Abstract
Adipose tissue metabolism is closely linked to insulin resistance, and differential fat distributions are associated with disorders like hypertension, diabetes, and cardiovascular disease. Adipose tissues vary in their impact on metabolic risk due to diverse gene expression profiles, leading to differences in lipolysis and in the production and release of adipokines and cytokines, thereby affecting the function of other tissues. In this paper, the roles of the various adipose tissues in obesity are summarized, with particular focus on mitochondrial function. In addition, we discuss how a functionally mitochondrial-targeted compound, the modified fatty acid tetradecylthioacetic acid (TTA), can influence mitochondrial function and decrease the size of specific fat depots.
Highlights
In a modern lifestyle people are chronically exposed to elevated amounts of lipids and nutrients, potentially leading to tissue dysfunction and disease [1]
While most of the genes involved in lipolysis, fatty acid β-oxidation, mitochondrial biosynthesis, and immune response were unchanged by tetradecylthioacetic acid (TTA) in all studied adipose tissues, Ucp1 was highly increased at the mRNA level in epididymal and mesenteric depots [123]
The different adipose depots have specific roles based on their level of lipolysis and rate of TG storage
Summary
In a modern lifestyle people are chronically exposed to elevated amounts of lipids and nutrients, potentially leading to tissue dysfunction and disease [1]. The adipose tissue is highly involved in the development of metabolic disorders such as cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM) It is the body’s largest storage site for triglycerides and plays an important role as an endocrine organ in energy homeostasis [2]. Adipose tissue inflammation due to the recruitment of T-cells and macrophages has been shown to contribute to insulin resistance in obese individuals This inflammation leads to a disturbed adipokine-balance and an uncontrolled release of free fatty acids and inflammatory cytokines [6]. The adipocyte size increases (hypertrophy), and they are eventually unable to store excess lipids even with enhanced adipocyte proliferation (hyperplasia) This redirects fatty acids to the liver promoting dyslipidemia, characterized by elevated plasma FFA, triglycerides (TGs), and small dense lowdensity lipoprotein (LDL), and the reduction of high-density lipoproteins (HDLi). Pharmacological treatments that target mitochondria have great potential in the treatment of obesity-related disorders, and their differential effect on adipose depots will be discussed
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