Age-Related Lifestyle Diseases Linked to Activity in Fat Cells
Health conditions such as high cholesterol, fatty liver, and diabetes are all illnesses, also known as 'lifestyle diseases.'
Regardless of how much an individual tries to delay or even fight it, aging will happen, and it is indeed a part of life. With age are health conditions, such as high cholesterol, fatty liver, and diabetes—illnesses also known as "lifestyle diseases."
Remarkably, a lot of these age-related illnesses are results of changes taking place inside the fat cells accountable for the excess energy storage, also known as adipocytes.
In a recent study published in Nature Communications, Osaka University researchers have unveiled how such changes result in the onset of lifestyle diseases, aiming to reverse the processes.
According to Tadashi Yamamuro, the study's lead author, adipocytes produce hormones and cytokines that control the other organs' function.
Changes in adipose tissue that are age-related, Yamamuro explained, lead to metabolic syndromes, which are closely linked to life-threatening cardiovascular diseases.
The lead author continued, "No one really knows what leads to adipocyte dysfunction in aged organisms."
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The Autophagy Process
The researchers shared that they decided to focus on the process in which the cells remove unwanted or malfunctioning cellular components known as autophagy.
Past research had shown that this process plays an essential role in preventing various age-related illnesses, and it is possibly involved in the process of aging. Autophagy is vital for healthy organs like the kidneys or liver, their functions, and longevity.
Yamamuro's team previously presented that Rubicon, a protein that hinders autophagy, is upregulated in aging tissues.
They then hypothesized that the said protein possibly gathers or mounts up in aged adipocytes, reducing the autophagic activity and serving as a contributor to the inception of metabolic orders.
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Autophagic Activity in Mice
Yamamuro also shared that they discovered that the levels of Rubicon were lowered in the aged mice's adipose, leading to a rise in autophagic activity.
To further study the underlying mechanism, the scientists devised a rodent line in which Rubicon was mainly deactivated in adipose tissues.
In Rubicon's absence, senior author Tamotsu Yoshimori said that the team observed extreme autophagy in adipocytes and a drop in its function.
Yoshimori added, "The mice established lifestyle diseases like diabetes and fatty liver." More so, the mice had considerably higher cholesterol levels despite being fed a similar diet as the control.
The researchers also continued to determine the particular proteins impacted by the increased autophagy levels.
Yoshimori explained that this is indeed, a thrilling finding with necessary therapy implications. And, since the age-reliant absence of Rubicon causes lifestyle illnesses via excess autophagy, preventing this absence in adipocytes may contribute to the prevention of these dominant and dangerous health conditions.
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Aug 18, 2020 11:46 PM EDT
