Fig 1: Catecholamine and hormone levels in wild-type and GHSR-null mice exercised to match the exhaustion time of the other genotype. Plasma (A) norepinephrine, (B) epinephrine, (C) insulin, (D) growth hormone, (E) glucagon, (F) corticosterone, and (G) IGF-1 levels in exercised mice time-matched (TM) to the exhaustion time (Exh) of the other genotype. Data were analyzed by Student's unpaired “t” test. *p < 0.05, **p < 0.01, significant difference. n = 7–12 per group. Data represented as mean ± S.E.M.
Fig 2: Relationship of food intake/body weight (BW) against active ghrelin, TSH, and IGF-1 in rats. N = 32 for the whole cohort. The food intake/BW negatively correlated with plasma active ghrelin and serum TSH levels (a, b). In contrast, it negatively correlated with IGF-1 serum levels (c).
Fig 3: Relationship among TSH, active ghrelin, total ghrelin, GH, and IGH-1 in rats. N = 32 for the whole cohort. Serum TSH levels positively correlated with plasma active ghrelin and total ghrelin levels (a, b). Conversely, serum IGF-1 levels negatively correlated with plasma TSH, active ghrelin, and total ghrelin levels (c, d, e).
Fig 4: Neural-specific Fto knockout mice are growth retarded.(A) The breeding scheme to generate neural-specific Fto knockout mice. (B) Western blot analysis of different tissues of FtoN+ and FtoN? mice. (C) Body weights of 7-day-old FtoN+/+, FtoN+/? and FtoN?/? pups. For each genotype (FtoN+/+/FtoN+/?/FtoN?/?), n = 17/7/9 (male), and 14/7/8 (female). (D) Growth curves of male and female FtoN+ and FtoN? mice. For each genotype (FtoN+/FtoN?), n = 30/25(male), and 24/20(female). (E, F) Body length (E) and femur bone mineral density (F) of 16-week-old FtoN+ and FtoN? mice measured by DEXA. For each genotype (FtoN+/FtoN?), n = 19/21(male), 19/17(female). (G) Relative serum IGF-1 levels of 4-week-old FtoN+ and FtoN? mice. For each genotype (FtoN+/FtoN?), n = 6/6(male), and n = 5/4(female). Statistical analyses were performed by one-way ANOVA (C) or unpaired t-test (D–G). **P<0.01. All values are mean ± s.e.m.
Fig 5: Effects of somatotroph-selective GHSR deletion and chronic acyl-ghrelin administration on GH secretion, GH mRNA levels, plasma IGF-1, food intake, body weight, and body composition. (A) Plasma acyl-ghrelin and (B) plasma GH measured before (indicated as “0”) and after 12 days (indicated as “12”) of chronic s.c. acyl-ghrelin infusion via osmotic minipumps. (C) Pituitary GH mRNA levels after 12 days of chronic s.c. acyl-ghrelin infusion. (D) Plasma IGF-1 levels before and after 12 days of chronic s.c. acyl-ghrelin infusion. (E) Daily food intake, (F) cumulative food intake, (G) body weight, and (H) % body weight gain over the 12-day course of ghrelin administration. (I) Fat mass, (J) lean mass, and (K) blood glucose measured on the last day of ghrelin administration. Data in A, B, D, E, G, and I–K were analyzed by repeated-measures two-way ANOVA followed by Sidak's multiple comparisons test. Data in C, F, and H were measured by unpaired Student t-test. n = 9–10 (for A-B and E-K), n = 8–9 (for C), n = 7–9 (for D). All the values are expressed as mean ± SEM. *P < 0.05, **P < 0.005, ***P < 0.001, ****P < 0.0001 for statistically significant changes or ns = no significant changes. fl/fl, mice homozygous for the loxP-flanked GHSR gene; –, absence or +, presence of GH-IRES-Cre.
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