Neural regulation of hindlimb muscle contraction-induced glucagon-like peptide-1 and peptide YY secretion in rats

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  • Ueda Shin-ya
    Graduate School of Health Sciences, Morinomiya University of Medical Sciences
  • Nakahara Hidehiro
    Graduate School of Health Sciences, Morinomiya University of Medical Sciences
  • Manabe Kou
    Graduate School of Health Sciences, Morinomiya University of Medical Sciences
  • Miyamoto Tadayoshi
    Graduate School of Health Sciences, Morinomiya University of Medical Sciences

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The physiological mechanisms underlying the increases observed in glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) plasma levels with exercise currently remain unknown. Previous studies reported that increases in plasma GLP-1 and PYY concentrations were mediated by a neural pathway, regardless of exercise. Therefore, we investigated the neural regulation of GLP-1 and PYY secretion during exercise in rats using a hindlimb muscle contraction model. Hindlimb muscle contraction was induced by electrically stimulating the sciatic nerve for 20 min (5 V, 5 Hz). A fasting arterial blood sample (Baseline) was taken. Rats were subjected to 20 min of hindlimb muscle contraction in vivo, and blood samples were collected at the end of the hindlimb muscle contraction protocol. Although GLP-1 and PYY levels were significantly increased after hindlimb muscle contraction (P < 0.001, respectively), no significant differences were observed in GLP-1 or PYY levels between sham and vagotomy trials. On the other hand, GLP-1 and PYY levels after hindlimb muscle contraction were significantly lower in the sciatic nerve deafferentation trial than in the sham trial (P < 0.01, respectively). These results indicate that the increases observed in GLP-1 and PYY plasma levels with exercise were mediated by the activation of skeletal muscle-derived afferent neurons, and not by mechanisms through the neural pathway of the vagus nerve.

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