimize, not too much, not too little,” Barrientos says. “If these microglia are eaten away too quickly, the ability of these spines to regrow and create new connections will be outstripped, so the memory won’t be able to consolidate or stabilize.”
The researchers will now extend their findings related to synaptic pruning and mitochondrial function to examine how the effects of palmitate and DHA work in primary brain cells from young and old animals.
Funding: This research was supported by grants from the National Institute on Aging and the National Institute of Dental and Craniofacial Research. Additional co-authors include Sabrina McKee Alfonso, Nashali Massa, and Kedryn Baskin, all from Ohio.
About this research news on diet, memory, and aging
author: emily caldwell
sauce: ohio state university
contact: Emily Caldwell – Ohio State University
image: Image credited to Neuroscience News
Original research: Open access.
“Dietary fatty acids differentially affect phagocytosis, inflammatory gene expression, and mitochondrial respiration in microglial and neuronal cell models” written by Ruth Barrientos et al. Frontiers of cellular neuroscience
abstract
Dietary fatty acids differentially affect phagocytosis, inflammatory gene expression, and mitochondrial respiration in microglial and neuronal cell models
Consumption of a diet high in saturated fatty acids and refined carbohydrates is associated with neuroinflammation, cognitive dysfunction, and neurodegenerative diseases. In contrast, a diet high in polliansat
Urine oxidized fatty acids are associated with anti-inflammatory and neuroprotective effects. We previously showed that high-fat diet (HFD) intake increases saturated fatty acids and decreases polyunsaturated fatty acids in the hippocampus.
We further showed that HFD induces excessive neuroinflammation and loss of synaptic elements, causing strong memory impairment in aged rats.
Here we investigate the effects of palmitate, a saturated fat abundant in food, on various cellular responses in BV2 microglia and HippoE-14 neurons, and the extent to which the omega-3 fatty acid docosahexaenoic acid (DHA) buffers them. I investigated whether to do so. We oppose these responses.
Our data show that DHA pretreatment prevents or partially attenuates palmitate-induced pro-inflammatory, endoplasmic reticulum stress, and mitochondrial damage-related gene expression changes in both cell types. .
Furthermore, we show that synaptic neurosomes isolated from HFD-fed aged mice are engulfed by BV2 microglia at a faster rate than synaptic neurosomes isolated from chow-fed aged mice, indicating that HFD signals at synapses. Our results suggest that it alters transmission and facilitates engulfment by microglia.
Consistent with this concept, we found a slight increase in complement proteins and a decrease in CD47 protein expression on synapneurosomes isolated from the hippocampus of older mice fed a HFD.
Interestingly, palmitate reduced phagocytosis of BV2 microglia, but only synapneurosomes isolated from chow-fed mice, and this effect was prevented by DHA pretreatment. Ta. Finally, we measured the effects of palmitate and DHA on mitochondrial function in both microglial and neuronal models using the Seahorse XFe96 Analyzer.
These data indicate that DHA pretreatment does not alleviate palmitate-induced mitochondrial respiration reduction in BV2 microglia and HippoE-14 neurons, suggesting that DHA acts downstream of mitochondrial function to exert a protective effect. This suggests that there is a possibility that
Taken together, this study provides evidence that DHA can ameliorate the negative effects of palmitate on various cellular functions of microglia and neuron-like cells.