Senescent adipocytes and type 2 diabetes – current knowledge and perspective concepts

Abstract

Among civilization diseases, the number of individuals suffering from type 2 diabetes (T2DM) is expected to increase to more than a billion in less than 20 years, which is associated with, e.g., populational aging, poor diet, sedentary lifestyle, genetic predispositions, and immunological factors. T2DM affects many organs and is characterized by insulin resistance, high glucose levels, and adipocyte dysfunction, which are related to senescence. Although this type of cellular aging has beneficial biological functions, it can also act unfavorable since senescent adipocytes resist apoptosis, enhance cytokine secretion, downregulate cell identity genes, and acquire the senescence-associated secretory phenotype that renders a more oxidative environment. Opposing T2DM is possible via a wide variety of senotherapies, including senolytics and senomorphics; nevertheless, further research is advised to expand therapeutic possibilities and benefits. Consequences that ought to be deeply researched include secretory phenotype, chronic inflammation, increasing insulin resistance, as well as impairment of adipogenesis and functioning of adipocyte cells. Herein, despite reviewing T2DM and fat tissue senescence, we summarized the latest adipocyte-related anti-diabetes solutions and suggested further research directions.

Red Oranges and Olive Leaf Waste-Derived Bioactive Extracts Promote Adipocyte Functionality In Vitro

“…Sustained positive energy balance prompts the enlargement of present adipocytes (hypertrophy) and/or a rise in the number of pre-adipocytes and adipocytes (hyperplasia) to accommodate surplus energy consumption [ 23 ]. When these alterations become significantly pronounced and unmanageable, dysfunction may result in insulin resistance not only within adipose tissue but also in the liver, muscles, and pancreas [ 22 ]. Dysfunctional adipocytes produce and release cytokines, including IL-6, tumor necrosis factor α (TNFα), and monocyte chemoattractant protein 1 (MCP-1), which trigger inflammation within adipose tissue, thereby promoting cellular aging, a process also known as cell senescence.…”

“…Chronic inflammation and dysregulation of cytokine signaling can lead to irregu ities in the deposition of fat and energy metabolism [22]. Sustained positive energy ance prompts the enlargement of present adipocytes (hypertrophy) and/or a rise in number of pre-adipocytes and adipocytes (hyperplasia) to accommodate surplus ene Interestingly, the preliminary results obtained following erastin treatment on differentiated adipocytes showed no cytotoxic effect compared to pre-adipocytes.…”