Fig. 7

Pegvisomant produces energy-saving adaptations in food-deprived mice. a Serum insulin-like growth factor-1 (IGF-1) concentration (t₍₁₄₎ = 4.089, P = 0.0011; n = 8). b Hypothalamic growth hormone-releasing hormone (GHRH mRNA levels (t₍₁₄₎ = 2.452, P = 0.0279; n = 8). c Energy expenditure (food restriction (F.R.) 1, F_(2, 23) = 1.83, P = 0.1829; F.R. 2, F_(2, 23) = 5.396, P = 0.012; F.R. 3, F_(2, 23) = 0.1271, P = 0.8813; F.R. 4, F_(2, 23) = 0.4397, P = 0.6496; n = 7–10). d Body weight changes (main effect of F.R. [F_(5, 125) = 1031, P < 0.0001], main effect of treatment [F_(2, 25) = 0.3717, P = 0.1163] and interaction [F_(10, 125) = 2.398, P = 0.0122]; n = 7–10). e Blood glucose levels (main effect of F.R. [F_(5, 125) = 116.6, P < 0.0001], main effect of treatment [F_(2, 25) = 4.747, P = 0.0179] and interaction [F_(10, 125) = 2.966, P = 0.0022]; n = 8–10; *P < 0.05, leptin vs. phosphate-buffered saline (PBS) treatment; ^#P < 0.05, leptin vs. pegvisomant treatment; Fisher's least significant difference (LSD) post-hoc test). f Scheme summarizing our findings highlighting that growth hormone (GH), parallel to the fall in leptin levels, is a critical cue that informs the brain about energy deficiency, triggering key adaptive responses to conserve body energy stores via activation of agouti-related protein (AgRP) neurons. All results were expressed as mean ± s.e.m.