Severe energy deficit up-regulates leptin receptors, leptin signaling and PTP1B in human skeletal muscle

In obesity, leptin receptors (OBR) and leptin signaling in skeletal muscle are down-regulated. To determine whether OBR and leptin signaling are up-regulated with a severe energy deficit fifteen overweight men were assessed before (PRE), after 4 days of caloric restriction (3.2 Kcal/kg BW/day) in combination with prolonged exercise (CRE) (8h walking + 45min single-arm cranking/day) to induce an energy deficit of ~5500 Kcal/d, and following 3 days of control diet (isoenergetic) and reduced exercise (CD). During CRE, the diet consisted solely of whey protein (n=8) or sucrose (n=7) (0.8 g/kg BW/day). Muscle biopsies were obtained from the exercised and the non-exercised deltoid muscles, and from the vastus lateralis. From PRE to CRE, serum glucose, insulin, and leptin were reduced. OBR expression was augmented in all examined muscles associated to increased maximal fat oxidation. Compared to PRE, after CD phospho-Tyr¹¹⁴¹OBR, phospho-Tyr⁹⁸⁵OBR, JAK2, and phospho-Tyr^1007/1008JAK2 protein expression were increased in all muscles, while STAT3 and phospho-Tyr705STAT3 were increased only in the arms. The expression of PTP1B in skeletal muscle was increased by 18 and 45%, after CRE and CD, respectively (P<0.05). SOCS3 tended to increase in the legs and decrease in the arm muscles (ANOVA interaction P<0.05). Myosin heavy chain I isoform was associated with OBR protein expression (r=-0.75), phospho-Tyr⁹⁸⁵OBR (r=0.88) and phospho-Tyr⁷⁰⁵STAT3 /STAT3 (r=0.74). In summary, despite increased PTP1B expression, skeletal muscle OBRs and signaling are up-regulated by a severe energy deficit with greater response in the arm than in the legs likely due to SOCS3 up-regulation in the leg muscles.

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