- People who are obese have a higher risk of developing insulin resistance and type 2 diabetes than people who are of a healthy weight.
- However, the conditions that lead to insulin resistance do not affect all obese people.
- Scientists are now investigating why some people are able to stay healthy while others have not discovered that adipose (fat) tissue can affect cell function.
- Their research in mouse models suggests that in some individuals, obesity inhibits the ability of macrophages to clear cellular debris, leading to inflammation and metabolic disorders.
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Obese people are
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obesity
However, many obese patients do not develop these symptoms, and scientists at the University of Gothenburg in Sweden may have discovered why some people are more likely to progress to metabolic disorders than others. be.
In a study on mice, researchers found that in some people, fat tissue interferes with the function of white blood cells called macrophages, making them unable to clear away collagen fragments.
This can cause inflammation and increase the likelihood of type 2 diabetes.
This research PNAS.
Genetic engineer Sebnem Anluisler from the London Institute of Regeneration, who was not involved in the study, commented: Today’s medical news:
“This study adds to the growing body of evidence highlighting the complex interplay between obesity, adipose tissue dysfunction, and metabolic disease. Understanding the mechanisms underlying these relationships will help improve type 2 This is critical to developing more effective strategies to prevent and treat conditions like diabetes.”
In this study, researchers fed seven-week-old mice a high-fat diet for one week, which resulted in a significant increase in adipose tissue compared to control mice fed a normal diet.
In mice fed a high-fat diet, more type 1 collagen was broken down into fragments and the number of macrophages in adipose tissue increased. These macrophages removed collagen fragments.
However, in obese, insulin-resistant male mice induced by a high-fat diet, macrophages were unable to remove the fragments and instead triggered an inflammatory response.
The researchers concluded that collagen fragments are not inactive metabolites, but simply markers of tissue remodeling, but alter the microenvironment within adipose tissue.
Professor Ingrid Wernsted Asterholm, corresponding author and research leader from the Department of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden, said: MNT:
“We are not 100% sure why macrophages are unable to take up fragmented collagen, but our data suggest that too high levels of nutrients promote this. We showed that when these macrophages become dysfunctional, they accumulate fragments in adipose tissue, and such fragments can cause inflammation and exacerbate adipose tissue dysfunction.”
“Dysfunctional adipose tissue cannot effectively store excess nutrients, resulting in harmful fat deposits in areas such as the liver. […] This can lead to systemic insulin resistance and ultimately metabolic disorders such as type 2 diabetes,” she continued.
Researchers saw similar effects in vitro when they treated human macrophages with palmitate, high glucose, and high insulin to mimic conditions that lead to obesity.
Professor Wernstead Asterholm said: “We found that human macrophages have similar functions and regulation. Our current research focuses on translating our findings in mice to the human environment, and so far It looks promising. We also want to know if and how this macrophage-collagen axis plays a role in other tissues, such as the heart.”
“Dysregulation of adipose tissue function, characterized by changes in collagen turnover and macrophage activity, is thought to be involved in the development of metabolic diseases. By understanding the specific cellular and molecular mechanisms involved, , could lead to new therapeutic strategies to manage these symptoms,” said Ann Ruisler.
The researchers behind this study found that isolated human cells responded similarly to mouse cells, but they would like further research to confirm that similar fat dysfunction occurs in humans. said Ann Lewisler.
“Results from animal studies can provide valuable insights, but care must be taken when applying them to humans. There are similarities between mice and humans, but there are potential implications for the interpretation of findings. “There are also some differences. Further studies in humans are needed to confirm these results,” she said. MNT.
And, as Professor Asterholm pointed out, the researchers said they were planning further research into both the treatment and diagnosis of type 2 diabetes.
“Hopefully, we will be able to identify macrophage targets that can be used to develop better treatments. However, in the nearer future, certain collagen fragments from adipose tissue will eventually enter the circulation and thereby It may be possible to use it as a biomarker to identify individuals who are at increased risk of developing type 2 diabetes. ”
Although still in its early stages, this study adds to evidence that obesity can lead to adipose tissue dysfunction and metabolic disease, and provides an explanation for why this occurs. It could help identify people at high risk for type 2 diabetes and could also help develop more effective treatments.
