Ageing is a conserved biological process, modulated by intrinsic and extrinsic factors, that leads to changes in life expectancy. In humans, ageing is characterized by greatly increased prevalence of cardiometabolic disease, type 2 diabetes and disorders associated with impaired immune surveillance. Adipose tissue displays species-conserved, temporal changes with ageing, including redistribution from peripheral to central depots, loss of thermogenic capacity and expansion within the bone marrow. Adipose tissue is localized to discrete depots, and also diffusely distributed within multiple organs and tissues in direct proximity to specialized cells. Thus, through their potent endocrine properties, adipocytes are capable of modulating tissue and organ function throughout the body. In addition to adipocytes, multipotent progenitor/stem cells in adipose tissue play a crucial role in maintenance and repair of tissues throughout the lifetime. Adipose tissue may therefore be a central driver for organismal ageing and age-associated diseases. Here we review the features of adipose tissue during ageing, and discuss potential mechanisms by which these changes affect whole-body metabolism, immunity and longevity. We also explore the potential of adipose tissue-targeted therapies to ameliorate age-associated disease burdens.
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http://dx.doi.org/10.1038/s42255-024-01046-3 | DOI Listing |
Mol Biol Rep
January 2025
Department of Pharmaceutical Sciences & Technology, BIT Mesra, Ranchi, 835215, India.
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View Article and Find Full Text PDFArch Dermatol Res
January 2025
Department of Biomedical Engineering, Central Tehran Branch, Islamic Azad University, Tehran, Iran.
Although the role of low-level laser therapy (LLLT) and human adipose-derived stem cells (hADSC) in accelerating diabetic wound healing has been proven, their synergistic effect is still debated. This study aimed to evaluate the individual and combined effects of LLLT and hADSC on wound healing and on biomechanical parameters in type 2 diabetic rabbits. In this experimental study, 40 rabbits with type 2 diabetes (induced by streptozotocin (STZ)) were included.
View Article and Find Full Text PDFAging (Albany NY)
January 2025
Department of Pathology, Yale University School of Medicine, New Haven, CT 06519, USA.
Studies of the aging transcriptome focus on genes that change with age. But what can we learn from age-invariant genes-those that remain unchanged throughout the aging process? These genes also have a practical application: they can serve as reference genes in expression studies. Reference genes have mostly been identified and validated in young organisms, and no systematic investigation has been done across the lifespan.
View Article and Find Full Text PDFLife Metab
December 2024
Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Clinical Center for Diabetes, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai 200233, China.
Type 2 diabetes mellitus (T2DM) is closely associated with obesity, while interactions between the two diseases remain to be fully elucidated. To this point, we offer this perspective to introduce a set of new insights into the interpretation of T2DM spanning the etiology, pathogenesis, and treatment approaches. These include a definition of T2DM as an energy surplus-induced diabetes characterized by the gradual decline of β cell insulin secretion function, which ultimately aims to prevent the onset of severe obesity through mechanisms of weight loss.
View Article and Find Full Text PDFLife Metab
February 2025
Hubei Key Laboratory of Cell Homeostasis, Department of Biochemistry, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Wuhan University, Wuhan, Hubei 430072, China.
Graphical Abstract Lipoprotein lipase (LPL) mediates peripheral tissue triglyceride (TG) uptake. Hepatic ANGPTL3 (A3) and ANGPTL8 (A8) form a complex and inhibit LPL activity in the white adipose tissue (WAT) via systematic circulation. ANGPTL4 (A4) is expressed in WAT and inhibits LPL activity locally.
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