Femoral Artery Infusion of αMSH Increases Muscle Thermogenesis and Promotes Glucose Uptake in Ovariectomized Ewes

Figures

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  Figure 1.. The effect of femoral artery infusion of α-melanocyte–stimulating hormone (αMSH) (0.1 µg/h) or saline on (A) skeletal muscle heat production and (B) food intake. Peripheral infusion of αMSH increased (****P < .0001) muscle temperature in the vastus lateralis muscle of the infusion limb. On the other hand, food intake was similar in saline- and αMSH-treated animals. All data are presented as the mean ± SEM.

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  Figure 2.. The effect of femoral artery infusion of α-melanocyte–stimulating hormone (αMSH) (0.1 µg/h) or saline on stages of cellular respiration in mitochondria isolated from the vastus lateralis muscle of the infusion limb. To assess mitochondrial respiration, we measured (A) substrate-driven respiration; (B) state 3 respiration; (C) state 4 respiration; (D) total respiratory capacity; and (E) the respiratory control ration (RCR). Substrate-driven and state 3 respiration as well as the total respiratory capacity was similar in αMSH- and saline-treated groups. In contrast, state 4 respiration was increased (*P < .05) and the RCR was reduced (*P < .05) by αMSH treatment. All data are presented as the mean ± SEM. Statistical analyses was performed using an unpaired t test.

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  Figure 3.. Serial measurement of plasma glucose and nonesterified fatty acids (NEFA) from the femoral and jugular vein in saline (circles) and α-melanocyte–stimulating hormone (αMSH)-treated (squares) animals. (A-D) The box depicts the feeding window and the bar depicts the period of infusion. In the femoral vein, infusion of αMSH (0.1 μg/h) decreased (*P < .05) A, the plasma concentration of glucose, although (B) there was no effect of αMSH treatment on glucose concentration in the jugular vein. With regard to NEFA, the onset of feeding reduced concentrations both in the (C) femoral and (D) jugular vein, but there was no effect of αMSH treatment. (E) The overall mean concentration of glucose in the femoral vein was lower (*P < .05) in αMSH-treated animals compared to their control counterparts. In contrast, the mean concentration of (G) glucose in the jugular vein and NEFA concentration both in the (F) femoral and (H) jugular veins were similar between αMSH- and saline-treated groups. All data are presented as the mean ± SEM.

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  Figure 4.. Effect of phentolamine and propranolol treatment on α-melanocyte–stimulating hormone (αMSH)-induced skeletal muscle heat production. There was no statistically significant effect of phentolamine or propranolol treatment on the longitudinal muscle temperature pattern in either (A) saline- or (B) αMSH-treated animals. The peak temperature response was greater in αMSH alone (*P < .05) and αMSH-phentolamine-treated (**P < .01) animals compared to the (C) saline controls. With regard to the area under the curve (AUC), this was greater both in αMSH-phentolamine (*P < .05) and αMSH-propranolol (***P < .001) compared to the (D) saline-treated controls. Notably, the peak temperature response or AUC in αMSH-treated animals was not altered by coadministration of either (C) phentolamine or (D) propranolol. (E) In contrast, β-blockade with propranolol attenuated the leptin-induced skeletal muscle heat production in female sheep. (E) Skeletal muscle temperature increased by leptin treatment (aP < .05, control vs leptin groups). (E) Furthermore, propranolol infusion mitigated (bP < .05 leptin, vs leptin/propranolol) the ability of leptin to increase heat production in skeletal muscle.