ISLAMABAD : According to the World Health Organisation (WHO) the number of people with obesity worldwide has tripled in the past 50 years. While the United States and Europe top the scale South East Asian and African countries are fast catching up.
People with obesity have a body mass index (BMI) of more than 30 although it must be remembered that BMI alone cannot determine whether that mass is made up of muscle or fatty tissue.
More usefully the WHO defines obesity as abnormal or excessive fat accumulation that presents a risk to health together with a BMI of more than 30.
Obesity increases the risk of several health conditions, which include high blood pressure high LDL (bad) cholesterol low HDL (good) cholesterol and high triglycerides sleep apnea and breathing problems coronary heart disease stroke some cancers type 2 diabetes.
However many people with obesity will not develop these conditions and scientists at the University of Gothenburg Sweden may have found a reason why some are more likely to progress to metabolic disorders than others.
Why do only some people with obesity develop diabetes?
In a mouse study, the researchers found that in some people adipose tissue disrupts the function of white blood cells called macrophages preventing them from cleaning up fragments of collagen. This may lead to inflammation increasing the likelihood of type 2 diabetes. The study is published in PNAS.
This study adds to a growing body of evidence highlighting the complex interplay between obesity adipose tissue dysfunction and metabolic disease. Understanding the mechanisms underlying these relationships is crucial for developing more effective strategies for preventing and treating conditions like type 2 diabetes. High fat diet leads to collagen breakdown:
Previous research found that excess adipose or fatty tissue can lead to activation of immune cells that cause inflammation and lead to insulin resistance.
For this study, the researchers placed 7 week old mice on a high fat diet for 1 week which resulted in a significant gain in adipose tissue compared with control mice fed a regular diet.
In the mice on the high fat diet more collagen type 1 was broken down into fragments and macrophage numbers in the adipose tissue increased. These macrophages cleared the collagen fragments. However, in high fat diet induced obese insulin resistant male mice the macrophages were unable to clear the fragments and instead caused an inflammatory reaction.
The researchers conclude that collagen fragments are not inert metabolites and solely markers of tissue remodeling but change the microenvironment within the adipose tissue. Dysfunctional adipose tissue leads to insulin resistance:
We are not 100% sure why the macrophages fail to take up fragmented collagen but our data suggest that too high levels of nutrients drive this. And when these macrophages fail there will be accumulation of fragments in adipose tissue and we show that such fragments trigger inflammation which may aggravate adipose tissue dysfunction.
Dysfunctional adipose tissue cannot effectively store excess nutrients which then leads to deleterious fat deposition in for example the liver, this will then lead to systemic insulin resistance that eventually can cause metabolic disorders such as type 2 diabetes she continued.
The 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.
Prof. Wernstedt Asterholm told us We show that human macrophages have similar function and regulation. Our current research focuses on translating our mouse findings to the human setting and it looks promising so far. I would also like to see whether and how this macrophage collagen axis plays a role in other tissues such as in the heart.
Potential for diabetes diagnosis and treatment:
Dysregulation of adipose tissue function characterized by altered collagen turnover and macrophage activity has been implicated in the pathogenesis of metabolic diseases. Understanding the specific cellular and molecular mechanisms involved could lead to novel therapeutic strategies for managing these conditions Unluisler told us.
Although the researchers behind this study found that isolated human cells reacted in a similar way to mouse cells Unluisler said that she would like to see further research to confirm that similar adipose dysfunction occurs in people.
While findings from animal studies can give us valuable insights we need to be cautious when applying them to humans. Mice and humans have similarities but also differences that might affect how findings translate. Further research with human subjects is necessary to confirm these results she told MNT.
And the researchers are planning more research into both treatment and diagnosis of type 2 diabetes as Prof. Asterholm noted
Hopefully, we will identify a macrophage target that can be used for developing better therapeutics... but in a more near future one could imagine that certain collagen fragments from adipose tissue end up in the circulation and thereby can be used as biomarkers to identify individuals that are at higher risk for developing type 2 diabetes. –Online
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