Abstract
Glycation stress (glycative stress) is a general concept of biological stress caused by a series of non-enzymatic glycation reactions, including advanced glycation end products (AGEs) formation, AGEs accumulation, glycation-associated dysfunction of proteins and cellular signaling, inflammation, oxidation, and/or tissue damage. There has been increasing evidence supporting a profound effect of AGEs on human diseases such as type 2 diabetes, cardiovascular disease, cancer, Alzheimer’s disease, osteoporosis, and dementia, as well as aging process itself. In addition, dietary AGEs intake has also been suggested to contribute to tissue dysfunction and development of the diseases. Skeletal muscle is the largest organ in the human body and important responsibility for maintaining our health as not only locomotor system but also metabolic and endocrine systems. Especially in past decades, numerous studies have suggested the contribution of glycation stress to skeletal muscle dysfunctions (e.g. muscle atrophy, reducing contractile property, and insulin resistance). In this chapter, we provide current evidence on the potential role of glycation stress in the impairment of skeletal muscle functions.
Highlights
Skeletal muscle is the largest organ in the human body, accounting for approximately 40% of body weight
Pinto-Junior et al [58] showed that injection of glycolaldehyde-derived advanced glycation end products (AGEs) (20 mg/kg/day) to rat for 12 weeks led to whole-body insulin resistance and decreased glucose transporter 4 (GLUT4) mRNA and protein levels in skeletal muscle
Increased signal transducer and activator of transcription 3 (STAT3) Tyr705 phosphorylation and decreased extracellular signal-regulated kinase (ERK) Thr202/Tyr204 phosphorylation were confirmed in the skeletal muscles of mice treated with a diet high in AGEs for 16 weeks. These results suggest that systemic AGEs modulate cellular signaling transduction pathways, such as STAT3 and insulin/insulin-like growth factor 1 (IGF-1) signaling, and thereby contribute to the impairment of skeletal muscle growth and development
Summary
Skeletal muscle is the largest organ in the human body, accounting for approximately 40% of body weight. It has recently been found that skeletal muscle is a secretary organ that produces and releases cytokines and other peptides, which is known as myokine, that function in manner similar to hormones [1]. After the age of 50, approximately 1–2% of muscle mass and 1.5–5% of muscle strength are lost per year [3]. These reductions in muscle mass, strength, and function, the so-called sarcopenia, link to numerous adverse consequences including frailty, disability, morbidity, and mortality [2]. We provide current evidence on the potential role of glycation stress in the impairment of skeletal muscle functions
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