Summary: High-fat foods induce hyperalgesic priming, a neurological change that represents the transition from acute to chronic pain, and allodynia, or pain, induced by normally non-painful stimuli.

Source: UT Dallas

A new study in mice by researchers at the University of Texas at Dallas suggests that short-term exposure to a high-fat diet can be linked to pain in the absence of pre-existing conditions such as obesity or obesity. Diabetes.

The study was published in the journal September 1 Scientific reportsComparing the effects of eight weeks of different diets on two groups of rats.

One group received regular chow, while the other received a diet that did not promote obesity or elevated blood sugar, both of which can cause diabetic neuropathy and other types of pain.

The researchers found that the high-fat diet induced hyperalgesic priming — a neurological change that signals the transition from acute to chronic pain — and allodynia, which is pain caused by stimuli that normally do not cause pain.

“This study shows you don’t need to be obese; you don’t need diabetes; you don’t need pathology or injury at all to trigger pain,” said Dr. Michael Burton, assistant professor of neuroscience in the School of Behavioral and Brain Sciences and co-author of the paper.

“It’s enough to eat a high-fat diet for a short period of time — a diet similar to what all of us in the United States ate at one time.”

The study also compared obese, diabetic mice with those that underwent a dietary change.

“Surprisingly, it became clear that there was no underlying pathology or obesity. All you need is nutrition,” Burton said. “This is the first study to show the effect of a short-term high-fat diet on allodynia or chronic pain.”

Western diets are high in fat—especially saturated fat, which has proven to be responsible for an epidemic of obesity, diabetes, and related diseases.

Individuals who eat high amounts of saturated fat, such as butter, cheese, and red meat, have large amounts of free fatty acids circulating in their blood, causing inflammation in the system.

Recently, scientists have shown that these high-fat foods increase the mechanical pain in the absence of obesity, and may aggravate pre-existing conditions or hinder recovery from injuries.

But no studies have clarified how high-fat foods alone can act as a trigger for pain, rather than non-painful stimuli, such as light touch on the skin, Burton said.

“We’ve seen in the past that only a subset of people or animals experience allodynia in diabetes or obesity, and if they do, it varies across the spectrum and it’s not clear why,” said Burton. We assumed there must be other triggering factors.

Burton and his team looked for saturated fatty acids in the blood of mice fed a high-fat diet. A type of fatty acid called palmitic acid, the most common saturated fatty acid in animals, binds to receptors on nerve cells, a process that causes inflammation and mimics damage to nerve cells.

“The metabolites in the diet cause inflammation before we see the development of pathology,” Burton said.

This shows the burger.
The researchers found that the high-fat diet induced hyperalgesic priming — a neurological change that signals the transition from acute to chronic pain — and allodynia, which is pain caused by stimuli that normally do not cause pain. The image is in the public domain.

“The diet itself caused symptoms of nerve damage. Now that we see that it is the sensory neurons that are affected, how is this happening? We found that if you take the receptor that palmitic acid binds to, you don’t see that excitatory effect on those neurons. That suggests there is a way to block it medicinally.

Burton says the next step will be to focus on neurons – how they are activated and how damage to them can be reversed. It is part of a larger effort to better understand the transition from acute to chronic pain.

“The mechanism behind this shift is important because chronic pain — from any source — is fueling the opioid epidemic,” he said.

“If we can figure out a way to prevent the transition from acute to chronic disease, it will do a lot of good.”

Burton said he hopes his research will encourage health care professionals to consider the role diet plays in influencing pain.

“The biggest reason we do this kind of research is because we want to fully understand our physiology,” he said.

“Now, when a patient goes to the clinic, they treat the symptoms based on the underlying disease or condition. Perhaps we should pay more attention to how the patient got there: the patient has inflammation caused by diabetes or obesity; Has a bad diet made you sicker than you realized? That’s a change.”

watch out

This shows the belly of a pregnant woman

Co-authors of the study were Calvin D. Ung, an assistant professor in Burton’s Neuroimmunology and Behavior Lab, and Jessica A. Tierney is now an MD/Ph.D. student at the UT Medical Branch in Galveston. Cognitive and neuroscience doctoral student and Eugene McDermott graduate Melissa E. Lennert and Terry Scholar alumna Marissa Williams also contributed.

About this disease and nutrition research news

Author: Press office
Source: UT Dallas
Contact: Press Office – UT Dallas
Image: The image is in the public domain.

Preliminary study: Open Access.
A high-fat diet causes mechanical allodynia in the absence of injury or diabetes pathology” by Jessica A. Tierney et al. Scientific reports


A high-fat diet causes mechanical allodynia in the absence of injury or diabetes pathology

Understanding the interactions between diet, obesity, and diabetes is important to tease out the mechanisms underlying trauma pathology. The Western diet is rich in fat, which produces large amounts of circulating bioactive metabolites.

However, no studies have evaluated how a high-fat diet (HFD) alone can sensitize a person with obesity or diabetes to non-painful stimuli.

To investigate this, we tested the ability of HFD to induce diet-induced hyperalgesic priming or food sensitization in male and female rats.

Our results showed that 8 weeks of HFD did not change baseline pain sensitivity, but both male and female HFD-fed animals showed stronger mechanical allodynia when exposed to subdermal doses of intraplantar Prostaglandin E.2 (PGE2) compared to mice on a chow diet.

Furthermore, calcium imaging increased the percentage of HFD capsaicin-responsive neurons in primary sensory neurons of both sexes compared with their chow counterparts. Immunohistochemistry (IHC) showed HFD-induced upregulation of ATF3, a marker of nerve damage, in the lumbar dorsal root ganglia (DRG). This suggests that HFD induces allodynia through feeding bodies in the absence of a preexisting condition or injury.

With this new understanding of how HFD contributes to pain relief, we can develop pharmacological interventions to effectively treat obesity and diabetes-related comorbidities.

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