TTF-1, a homeodomain-containing transcription factor, regulates feeding behavior in the rat hypothalamus

2006 ◽  
Vol 349 (3) ◽  
pp. 969-975 ◽  
Author(s):  
Jae Geun Kim ◽  
Il Seong Nam-Goong ◽  
Chang Ho Yun ◽  
Jin Kwon Jeong ◽  
Eun Sook Kim ◽  
...  
Gene Therapy ◽  
2004 ◽  
Vol 11 (9) ◽  
pp. 797-804 ◽  
Author(s):  
A J Noordmans ◽  
D K Song ◽  
C J Noordmans ◽  
M Garrity-Moses ◽  
M J During ◽  
...  

1998 ◽  
Vol 68 (6) ◽  
pp. 420-427 ◽  
Author(s):  
Marie-Louise Håkansson ◽  
Björn Meister

2020 ◽  
Vol 14 ◽  
Author(s):  
Helia Cheng ◽  
Schuyler J. Pablico ◽  
Jisu Lee ◽  
Ji Suk Chang ◽  
Sangho Yu

The central nervous system controls feeding behavior and energy expenditure in response to various internal and external stimuli to maintain energy balance. Here we report that the newly identified transcription factor zinc finger and BTB domain containing 16 (Zbtb16) is induced by energy deficit in the paraventricular (PVH) and arcuate (ARC) nuclei of the hypothalamus via glucocorticoid (GC) signaling. In the PVH, Zbtb16 is expressed in the anterior half of the PVH and co-expressed with many neuronal markers such as corticotropin-releasing hormone (Crh), thyrotropin-releasing hormone (Trh), oxytocin (Oxt), arginine vasopressin (Avp), and nitric oxide synthase 1 (Nos1). Knockdown (KD) of Zbtb16 in the PVH results in attenuated cold-induced thermogenesis and improved glucose tolerance without affecting food intake. In the meantime, Zbtb16 is predominantly expressed in agouti-related neuropeptide/neuropeptide Y (Agrp/Npy) neurons in the ARC and its KD in the ARC leads to reduced food intake. We further reveal that chemogenetic stimulation of PVH Zbtb16 neurons increases energy expenditure while that of ARC Zbtb16 neurons increases food intake. Taken together, we conclude that Zbtb16 is an important mediator that coordinates responses to energy deficit downstream of GCs by contributing to glycemic control through the PVH and feeding behavior regulation through the ARC, and additionally reveal its function in controlling energy expenditure during cold-evoked thermogenesis via the PVH. As a result, we hypothesize that Zbtb16 may be involved in promoting weight regain after weight loss.


2015 ◽  
Vol 8 (1) ◽  
Author(s):  
Mingkwan Greenwood ◽  
Michael P. Greenwood ◽  
Andre S. Mecawi ◽  
Su Yi Loh ◽  
José Antunes Rodrigues ◽  
...  

Endocrinology ◽  
2007 ◽  
Vol 149 (3) ◽  
pp. 1295-1301 ◽  
Author(s):  
Daisuke Kohno ◽  
Masanori Nakata ◽  
Yuko Maejima ◽  
Hiroyuki Shimizu ◽  
Udval Sedbazar ◽  
...  

Nesfatin-1, a newly discovered satiety molecule, is located in the hypothalamic nuclei, including the paraventricular nucleus (PVN) and supraoptic nucleus (SON). In this study, fine localization and regulation of nesfatin-1 neurons in the PVN and SON were investigated by immunohistochemistry of neuropeptides and c-Fos. In the PVN, 24% of nesfatin-1 neurons overlapped with oxytocin, 18% with vasopressin, 13% with CRH, and 12% with TRH neurons. In the SON, 35% of nesfatin-1 neurons overlapped with oxytocin and 28% with vasopressin. After a 48-h fast, refeeding for 2 h dramatically increased the number of nesfatin-1 neurons expressing c-Fos immunoreactivity by approximately 10 times in the PVN and 30 times in the SON, compared with the fasting controls. In the SON, refeeding also significantly increased the number of nesfatin-1-immunoreactive neurons and NUCB2 mRNA expression, compared with fasting. These results indicate that nesfatin-1 neurons in the PVN and SON highly overlap with oxytocin and vasopressin neurons and that they are activated markedly by refeeding. Feeding-activated nesfatin-1 neurons in the PVN and SON could play a role in the postprandial regulation of feeding behavior and energy homeostasis.


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