Adipose tissue aging: pathophysiological and clinical aspects
Adipose tissue is one of the most spread tissues; it forms fat depots, varied in their structural and functional characteristics. Adipose tissue is plastic. During human’s life, it undergoes many changes and restructuring. With age, the proportion of different types of adipose tissue and the microenvironment of adipocytes change, including the stromal component, immune cells and the microcirculation. In addition, energy storage strategies differ between younger and older adults. A redistribution of adipose tissue into visceral depots is observed even in patients with adequate body mass index. These changes aggravate metabolic disorders and contribute to insulin resistance. Along with increased proinflammatory potential and endothelial dysfunction, aging of adipose tissue increases the risk of cardiovascular outcomes. At the same time, the described changes are also observed in obesity, even in relatively young patients. It is assumed that the peculiarities of lipid accumulation due to adipocyte hypertrophy entail the development of dysfunction of adipose tissue, which is reflected in changes in its cytokine and hormonal profile. Such pathological processes are characteristic of the so-called “metabolically unhealthy” obesity.This review provides current knowledge about the changes that different types of adipose tissue undergo over time, as well as the connection between pathophysiological processes and clinical manifestations observed with aging and dysfunction of adipose tissue.
Authors
- Г. В. Семикова (ORCID: https://orcid.org/0000-0003-0791-4705)
- А. Р. Волкова (ORCID: https://orcid.org/0000-0002-5189-9365)
- Yu. Sh. Khalimov (ORCID: https://orcid.org/0000-0002-7755-7275)
Institutions
- First Pavlov State Medical University of St. Petersburg (RU)
Publication Details
- Journal
- Obesity and metabolism
- Published
- 2025-05-24
- DOI
- https://doi.org/10.14341/omet13069
- Primary Topic
- Adipose Tissue and Metabolism
- Type
- article
- Field-Weighted Citation Impact
- 0.00