scholarly journals Leucine sensing in rainbow trout hypothalamus is direct but separate from mTOR signalling in the regulation of food intake

Aquaculture ◽  
2021 ◽  
pp. 737009
Author(s):  
Sara Comesaña ◽  
Cristina Velasco ◽  
José L. Soengas
2011 ◽  
Vol 107 (11) ◽  
pp. 1714-1725 ◽  
Author(s):  
A. Cláudia Figueiredo-Silva ◽  
Sadasivam Kaushik ◽  
Frédéric Terrier ◽  
Johan W. Schrama ◽  
Françoise Médale ◽  
...  

We examined the long-term effect of feeding coconut oil (CO; rich in lauric acid, C12) on voluntary food intake and nutrient utilisation in rainbow trout (Oncorhynchus mykiss), with particular attention to the metabolic use (storage or oxidation) of ingested medium-chain TAG. Trout were fed for 15 weeks one of the four isoproteic diets containing fish oil (FO) or CO as fat source (FS), incorporated at 5 % (low fat, LF) or 15 % (high fat, HF). Fat level or FS did not modify food intake (g/kg0·8per d), despite higher intestinal cholecystokinin-T mRNA in trout fed the HF-FO diet. The HF diets relative to the LF ones induced higher growth and adiposity, whereas the replacements of FO by CO resulted in similar growth and adiposity. This, together with the substantial retention of C12 (57 % of intake), suggests the relatively low oxidation of ingested C12. The down-regulation of carnitine palmitoyl-transferase-1 (CPT-1) confirms the minor dependency of medium-chain fatty acids (MCFA) on CPT-1 to enter the mitochondria. However, MCFA did not up-regulate mitochondrial oxidation evaluated using hepatic hydroxyacyl-CoA dehydrogenase as a marker, in line with their high retention in body lipids. At a low lipid level, MCFA increased mRNA levels of fatty acid synthase, elongase and stearoyl-CoA desaturase in liver, showing the hepatic activation of fatty acid synthesis pathways by MCFA, reflected by increased 16 : 0, 18 : 0, 16 : 1, 18 : 1 body levels. The high capacity of trout to incorporate and transform C12, rather than to readily oxidise C12, contrasts with data in mammals and may explain the absence of a satiating effect of CO in rainbow trout.


2012 ◽  
Vol 178 (1) ◽  
pp. 131-138 ◽  
Author(s):  
Marta Conde-Sieira ◽  
Marta Librán-Pérez ◽  
Marcos A. López Patiño ◽  
José L. Soengas ◽  
Jesús M. Míguez

2013 ◽  
Vol 98 (12) ◽  
pp. 1696-1704 ◽  
Author(s):  
Weizhen Zhang ◽  
Chao Zhang ◽  
Danielle Fritze ◽  
Biaoxin Chai ◽  
Jiyao Li ◽  
...  

2015 ◽  
Vol 226 (2) ◽  
pp. 103-119 ◽  
Author(s):  
Barry N Madison ◽  
Sara Tavakoli ◽  
Sarah Kramer ◽  
Nicholas J Bernier

To gain a better understanding of the mechanisms by which cortisol suppresses growth during chronic stress in fish, we characterized the effects of chronic cortisol on food intake, mass gain, the expression of appetite-regulating factors, and the activity of the GH/IGF axis. Fish given osmotic pumps that maintained plasma cortisol levels at ∼70 or 116 ng/ml for 34 days were sampled 14, 28 and 42 days post-implantation. Relative to shams, the cortisol treatments reduced food intake by 40–60% and elicited marked increases in liver leptin (lep-a1) and brain preoptic area (POA) corticotropin-releasing factor (crf) mRNA levels. The cortisol treatments also elicited 40–80% reductions in mass gain associated with increases in pituitarygh, liverghreceptor (ghr), liverigfIandigfbinding protein (igfbp)-1 and -2 mRNA levels, reduced plasma GH and no change in plasma IGF1. During recovery, while plasma GH and pituitarygh, liverghrandigfIgene expression did not differ between treatments, the high cortisol-treated fish had lower plasma IGF1 and elevated liverigfbp1mRNA levels. Finally, the cortisol-treated fish had higher plasma glucose levels, reduced liver glycogen and lipid reserves, and muscle lipid content. Thus, our findings suggest that the growth-suppressing effects of chronic cortisol in rainbow trout result from reduced food intake mediated at least in part by increases in liverlep-a1and POAcrfmRNA, from sustained increases in hepaticigfbp1expression that reduce the growth-promoting actions of the GH/IGF axis, and from a mobilization of energy reserves.


Aquaculture ◽  
1992 ◽  
Vol 100 (1-3) ◽  
pp. 326
Author(s):  
I.D. McCarthy ◽  
C.G. Carter ◽  
D.F. Houlihan

2005 ◽  
Vol 289 (4) ◽  
pp. R982-R990 ◽  
Author(s):  
Nicholas J. Bernier ◽  
Paul M. Craig

Hypoxia stress suppresses appetite in a variety of fish species, but the mechanisms mediating this response are not known. Therefore, given their anorexigenic and hypophysiotropic properties, we investigated the contribution of forebrain corticotropin-releasing factor (CRF) and urotensin I (UI) to the regulation of food intake and the hypothalamic-pituitary-interrenal (HPI) stress axis in hypoxic rainbow trout. Exposure to 50 and 35% O2 saturation for 24 h decreased food intake by 28 and 48%, respectively. The 35% O2 treatment also increased forebrain CRF and UI mRNA levels, plasma cortisol, and lactate. Exposure for 72 h to the same conditions resulted in similar reductions in food intake, increases in plasma cortisol proportional to the hypoxia severity, and increases in forebrain CRF and UI mRNA levels in the 50% O2 treatment. Relative to saline-infused fish, chronic intracranial infusion of the CRF receptor antagonist α-helical CRF(9–41) reduced the appetite-suppressing effects of 24-h exposure to 35% O2 and blocked the hypoxia-induced increase in plasma cortisol. Finally, forebrain microdissection revealed that 50 and 35% O2 exposure for 24 h specifically increases preoptic area CRF and UI mRNA levels in proportion to the severity of the hypoxic challenge and either has no effect or elicits small decreases in other forebrain regions. These results show that CRF-related peptides play a physiological role in regulating the HPI axis and in mediating at least a portion of the reduction in food intake under hypoxic conditions in rainbow trout and demonstrate that the response of forebrain CRF and UI neurons to this stressor is region specific.


2017 ◽  
Vol 59 (4) ◽  
pp. 377-390 ◽  
Author(s):  
Cristina Velasco ◽  
Cristina Otero-Rodiño ◽  
Sara Comesaña ◽  
Jesús M Míguez ◽  
José L Soengas

We assessed in rainbow trout hypothalamus the effects of oleate and octanoate on levels and phosphorylation status of two transcription factors, FoxO1 and CREB, possibly involved in linking activation of fatty acid sensing with modulation of food intake through the expression of brain neuropeptides. Moreover, we assessed changes in the phosphorylation status of three proteins possibly involved in modulation of these transcription factors such as Akt, AMPK and mTOR. In a first experiment, we evaluated, in pools of hypothalamus incubated for 3 h and 6 h at 15°C in a modified Hanks’ medium containing 100 or 500 µM oleate or octanoate, the response of fatty acid sensing, neuropeptide expression and phosphorylation status of proteins of interest. The activation of fatty acid sensing and enhanced anorectic potential occurred in parallel with the activation of Akt and mTOR, and the inhibition of AMPK. The changes in these proteins would relate to a neuropeptide expression through changes in the phosphorylation status of transcription factors under their control, such as CREB and FoxO1, which displayed inhibitory (CREB) or activatory (FoxO1) responses when tissues were incubated with oleate or octanoate. In a second experiment, we incubated hypothalamus for 6 h with 500 µM oleate or octanoate alone or in the presence of specific inhibitors of Akt, AMPK, mTOR, CREB or FoxO1. The presence of inhibitors counteracted the effects of oleate or octanoate on the phosphorylation status of the proteins of interest. The results support, for the first time in fish, the involvement of these proteins in the regulation of food intake by fatty acids.


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