The interplay between obesity, immunosenescence, and insulin resistance

Abstract

Obesity, which is the accumulation of fat in adipose tissue, has adverse impacts on human health. Obesity-related metabolic dysregulation has similarities to the metabolic alterations observed in aging. It has been shown that the adipocytes of obese individuals undergo cellular aging, known as senescence. Senescence can be transmitted to other normal cells through a series of chemical factors referred to as the senescence-associated secretory phenotype (SASP). Most of these factors are pro-inflammatory compounds. The immune system removes these senescent T-cells, but immunosenescence, which is the senescence of immune cells, disrupts the clearance of senescent T-cells. Immunosenescence occurs as a result of aging or indirectly through transmission from senescent tissues. The significant occurrence of senescence in obesity is expected to cause immunosenescence and impairs the immune response to resolve inflammation. The sustained and chronic inflammation disrupts insulin's metabolic actions in metabolic tissues. Therefore, this review focuses on the role of senescent adipocyte cells in obesity-associated immunosenescence and subsequent metabolic dysregulation. Moreover, the article suggests novel therapeutic approaches to improve metabolic syndrome by targeting senescent T-cells or using senotherapeutics. Graphical Abstract

Anthocyanins and Type 2 Diabetes: An Update of Human Study and Clinical Trial

“…Evidence from numerous investigations has shown that elevated levels of reactive oxygen species (ROS) in the bloodstream resulting from deposited fat have been linked to activating insulin resistance (IR) in various adipose tissues and skeletal muscles [ 58 , 61 ]. IR is a common feature of type 2 diabetes, and resistance occurs long before the onset of the disease.…”

“…In diabetic patients, daily supplementation with 320 mg of ACNs was found to inhibit the expression of proinflammatory factors related to NF-κB pathways, including TNF-α, IL-6, and IL-18 [ 71 ]. At the cellular level, the activated transcription factor NF-κB induced the activity of TNF-α and the interleukins, thereby altering insulin sensitivity [ 46 , 61 ]. Therefore, the use of anthocyanin, which has been shown to have positive effects on the process of inflammation, may contribute to the development of treatment approaches focused on inhibiting NF-κB.…”

Correction: The interplay between obesity, immunosenescence, and insulin resistance

“…Following publication of the original article [ 1 ], the authors reported a typo found in the graphical abstract, the word “inflamation “ needs to be corrected to “inflammation “. The corrected graphical abstract is presented below.…”