Effects of neuropeptides B and W on the secretion and growth of rat adrenocortical cells

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Abstract. Neuropeptide B/W receptor 1 (NPBWR1) and neuropeptide B/W receptor 2 (NPBWR2) are two structurally related orphan receptors linked to protein G. In rodents NPBWR2 is absent, and its counterpart is described as being similar to neuropeptide B/W receptor 2. Endogenous ligands of these receptors have been identified. One of them is 29 amino acid residues long, uniquely modified with bromine and, thus, termed neuropeptide B (NPB). The other, neuropeptide W (NPW), has been identified in two molecular forms of 23 and 30 amino acids (NPW23 and NPW30), respectively. Both NPB and NPW affect food intake and energy expenditure. Since leptin, a potent anti-obesity hormone, and insulin are involved in the control of energy homeostasis, the present study aimed to investigate whether NPB and NPW affect leptin and insulin secretion in the rat. RT-PCR technique revealed the presence of ppNPB, ppNPW, NPBWR1 and NPBWR2-like mRNAs in isolated pancreatic islets of the rat. NPB and NPW immunoreactivities were observed in all of the cells of the pancreatic islets. Only when a higher dose was administered (3 nmol/100 g body weight) did NPW transiently lower blood insulin levels whereas NPB injection did not alter insulinaemia in the studied rats. At 30 min, but not 60, of the experiment, NPW notably lowered blood leptin concentrations at both tested doses. On the contrary, NPB injections had no effect on blood leptin and insulin concentrations. Thus, the results suggest that NPW but not NPB exerts a potent suppressive effect on blood leptin concentrations in the rat, and this mechanism may be involved in NPW regulation of energy homeostasis.

Section: Discussionsupporting

confidence: 74%

Section: Discussionsupporting

confidence: 67%

Section: Discussionmentioning

confidence: 99%

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Neuropeptide W exerts a potent suppressive effect on blood leptin and insulin concentrations in the rat

Ruciński

Nowak²,

Chmielewska³

et al. 2007

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“…Semiquantitative real-time PCR was performed as previously detailed (22)(23)(24) in a Roche LightCycler 2.0 with software version 4.0, using the following primers: i) StAR sense (684-703), 5'-CCTGAGCAAAGCGG TGTCAT-3' and antisense (850-870), 5'-GCAAGTGGCTGG CGAACTCTA-3' (amplifon, 187 bp; accession number, NM-03155); and ii) HPRT (hypoxanthine guanine phosphoribosyl transferase 1) sense (391-412), 5'-CAGTCAACGGGGG ACATAAAAG-3' and antisense (515-536), 5'-ATTTTGG GGCTGTACTGCTTGA-3' (amplicon, 146 bp; accession number, NM-01258). The PCR program was: denaturation step at 95˚C for 10 min, 45 cycles of three amplification steps (95˚C for 10 sec, annealing at 58˚C for 5 sec, and extension at 72˚C for 10 sec), and melting curve at 60-90˚C with a heating rate of 0.1˚C/sec.…”

Section: Reverse Transcription (Rt)-polymerase Chain Reaction (Pcr)mentioning

confidence: 99%

Steroidogenic acute regulatory protein gene expression, steroid-hormone secretion and proliferative activity of adrenocortical cells in the presence of proteasome inhibitors: In vivo studies on the regenerating rat adrenal cortex

Ruciński¹,

Tortorella²,

Ziółkowska³

et al. 2008

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Abstract.Previous studies have shown that proteasome inhibitors promote the accumulation of steroidogenic acute regulatory protein (StAR) in cultured rat adrenocortical cells. Unexpectedly, this response was associated with a moderate lowering in the corticosterone secretion and proliferation rate of cultured cells. Hence, we studied the effects of proteasome inhibitors MG115 and MG132 on the secretion and proliferative activity of the regenerating adrenal cortex in rats 5 days after surgery. Animals were given two subcutaneous injections of 0.15 or 1.5 nmol/100 g of inhibitors 24 and 12 h before decapitation. Real-time PCR and Western blotting showed that StAR expression, both mRNA and protein, was markedly lower in regenerating adrenals than in the intact gland of sham-operated rats. Neither MG115 nor MG132 affected StAR expression in regenerating gland. Inhibitors induced a slight decrease in the plasma concentrations of aldosterone and corticosterone, but did not significantly alter metaphase index of the regenerating adrenal cortex. Our findings provide the first evidence that down-regulation of StAR occurs during the early stages of adrenal regeneration. Moreover, this suggests that the steroidogenic pathway is more sensitive to proteasome inhibitors than that regulating proliferative activity of regenerating adrenal cortex in the rat.

“…Aldosterone and corticosterone were extracted from plasma, and corticosterone from culture incubation media, and measured by RIA, as detailed earlier (51,52). Aldosterone RIA: sensitivity, 5 pg/ml, intra-and interassay CVs, 5 and 7%, respectively.…”

Section: Rt-pcrmentioning

confidence: 99%

Effects of neuromedin-U on immature rat adrenocortical cells: In vitro and in vivo studies

Ziółkowska¹,

Macchi²,

Trejter³

et al. 2008

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Abstract. Neuromedin U (NMU) is a brain-gut peptide, that in the peripheral organs and tissues acts via a G protein-coupled receptor, called NMUR1. Reverse transcription-polymerase chain reaction showed the expression of NMUR1 mRNA in either cortex and medulla or dispersed zona glomerulosa and zona fasciculata-reticularis cells of the immature rat adrenals. Accordingly, immunocytochemistry demonstrated the presence of NMUR1-like immunoreactivity in the cortex and medulla of immature adrenals. NMU8 administration to immature rats was found to raise aldosterone, but not corticosterone, plasma concentration, without altering adrenal growth. Conversely, the exposure to NMU8 markedly enhanced the proliferative activity of immature rat inner adrenocortical cells in primary in vitro culture, without significantly affecting their corticosterone secretion. Collectively, our findings suggest that adrenals of immature rats may be a target for circulating NMU. However, the physiological significance and relevance of the adrenal effects of NMU remain to be ascertained.