The two faces of reactive oxygen species (ROS) in adipocyte function and dysfunction

Abstract

White adipose tissue (WAT) is actively involved in the regulation of whole-body energy homeostasis via storage/release of lipids and adipokine secretion. Current research links WAT dysfunction to the development of metabolic syndrome (MetS) and type 2 diabetes (T2D). The expansion of WAT during oversupply of nutrients prevents ectopic fat accumulation and requires proper preadipocyte-to-adipocyte differentiation. An assumed link between excess levels of reactive oxygen species (ROS), WAT dysfunction and T2D has been discussed controversially. While oxidative stress conditions have conclusively been detected in WAT of T2D patients and related animal models, clinical trials with antioxidants failed to prevent T2D or to improve glucose homeostasis. Furthermore, animal studies yielded inconsistent results regarding the role of oxidative stress in the development of diabetes. Here, we discuss the contribution of ROS to the (patho)physiology of adipocyte function and differentiation, with particular emphasis on sources and nutritional modulators of adipocyte ROS and their functions in signaling mechanisms controlling adipogenesis and functions of mature fat cells. We propose a concept of ROS balance that is required for normal functioning of WAT. We explain how both excessive and diminished levels of ROS, e.g. resulting from over supplementation with antioxidants, contribute to WAT dysfunction and subsequently insulin resistance.

Adipose Mitochondrial Respiratory Capacity in Obesity is Impaired Independently of Glycemic Status of Tissue Donors

“…Nonetheless, from a clinical point of view, reduced adipocyte OXPHOS capacity in sc adipose tissue, in spite of unaltered ATP production maintained via glycolysis, could occur in parallel with mitochondrial reactive oxygen species (ROS) production caused by disturbances in electron transport chain complex formation . Increased ROS could lead to a low‐grade inflammatory environment, representing a potential link between mitochondrial dysfunction in adipose tissue and the manifestation of comorbidities . Furthermore, ROS can stimulate glucose uptake and inhibit respiration in adipocytes , which could be an explanation for the high glycolytic and low respiratory rates of adipocytes from individuals with obesity that were observed in our study.…”

Strawberry and Achenes Hydroalcoholic Extracts and Their Digested Fractions Efficiently Counteract the AAPH-Induced Oxidative Damage in HepG2 Cells

“…In the last decades, oxidative stress has been recognized as one of the determining factors in the development and progression of most chronic noncommunicable diseases, including cardiovascular diseases, type 2 diabetes, and cancer [25,26]. …”

Happily (n)ever after: Aging in the context of oxidative stress, proteostasis loss and cellular senescence

“…“A disturbance in the pro-oxidant-antioxidant balance in favor of the former”, this was how oxidative stress was initially viewed, and known to promote damage in different cellular constituents [37]. However, it should be kept in mind, that recent insights on specific redox regulatory effects of oxidants support the idea that, when balanced, ROS play an important role in signal transduction cascades enhancing or suppressing cellular fates such as proliferation or differentiation [37], [38]. Recently, Sies reviewed and altered his own definition to “A disturbance in the prooxidant-antioxidant balance in favor of the former leading to a disruption in redox signaling” [37].…”