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In diet-induced obese mice, glucagon-driven energy expenditure depended on hepatic not adipose glucagon-receptor signaling and on sustained cAMP/PKA activation, and, strikingly, the energy-expenditure effect appeared in obese but not lean animals

This effect was likely due to attenuation of spinogenesis promoted by HGF and Dihexa treatments since, without the antagonizing effect of Hinge, each agonist increased mini-AMPA frequencies (Figure 13 A-B and Figure 10) thus forming functional synaptic connections