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Whether Leptin Levels are Associated with Ectopic Inflammation

As aging, chronic inflammation can cause sarcopenia. Previous studies have suggested that the accumulation of adipose tissue in skeletal muscle, referred to as intermuscular adipose tissue (IMAT), increases with age and is associated with inflammation. However, the mechanism governing ectopic inflammation in skeletal muscle due to aging is not fully understood. Leptin, an adipocytokine derived from adipose tissue, is an important mediator of inflammatory processes.
Sarcopenia is the reduction in skeletal muscle mass and function with age, and is a major public health concern. The sarcopenia-related morbidity rate is 5-13% in 60 to 70-year-old individuals, and 11-50% in those above 80 years old. Sarcopenia can lead to a rise in the incidence of falls and the risk of fractures in the elderly, and is therefore linked to physical disability, and increased mortality, morbidity, and health care costs . Although a number of factors are implicated in the pathophysiology of sarcopenia, its pathophysiology remains elusive. So some researchers examined changes in leptin levels with age and whether leptin contributes to ectopic inflammation.
To evaluate ectopic inflammation in skeletal muscle, researchers measured alterations to the expression of inflammatory cytokine genes (IL1B, IL6, and Tnfa) and muscle break down-related gene (MuRF1 and Atrogin1) in the quadricep muscles of young (10 weeks) and aged (48 weeks) female rats using quantitative reverse-transcription polymerase chain reaction (Q-RT-PCR). Histological examination was performed to identify the extent of IMAT. Leptin mRNA and leptin protein expression were examined using Q-RT-PCR and enzyme-linked immunosorbent assay, respectively. The effect of leptin on the mRNA expression of Il1b, Il6, and Tnfa in quadricep muscle-derived cells was also examined by stimulating the cells with 0 (control), 1, or 10 μg/mL rat recombinant leptin using Q-RT-PCR. Then the experiment result shows that aged rats had significantly higher IL6, MuRF1, and Atrogin1 but not IL1b and Tnfa, expression and greater levels of IMAT in their quadricep muscles than young rats. Aged rats also had significantly higher leptin expression and leptin protein concentration in their quadricep muscles than young rats. The addition of exogenous leptin to quadricep muscle-derived cells significantly increased the gene expression of Il1b and Il6 but not Tnfa.
Their results suggest that elevated leptin levels due to aging cause ectopic inflammation through IL-6 in the skeletal muscle of aged rats.
 

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