Arginine vasopressin: Direct and indirect action on metabolism

Abstract

From its identification and isolation in 1954, arginine vasopressin (AVP) has attracted attention, not only for its peripheral functions such as vasoconstriction and reabsorption of water from kidney, but also for its central effects. As there is now considerable evidence that AVP plays a crucial role in feeding behavior and energy balance, it has become a promising therapeutic target for treating obesity or other obesity-related metabolic disorders. However, the underlying mechanisms for AVP regulation of these central processes still remain largely unknown. In this review, we will provide a brief overview of the current knowledge concerning how AVP controls energy balance and feeding behavior, focusing on physiological aspects including the relationship between AVP, circadian rhythmicity, and glucocorticoids.

Keywords: Arginine vasopressin; Circadian rhythm; Energy balance; HPA axis; Hypothalamus.

Fig. 1

Chemogenetic activation of AVP neurons using transgenic rats. (A) Construction strategy of an AVP-hM3Dq-mCherry transgenic rat line are shown. (B) Robust Fos induction was observed 90 min after intraperitoneal (i.p.) injection of clozapine-N-oxide (CNO, 1 mg/kg) in the SON and PVN. Circadian activity (C) and circadian core body temperature (D) were significantly disrupted after chemogenetic activation of AVP neurons at the start of the dark phase. Cumulative food intake (E), water intake (F), and urine volume (G) were significantly suppressed after chemogenetic activation of AVP neurons. The figure was modified from Sci. Rep. 7, 2017 [17].

Fig. 2

The HPA axis. In response to stress, CRH neurons originating from the pPVN and projecting to the median eminence, release both CRH and AVP into the portal circulation reaching the anterior pituitary. Here, CRH and AVP bind and activate the CRH-type1 receptor (Crhr1) and the V1b receptor respectively; the two cognate receptors that are expressed on corticotrophes within the anterior pituitary and stimulate ACTH secretion. ACTH travels through the peripheral ACTH circulation to reach the adrenal cortex where it induces steroidogenesis, effectively increasing secretion of glucocorticoid hormone (corticosterone in rodents and cortisol in humans). In turn, glucocorticoids enter the circulation and travel back to the pituitary and hypothalamus to act in a classical negative feedback loop to prevent further glucocorticoid release, effectively terminating the stress response Created with BioRender.com.