Figure 1. Mitochondrial and transcriptional effects of ghrelin are UCP2-mediated.

a–c, Ghrelin alters hypothalamic mitochondrial respiration. a, Oligomycin inhibits ATP synthase and uncouples substrate oxidation from ATP phosphorylation. The resulting increase in uncoupled oxygen consumption in ghrelin-treated mice is due to UCP2, as Ucp2^–/– mice exhibit no response to ghrelin. b, Ghrelin enhances respiration after palmitate addition in wild-type but not Ucp2^–/– mice. [Author: Revised sentence ok?Yes.] c, An increase in respiration after FCCP shows that ghrelin enhances the maximal respiratory capacity in wild-type but not in Ucp2^–/– mice. d, Ghrelin increases (10 nmol) hypothalamic Ucp2 mRNA expression as measured by real-time PCR (n = 6). The data are expressed as a fold increase relative to saline levels. e, Arcuate Npy gene expression is increased in response to ghrelin in wild-type but not Ucp2^–/– mice (n = 6). f, Ghrelin promotes mitochondrial proliferation in a UCP2-dependent manner in arcuate NPY/AgRP cells. [Author: Should this be NPY/AgRP cells, as per panel label?Yes.] g, Ghrelin increases Nrf1 mRNA expression in the hypothalamus of wild-type but not Ucp2^–/– mice. h, Representative traces showing that ghrelin decreases the mitochondrial membrane potential after addition of energy substrates (state 2) and after addition of oligomycin (state 4). Asterisk indicates statistically significant differences (P < 0.05) with respect to saline controls. All error bars indicate s.e.m. [Author: Correct definition of error bars?Yes.] Olig, oligomycin; Palm, palmitate; Pyr/Mal, pyruvate and malate. [Author: Correct definitions? ΔΨ_m correct for y axis label?Yes.]