Mini Oral ANZOS-OSSANZ-AOCO Joint Annual Scientific Meeting 2017

Impaired of inflammatory cell recruitment was one of the key factors for attenuating muscle regeneration in obese mice fed with high-fructose diet (#193)

Yen-Hui Chiu 1 , Yu-Ning Liu 1 , Hung-Yu Chien 2 , Wan-Chun Li 3
  1. Department of Education and Research, Taipei City Hospital, Taipei, Taiwan
  2. Department of Endocrinology & Metabolism, Taipei City Hospital, Taipei, Taiwan
  3. Institute of Oral Biology, School of Dentistry, National Yang-Ming University, Taipei, Taiwan


The quality and quantity of skeletal muscles are particularly important; not only for maintaining normal physiological functions, but also for preventing the individuals from insulin resistance. Moreover, obese individuals often demonstrated abnormal wound healing associated with immune dysfunction. We therefore analyzed the inflammatory cell infiltration during muscle regeneration in mice fed with high fructose corn syrup.

Materials and methods:

C57BL6/J mice were received ad libitum either with standard chow with water (NC) or with 10% high fructose corn syrup added in the drinking water (HFr) at 8-10 weeks of age. After 20 weeks of feeding, snake myotoxin was injected to the left tibialis anterior of the mice and left the right muscle as non-injured control. The ability of satellite cell activation, as well as inflammatory response were addressed by morphological and immunostaining assays.


After 20 weeks of feeding, body weight of HFr mice increased by 25% (41.2 ± 0.6 g) compared to that of the NC group (32.8 ± 1.6 g) with relatively normal blood glucose level (116 ± 9.5 vs. 111 ± 10.2 mg/dL). At day 3 post injury, there is no difference in the number of MyoD+ cells in HFr mice but dramatically reduced the number of inflammatory cells recruited compared to that of the NC controls. After 7 days of injury, the inflammatory cells were significantly accumulated in damaged muscle and prolonged desmin expression in regenerating fibers in HFr mice while the muscle of NC mice had been replaced by regenerated muscles with low desmin expression.


The early activation of satellite cell was not hindered in obese mice while inflammatory cell infiltration was dramatically reduced. We hypotheses the muscle of obese individuals fail to secret significant amount of cytokines to recruit inflammatory cells to the site of injury leading to attenuation of muscle regeneration.