Paraventricular NUCB2/nesfatin-1 is directly targeted by leptin and mediates its anorexigenic effect

Gantulga, Darambazar; Nakata, Masao; Okada, Takashi; Wang, Lei; Li, EnXu; Shinozaki, Atsumi; Motoshima, M; Mori, Masataka; Yada, Toshihiko

doi:10.1016/j.bbrc.2014.12.065

Cited by 32 publications

(22 citation statements)

References 27 publications

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“…Rather, nesfatin-1 signaling seems to be important in mediating leptin-induced anorexia. Recently, it was shown that leptin increases Nucb2 mRNA expression in the PVN both in vitro and in vivo (Darambazar et al 2015). In agreement with this, in PVN NUCB2-knockdown mice, both peripheral and central administration of leptin failed to induce anorexia (Darambazar et al 2015).…”

Section: Energy Homeostasissupporting

confidence: 55%

“…Recently, it was shown that leptin increases Nucb2 mRNA expression in the PVN both in vitro and in vivo (Darambazar et al 2015). In agreement with this, in PVN NUCB2-knockdown mice, both peripheral and central administration of leptin failed to induce anorexia (Darambazar et al 2015). Moreover, central co-administration of leptin and nesfatin-1 did not yield larger effects on energy expenditure than nesfatin-1 or leptin alone, possibly suggesting common downstream signaling mechanisms (Wernecke et al 2014).…”

Section: Energy Homeostasissupporting

confidence: 54%

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Nesfatin-1: functions and physiology of a novel regulatory peptide

Dore

Levata

Lehnert

et al. 2017

Journal of Endocrinology

114

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Nesfatin-1 was identified in 2006 as a potent anorexigenic peptide involved in the regulation of homeostatic feeding. It is processed from the precursor-peptide NEFA/ nucleobindin 2 (NUCB2), which is expressed both in the central nervous system as well as in the periphery, from where it can access the brain via non-saturable transmembrane diffusion. In hypothalamus and brainstem, nesfatin-1 recruits the oxytocin, the melancortin and other systems to relay its anorexigenic properties. NUCB2/nesfatin-1 peptide expression in reward-related areas suggests that nesfatin-1 might also be involved in hedonic feeding. Besides its initially discovered anorexigenic properties, over the last years, other important functions of nesfatin-1 have been discovered, many of them related to energy homeostasis, e.g. energy expenditure and glucose homeostasis. Nesfatin-1 is not only affecting these physiological processes but also the alterations of the metabolic state (e.g. fat mass, glycemic state) have an impact on the synthesis and release of NUCB2 and/or nesfatin-1. Furthermore, nesfatin-1 exerts pleiotropic actions at the level of cardiovascular and digestive systems, as well as plays a role in stress response, behavior, sleep and reproduction. Despite the recent advances in nesfatin-1 research, a putative receptor has not been identified and furthermore potentially distinct functions of nesfatin-1 and its precursor NUCB2 have not been dissected yet. To tackle these open questions will be the major objectives of future research to broaden our knowledge on NUCB2/nesfatin-1.

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Section: Energy Homeostasissupporting

confidence: 55%

Section: Energy Homeostasissupporting

confidence: 54%

Nesfatin-1: functions and physiology of a novel regulatory peptide

Dore

Levata

Lehnert

et al. 2017

Journal of Endocrinology

114

View full text Add to dashboard Cite

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“…The detail information of vector construction was reported as previously described (18). Target sequence for mouse NUCB2 was chosen to design shRNAs (accession number NM 016773, 5Ј-GGATCATCCAAGTACAGTA-3Ј; 298 -316).…”

Section: Construction Of Short Hairpin Rnas (Shrnas) and Viral Vectormentioning

confidence: 99%

Paraventricular NUCB2/Nesfatin-1 Supports Oxytocin and Vasopressin Neurons to Control Feeding Behavior and Fluid Balance in Male Mice

et al. 2016

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Nesfatin-1, derived from nucleobindin-2 (NUCB2), is expressed in the hypothalamus, including the paraventricular nucleus (PVN), an integrative center for energy homeostasis. However, precise role of the NUCB2/nesfatin-1 in PVN remains less defined. The present study aimed to clarify physiological and/or pathophysiological roles of endogenous NUCB2/nesfatin-1 in PVN by using adeno-associated virus vectors encoding short hairpin RNAs targeting NUCB2 in mice. PVN-specific NUCB2 knockdown primarily increased food intake and decreased plasma oxytocin level specifically in light phase, leading to increased body weight gain without affecting energy expenditure. Furthermore, high-salt diet increased the systolic blood pressure, plasma arginine vasopressin (AVP) and AVP mRNA expression in PVN, and all these changes were blunted by PVN-specific NUCB2 knockdown. These results reveal that the endogenous NUCB2/nesfatin-1 in PVN regulates PVN AVP and oxytocin and consequently the fluid and energy balance.

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“…Transverse liver slices were prepared from 5 weeksold male C57BL/6 mice [18]. Liver was isolated from anesthetized mice, from which slices of 300 µm thickness were prepared with a vibratome.…”

Section: Liver Slice Culturementioning

confidence: 99%