Prolactin-releasing peptide improved leptin hypothalamic signaling in obese mice

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   Figure 1

   Chronic effect of palm¹¹-PrRP31 on (A) food intake and (B and C) body weight in DIO mice. Mice were subcutaneously injected twice a day with saline for 28 days (saline group), with palm¹¹-PrRP31 (5 mg/kg) for 28 days (palm¹¹-PrRP31 group) or with palm¹¹-PrRP31 (5 mg/kg) for 14 days and for the following 14 days with saline (palm¹¹-PrRP31 + saline group). Data are presented as means ± s.e.m. Statistical analysis was performed by One-way ANOVA with Bonferroni post hoc test, significance is ***P < 0.001 vs the saline treated group (n = 14). No significant difference was found between the groups treated with palm¹¹-PrRP31 for 14 or 28 days.
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   Figure 2

   (A) The FOSB immunoreactive cells activation and (B) the amount of immunoreactive cells in selected brain nuclei (ARC, NTS, PVN, DMN) involved in food intake regulation. Mice were subcutaneously injected twice a day with saline for 28 days (saline group), with palm¹¹-PrRP31 (5 mg/kg) for 28 days (palm¹¹-PrRP31 group) or with palm¹¹-PrRP31 (5 mg/kg) for 14 days and for the following 14 days with saline (palm¹¹-PrRP31 + saline group). After the treatment, mice were deeply anesthetized and perfused transcardially. The brains were dissected and cut into coronal sections. The FOSB immunoreactive cells were counted separately on each side of the appropriate coronal sections. Data are presented as means ± s.e.m. Statistical analysis was performed by unpaired t-test. Significance is **P < 0.01, ***P < 0.001 vs the saline treated group, ⁺⁺P < 0.01, ⁺⁺⁺P < 0.001 palm¹¹-PrRP31 + saline vs palm¹¹-PrRP31 (n = 4). ARC, nucleus arcuatus; NTS, nucleus of solitary tract; PVN, paraventricular nucleus; DMN, dorsomedial nucleus.
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   Figure 3

   Signaling pathways in hypothalamus. Signaling pathways were measured in hypothalamic lysates using Western blotting. Densitometric quantification of Western blots is normalized to β-actin. Leptin-related signaling pathways – total IRS1, total PI3 kinase, phospho-AKT (Ser473), total AKT, phospho-ERK1/2 and total ERK. IRS1, insulin receptor substrate 1; PI3 kinase, phospho-inositol-3 kinase; AKT, protein kinase B.
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   Figure 4

   The apoptotic pathway in hypothalamus – total JNK, phospho-c-JUn and total c-JUN. JAK2/STAT3 pathway in hypothalamus – total SOCS3, phospho-STAT3 and total STAT3. JNK, c-JUN N-terminal kinase.
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   Figure 5

   Phosphorylation of leptin receptor in hypothalamus. Data are presented as means ± s.e.m. Statistical analysis was performed by unpaired t-test. Significance is *P < 0.05, **P < 0.01, ***P < 0.001 vs saline treated group, ⁺P < 0.05, ⁺⁺P < 0.01, ⁺⁺⁺P < 0.001 palm¹¹-PrRP31 + saline vs palm¹¹-PrRP31 (n = 8).
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   Figure 6

   Chronic effect of palm¹¹-PrRP31 on mRNA expressions in DIO mice. (A) Ucp1 in BAT, (B) Lep in SCAT, (C) Lep in IPAT, (D) Srebf, (E) Acaca, (F) Lpl, (G) Cpt1a and (H) Cpt1b in liver. Mice were subcutaneously injected twice a day with saline for 28 days (saline group), with palm¹¹-PrRP31 (5 mg/kg) for 28 days (palm¹¹-PrRP31 group) or with palm¹¹-PrRP31 (5 mg/kg) for 14 days and for the following 14 days with saline (palm¹¹-PrRP31 + saline group). After the treatment the mRNA expressions were determined. Data are presented as mean ± s.e.m. The data were normalized to beta-2-microglobulin and analyzed by unpaired t-test, significance is *P < 0.05, **P < 0.01 vs the saline treated group, ⁺P < 0.05 palm¹¹-PrRP31 + saline vs palm¹¹-PrRP31 (n = 10). Ucp1, uncoupling protein-1; Lep, leptin; Lpl, lipoprotein lipase; Cpt1b, carnitine palmitoyltransferase 1b; BAT, brown adipose tissue; IPAT, intraperitoneal adipose tissue; SCAT, subcutaneous adipose tissue

• © 2018 Society for Endocrinology