Effects of meteorin-like hormone on endocrine function of hypothalamo-hypophysial system and peripheral uncoupling proteins in rats

被引:6
作者
Sekerci, Guldeniz [1 ]
Erden, Yavuz [2 ]
Tekin, Suat [1 ]
机构
[1] Inonu Univ, Fac Med, Dept Physiol, Malatya, Turkey
[2] Bartin Univ, Fac Sci, Dept Mol Biol & Genet, Bartin, Turkey
关键词
Metrnl; Thyroid hormones; Energy use; UCP1; UCP3; PITUITARY-THYROID AXIS; ADIPOSE-TISSUE; INTRACEREBROVENTRICULAR INFUSION; FEEDING-BEHAVIOR; HYPOTHALAMUS; EXPRESSION; LEPTIN; MITOCHONDRIA; APELIN-13; IRISIN;
D O I
10.1007/s11033-022-07374-5
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background Meteorin-like hormone (Metrnl) is a peptide secreted from the adipose tissue and modulates the whole-body energy metabolism. Metrnl release into the circulation is influenced by obesity, cold exposure, and exercise. Thyroid hormones also exert many of their effects on metabolism through uncoupling proteins (UCPs). This study aimed to determine effect of Metrnl on hypothalamo-hypophysier-thyroid axis and energy metabolism and reveal the possible involvement of UCPs in this process. Methods and results Fourty male Sprague-Dawley rats were divided into 4 groups with 10 animals in each group: control, sham, 10 and 100 nM Metrnl. Hypothalamus, muscle, white adipose tissue (WAT) and brown adipose tissue (BAT) samples were collected to detect thyrotropin-releasing hormone (TRH), and UCP1 and UCP3 protein levels by western blot analysis. Serum thyroid-stimulating hormone (TSH), triiodothyronine (T3) and thyroxine (T4) hormone levels were determined by enzyme-linked immunosorbent assay. Central infusion of Metrnl caused significant increase in serum TSH, T3 and T4 levels compared to control (p < 0.05). After Metrnl treatment, there were significant increases in TRH in hypothalamus tissue, UCP1 in WAT and BAT; and UCP3 protein in the muscle tissue (p < 0.05). Conclusions The findings that Metrnl induced increases in the peripheral UCPs and hypothalamus-pituitary-thyroid axis hormones implicate a role for this hormone in body energy homeostasis through UCP-mediated mechanisms.
引用
收藏
页码:5919 / 5925
页数:7
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