Downregulation of prolactin-releasing peptide gene expression in the hypothalamus and brainstem of diabetic rats

We investigated the prolactin-releasing peptide (PrRP) mRNA levels in the hypothalamus and brainstem of streptozotocin (STZ)-induced diabetic rats and fa/ fa Zucker diabetic rats, using in situ hybridization histochemistry. PrRP mRNA levels in the hypothalamus and brainstem of STZ-induced diabetic r...

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Published inPeptides (New York, N.Y. : 1980) Vol. 28; no. 8; pp. 1596 - 1604
Main Authors Mera, Takashi, Fujihara, Hiroaki, Saito, Jun, Kawasaki, Makoto, Hashimoto, Hirofumi, Saito, Takeshi, Shibata, Minori, Onaka, Tatsushi, Tanaka, Yoshiya, Oka, Takakazu, Tsuji, Sadatoshi, Ueta, Yoichi
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.08.2007
Elsevier Science
Subjects
PVN
s.c
CCK
i.p
NTS
RTS
NA
VLM
NPY
STZ
CRH
HPA
DMH
Rat
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Summary:We investigated the prolactin-releasing peptide (PrRP) mRNA levels in the hypothalamus and brainstem of streptozotocin (STZ)-induced diabetic rats and fa/ fa Zucker diabetic rats, using in situ hybridization histochemistry. PrRP mRNA levels in the hypothalamus and brainstem of STZ-induced diabetic rats were significantly reduced in comparison with those of control rats. PrRP mRNA levels in the diabetic rats were reversed by both insulin and leptin. PrRP mRNA levels in the fa/ fa diabetic rats were significantly reduced in comparison with those of Fa/ ? rats. PrRP mRNA levels in the fa/ fa diabetic rats were significantly increased by insulin-treatment, but did not reach control levels in the Fa/ ? rats. We also investigated the effect of restraint stress on PrRP mRNA levels in STZ-induced diabetic rats. The PrRP mRNA levels in the control and the STZ-induced diabetic rats increased significantly after restraint stress. The diabetic condition and insulin-treatment may affect the regulation of PrRP gene expression via leptin and other factors, such as plasma glucose level. The diabetic condition may not impair the role of PrRP as a stress mediator.
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ISSN:0196-9781
1873-5169
DOI:10.1016/j.peptides.2007.06.023