作者: Carolin S Hoefig , Simon F Jacobi , Amy Warner , Lisbeth Harder , Nancy Schanze
DOI: 10.1111/BPH.13131
关键词: Hypothermia 、 Bradycardia 、 Blood pressure 、 Thermoregulatory functions 、 Biology 、 Heart rate 、 Endocrinology 、 Thermogenesis 、 Brown adipose tissue 、 Internal medicine 、 Triiodothyronine
摘要: Background and Purpose 3-Iodothyronamine (3-T1AM) is an endogenous thyroid hormone derivative reported to induce strong hypothermia bradycardia within minutes upon injection in rodents. Although 3-T1AM rapidly converted several other metabolites vivo, these pharmacological responses were solely attributed 3-T1AM, leaving potential contributions of downstream products untested. We therefore examined the cardiometabolic effects 3-iodothyroacetic acid (TA1), main degradation product 3-T1AM. Experimental Approach We used a sensitive implantable radiotelemetry system C57/Bl6J mice study TA1 on body temperature heart rate, as well metabolic parameters. Key Results Interestingly, despite using doses, we observed no rate or after single (50 mg·kg−1, i.p.) compared sham-injected controls. Repeated administration (5 mg·kg−1, i.p. for 7 days) likewise did not alter weight, food water intake, blood pressure, brown adipose tissue (BAT) thermogenesis temperature. Moreover, mRNA expression specific genes heart, kidney, liver, BAT lung was also altered by controls. Conclusions Implications Our data conclusively demonstrate that does contribute cardiovascular thermoregulatory mice, suggesting oxidative deamination constitutes important deactivation mechanism with possible implications functions.