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High-fat diet may cause pain sensitivity without obesity or diabetes

Summary: High-fat diets induce hyperalgesic priming, a neurological change that represents the transition from acute pain to chronic pain, and allodynia or pain resulting from stimuli that do not normally cause pain.

Source: UT Dallas

A new mouse study by researchers at the University of Texas at Dallas suggests that short-term exposure to a high-fat diet may be linked to feelings of pain even in the absence of previous injury or pain. a pre-existing condition such as obesity or diabetes.

The study, published September 1 in the journal Scientific reportscompared the effects of eight weeks of different diets on two cohorts of mice.

One group received normal food, while the other received a high-fat diet in a way that did not precipitate the development of obesity or hyperglycemia, two conditions that can lead to diabetic neuropathy. and other types of pain.

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

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

“A high-fat diet for a short time is enough, a diet similar to what almost all of us eat in the United States at some point.”

The study also compared obese and diabetic mice to those that had just undergone dietary changes.

“It became surprisingly clear that you don’t need an underlying pathology or obesity. You just needed the diet,” Burton said. “This is the first study to demonstrate the influential role of short exposure to a high-fat diet on allodynia or chronic pain.”

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

People who eat large amounts of saturated fat, such as butter, cheese, and red meat, have large amounts of free fatty acids circulating in their bloodstream which, in turn, induce systemic inflammation.

Recently, scientists have shown that these high-fat diets also increase existing mechanical pain sensitivity in the absence of obesity, and may aggravate pre-existing conditions or impede recovery from injury.

No study, however, has clarified how sensitizing high-fat diets alone can be in inducing pain from nonpainful stimuli, such as light touch to the skin, Burton said.

“We’ve seen in the past that in models of diabetes or obesity, only a subsection of people or animals has allodynia, and if so, it varies on a spectrum, and we don’t know why,” Burton said. . “We hypothesized that there must be other precipitating factors.”

Burton and his team looked for saturated fatty acids in the blood of mice fed a high-fat diet. They found that a type of fatty acid called palmitic acid – the most common saturated fatty acid in animals – binds to a particular receptor on nerve cells, a process that leads to inflammation and mimics damage to neurons. .

“Metabolites in the diet cause inflammation before pathology develops,” Burton said.

The researchers found that the high-fat diet induced hyperalgesic priming – a neurological change that represents the transition from acute pain to chronic pain – and allodynia, which is pain resulting from stimuli that do not normally cause pain. . Image is in public domain

“The diet itself caused markers of neuronal damage. Now that we see that it’s the sensory neurons that are affected, what happens? We found that if you take away the receptor that palmitic acid binds to , you don’t see this sensitizing effect on these neurons. This suggests that there is a way to block it pharmacologically.

Burton said the next step will be to focus on the neurons themselves, how they are activated and how injuries can be reversed. This is part of a larger effort to better understand the transition from acute pain to chronic pain.

“The mechanism behind this transition is important because it is the presence of chronic pain – whatever the source – that is fueling the opioid epidemic,” he said.

“If we find a way to prevent this transition from acute to chronic, it could do a lot of good.”

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

“The main reason we do research like this is because we want to completely understand our physiology,” he said.

“Now when a patient comes to a clinician they are treating a symptom, based on an underlying disease or condition. Maybe we need to pay more attention to how the patient got there: Does the patient have inflammation induced by diabetes or obesity?Has a terrible diet made them more sensitive to pain than they thought?That would be a paradigm shift.

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The study’s co-senior authors are Calvin D. Uong, lab assistant in Burton’s Neuroimmunology and Behavior Laboratory, and Jessica A. Tierney, now MD/Ph.D. student at the medical branch of UT in Galveston. Melissa E. Lenert, PhD student in cognition and neuroscience and Eugene McDermott graduate fellow, and Marisa Williams, former Terry fellow, also contributed.

About this pain and diet research news story

Author: Press office
Source: UT Dallas
Contact: Press Office – UT Dallas
Image: Image is in public domain

Original research: Free access.
A high-fat diet causes mechanical allodynia in the absence of injury or diabetic pathology” by Jessica A. Tierney et al. Scientific reports


Summary

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

Understanding the interactions between diet, obesity and diabetes is important for unraveling the mechanisms of painful pathology. The Western diet is high in fat, producing large amounts of circulating bioactive metabolites.

However, no research has evaluated how a high-fat diet (HFD) alone can sensitize an individual to non-painful stimuli in the absence of obesity or diabetic pathology.

To investigate this, we tested the ability of an HFD to stimulate food-induced hyperalgesic priming or food sensitization in male and female mice.

Our results revealed that 8 weeks of HFD did not alter baseline pain sensitivity, but HFD-fed male and female animals exhibited robust mechanical allodynia when exposed to a subthreshold dose of intraplantar prostaglandin E. .2 (EGP2) compared to diet mice.

Additionally, calcium imaging in isolated primary sensory neurons of both sexes revealed that HFD induced an increased percentage of capsaicin-responsive neurons compared to their chow counterparts. Immunohistochemistry (IHC) showed HFD-induced upregulation of ATF3, a neuronal marker of injury, in lumbar thoracic root ganglia (DRG). This suggests that an HFD induces allodynia in the absence of a pre-existing condition or injury via dietary components.

With this new understanding of how an HFD can contribute to the onset of pain, we can understand the dissociation behind the comorbidities associated with obesity and diabetes to develop pharmacological interventions to treat them more effectively.

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