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. Author manuscript; available in PMC: 2015 Apr 1.
Published in final edited form as: Cell Metab. 2014 Apr 1;19(4):667–681. doi: 10.1016/j.cmet.2014.03.005

Figure 6. Hyperlucagonemia is linked to liver kisspeptin1 production in HFD fed and Leprdb/db mice.

Figure 6

HFD fed mice: Panels A–F

Leprdb/db mice: Panels G–M

A, G Plasma glucagon levels in the fed state 60 min after treatment with GAI or GAC. Plasma glucagon levels remain unchanged after GAI or GAC treament.

B, H Representative liver IB for pCREB, total CREB and kisspeptin1 in GAI and GAC treated mice. Phospho-CREB is reduced in mice treated with GAI but not GAC.

C, I qRT-PCR of indicated genes of the gluconeogenic program in livers of GAI or GAC treated mice. GAI but not GAC treatment downregulates Pparg1a, Src1, G6P and Pck1 mRNA (mean±SEM, *P<0.05).

D, J qRT-PCR of Kiss1 in livers of GAI and GAC treated mice. GAI but not GAC treatment downregulates liver Kiss1 mRNA (mean±SEM, *P<0.05).

E, K In vivo ChIP of CREB occupancy on (left) CRE1 and (right) CRE2 half-sites of the Kiss1 promoter in livers of GAI or GAC treated SD mice, HFD and Leprdb/db mice. GAI reduces CREB occupancy on Kiss1 CRE 1 & 2 to levels similar to those in control mice (mean±SEM, *P<0.05).

F, L ipGTT in GAI or GAC treated mice. GAI treatment improves GT as compared to GAC treatment (mean±SEM, *P<0.05).