Why the study?
Understanding adipose tissue dysfunction in obesity may clarify the mechanisms driving metabolic dysfunction and accelerated aging processes.
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Design
Review
Obesity shares aging-like phenotypes; hypothesis-generating for shared pathways without current practice implications.
Obesity is associated with an increased risk of acute and chronic diseases, including hypertension, stroke, myocardial infarction, cardiovascular disease, diabetes, cancer, and reduces life expectancy by up to 20 years, increasing the risk of premature death. It has been shown that the metabolic changes associated with obesity are similar to those observed with aging. Thus, obesity and aging have a similar range of phenotypes, such as impaired genome integrity, mitochondrial function, accumulation of intracellular macromolecules, weakened immunity, and systemic inflammation. The commonality of mechanisms may underlie the acceleration of aging processes, both at the molecular and systemic levels. Thus, understanding the mechanisms of adipose tissue dysfunction in obesity can provide insight into the processes that contribute to the metabolic dysfunction associated with the aging process. The current review will examine the molecular and cellular mechanisms that underlie obesity and aging, and how obesity can activate the aging process, initiating the early onset of aging-associated chronic diseases.
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Dyleva et al. (2023) studied this question.
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