scholarly journals Leptin signalling in teleost fish with emphasis in food intake regulation

2021 ◽  
Vol 526 ◽  
pp. 111209
Author(s):  
Ayelén Melisa Blanco ◽  
José Luis Soengas
2006 ◽  
Vol 3 (3) ◽  
pp. 223-229 ◽  
Author(s):  
Tetsuya Yamada ◽  
Hideki Katagiri ◽  
Yasushi Ishigaki ◽  
Takehide Ogihara ◽  
Junta Imai ◽  
...  

2020 ◽  
Vol 223 (17) ◽  
pp. jeb227330
Author(s):  
Cristina Velasco ◽  
Marta Conde-Sieira ◽  
Sara Comesaña ◽  
Mauro Chivite ◽  
Adrián Díaz-Rúa ◽  
...  

ABSTRACTWe hypothesized that the free fatty acid receptors FFA1 and FFA4 might be involved in the anorectic response observed in fish after rising levels of long-chain fatty acids (LCFAs) such as oleate. In one experiment we demonstrated that intracerebroventricular (i.c.v.) treatment of rainbow trout with FFA1 and FFA4 agonists elicited an anorectic response 2, 6 and 24 h after treatment. In a second experiment, the same i.c.v. treatment resulted after 2 h in an enhancement in the mRNA abundance of anorexigenic neuropeptides pomca1 and cartpt and a decrease in the values of orexigenic peptides npy and agrp1. These changes occurred in parallel with those observed in the mRNA abundance and/or protein levels of the transcription factors Creb, Bsx and FoxO1, protein levels and phosphorylation status of Ampkα and Akt, and mRNA abundance of plcb1 and itrp3. Finally, we assessed in a third experiment the response of all these parameters after 2 h of i.c.v. treatment with oleate (the endogenous ligand of both free fatty acid receptors) alone or in the presence of FFA1 and FFA4 antagonists. Most effects of oleate disappeared in the presence of FFA1 and FFA4 antagonists. The evidence obtained supports the involvement of FFA1 and FFA4 in fatty acid sensing in fish brain, and thus involvement in food intake regulation through mechanisms not exactly comparable (differential response of neuropeptides and cellular signalling) to those known in mammals.


2018 ◽  
Vol 818 ◽  
pp. 43-49 ◽  
Author(s):  
Zahra. Mirmohammadsadeghi ◽  
Masoud. Shareghi Brojeni ◽  
Abbas. Haghparast ◽  
Afsaneh. Eliassi

1973 ◽  
Vol 103 (4) ◽  
pp. 608-617 ◽  
Author(s):  
Y. Peng ◽  
J. Gubin ◽  
A. E. Harper ◽  
M. G. Vavich ◽  
A. R. Kemmerer

2018 ◽  
Vol 107 (1) ◽  
pp. 91-104 ◽  
Author(s):  
Yuko Maejima ◽  
Shoko Yokota ◽  
Katsuhiko Nishimori ◽  
Kenju Shimomura

Oxytocin was discovered in 1906 as a peptide that promotes delivery and milk ejection; however, its additional physiological functions were determined 100 years later. Many recent articles have reported newly discovered effects of oxytocin on social communication, bonding, reward-related behavior, adipose tissue, and muscle and food intake regulation. Because oxytocin neurons project to various regions in the brain that contribute to both feeding reward (hedonic feeding) and the regulation of energy balance (homeostatic feeding), the mechanisms of oxytocin on food intake regulation are complicated and largely unknown. Oxytocin neurons in the paraventricular nucleus (PVN) receive neural projections from the arcuate nucleus (ARC), which is an important center for feeding regulation. On the other hand, these neurons in the PVN and supraoptic nucleus project to the ARC. PVN oxytocin neurons also project to the brain stem and the reward-related limbic system. In addition to this, oxytocin induces lipolysis and decreases fat mass. However, these effects in feeding and adipose tissue are known to be dependent on body weight (BW). Oxytocin treatment is more effective in food intake regulation and fat mass decline for individuals with leptin resistance and higher BW, but is known to be less effective in individuals with normal BW. In this review, we present in detail the recent findings on the physiological role of oxytocin in feeding regulation and the anorexigenic neural pathway of oxytocin neurons, as well as the advantage of oxytocin usage for anti-obesity treatment.


2022 ◽  
pp. 667-693
Author(s):  
Mark A. Cline ◽  
Mike Denbow ◽  
Elizabeth Gilbert ◽  
Sami Dridi

1999 ◽  
Vol 24 ◽  
pp. 37-54 ◽  
Author(s):  
K. L. Ingvartsen ◽  
N. C. Friggens ◽  
P. Faverdin

AbstractThe dip in food intake, which starts in late pregnancy and continues into early lactation, has traditionally been interpreted as a depression in intake due to physical constraints. However, the rôle of physical constraints on intake has been overemphasized, particularly in early lactation. There is mounting evidence that the presence and mobilization of body reserves in early lactation play an important rôle in regulating intake at this time.Conceptually, the dip in intake in early lactation observed when cows have access to non-limiting foods can be accounted for by assuming that the cow has a desired level of body reserves. When the cow is not compromised, the changes with time in body reserves and the dip in intake represent the normal case and provide the basis against which to assess true depressions in intake which may occur when the cow is compromised by limiting nutrition or environment.The regulation of body reserves and intake in the periparturient cow is orchestrated through nervous and hormonal signals. Likely factors that are involved in intake regulation are reproductive hormones, neuropeptides, adrenergic signals, insulin and insulin resistance and leptin. Furthermore, oxidation of NEFA in the liver may result in feedback signals that reduce intake. The relative importance of these is discussed. A better understanding of the physiological signals involved in intake regulation and their interrelations with body weight regulation may provide important indicators of the degree of compromise that periparturient cows may experience.


1977 ◽  
Vol 135 (2) ◽  
pp. 325-336 ◽  
Author(s):  
Jan Van Der Gugten ◽  
E.Ronald De Kloet ◽  
Dirk H.G. Versteeg ◽  
Jef L. Slangen

Sign in / Sign up

Export Citation Format

Share Document