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3-Iodothyronamine Induces Tail Vasodilation Through Central Action in Male Mice.

Abstract：

:3-Iodothyronamine (3-T1AM) is an endogenous thyroid hormone (TH)-derived metabolite that induces severe hypothermia in mice after systemic administration; however, the underlying mechanisms have remained enigmatic. We show here that the rapid 3-T1AM-induced loss in body temperature is a consequence of peripheral vasodilation and subsequent heat loss (e.g., over the tail surface). The condition is subsequently intensified by hypomotility and a lack of brown adipose tissue activation. Although the possible 3-T1AM targets trace amine-associated receptor 1 or α2a-adrenergic receptor were detected in tail artery and aorta respectively, myograph studies did not show any direct effect of 3-T1AM on vasodilation, suggesting that its actions are likely indirect. Intracerebroventricular application of 3-T1AM, however, replicated the phenotype of tail vasodilation and body temperature decline and led to neuronal activation in the hypothalamus, suggesting that the metabolite causes tail vasodilation through a hypothalamic signaling pathway. Consequently, the 3-T1AM response constitutes anapyrexia rather than hypothermia and closely resembles the heat-stress response mediated by hypothalamic temperature-sensitive neurons. Our results thus underline the well-known role of the hypothalamus as the body's thermostat and suggest an additional molecular link between TH signaling and the central control of body temperature.

journal_name

Endocrinology

journal_title

Endocrinology

authors

Gachkar S,Oelkrug R,Martinez-Sanchez N,Rial-Pensado E,Warner A,Hoefig CS,López M,Mittag J

doi

10.1210/en.2016-1951

subject

Has Abstract

pub_date

2017-06-01 00:00:00

pages

1977-1984

issue

6

eissn

0013-7227

issn

1945-7170

pii

3078999

journal_volume

158

pub_type

杂志文章

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