کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5585125 | 1568114 | 2017 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The impact of peripheral serotonin on leptin-brain serotonin axis, bone metabolism and strength in growing rats with experimental chronic kidney disease
ترجمه فارسی عنوان
تأثیر سروتونین محیطی بر محور سروتونین مغز لپتین مغز، متابولیسم استخوان و قدرت در موش های در حال رشد با بیماری مزمن کلیوی
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کلمات کلیدی
BDSTRACP 5bPER-1CKD-MBDCol1α1SNS5-HT1B5-HIAAGDSCREBtph25-HTATF4RANKLFOXO1VMARUNX2Trp5-Hydroxyindoleacetic acid - 5-هیدروکسی سدیم اسیدbiomechanical tests - آزمایش های بیومکانیکALP - آلکالن فسفاتازBone - استخوان Vanillylmandelic acid - اسید وانیلیلیماندلیکchronic kidney disease - بیماری مزمن کلیویtryptophan hydroxylase-2 - تریپتوفان هیدروکسیلاز 2Genes - زایه یا ژنSerotonin - سروتونینsympathetic nervous system - سیستم عصبی سمپاتیکLeptin - لپتین CKD - نارسایی مزمن کلیه
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی تکاملی
چکیده انگلیسی
Chronic kidney disease (CKD) results in decreased bone strength. Serotonin (5-HT) is one of the critical regulators of bone health, fulfilling distinct functions depending on its synthesis site: brain-derived serotonin (BDS) favors osteoblast proliferation, whereas gut-derived serotonin (GDS) inhibits it. We assessed the role of BDS and peripheral leptin in the regulation of bone metabolism and strength in young rats with 5/6 nephrectomy. BDS synthesis was accelerated during CKD progression. Decreased peripheral leptin in CKD rats was inversely related to BDS content in the hypothalamus, brainstem and frontal cortex. Serotonin in these brain regions affected bone strength and metabolism in the studied animals. The direct effect of circulating leptin on bone was not shown in uremia. At the molecular level, there was an inverse association between elevated GDS and the expression of cAMP responsive element-binding protein (Creb) gene in bone of CKD animals. In contrast, increased expression of activating transcription factor 4 (Atf4) was shown, which was associated with GDS-dependent transcription factor 1 (Foxo1), clock gene - Cry-1, cell cycle genes: c-Myc, cyclins, and osteoblast differentiation genes. These results identified a previously unknown molecular pathway, by which elevated GDS can shift in Foxo1 target genes from Creb to Atf4-dependent response, disrupting the leptin-BDS - dependent gene pathway in the bone of uremic rats. Thus, in the condition of CKD the effect of BDS and GDS on bone metabolism and strength can't be distinguished.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Bone - Volume 105, December 2017, Pages 1-10
Journal: Bone - Volume 105, December 2017, Pages 1-10
نویسندگان
Dariusz Pawlak, Tomasz Domaniewski, Beata Znorko, Ewa Oksztulska-Kolanek, PaweÅ Lipowicz, MichaÅ Doroszko, Malgorzata Karbowska, Krystyna Pawlak,