scholarly journals Chronic cortisol and the regulation of food intake and the endocrine growth axis in rainbow trout

2015 ◽  
Vol 226 (2) ◽  
pp. 103-119 ◽  
Author(s):  
Barry N Madison ◽  
Sara Tavakoli ◽  
Sarah Kramer ◽  
Nicholas J Bernier
Keyword(s):  
Rainbow Trout ◽  
Food Intake ◽  
Mass Gain ◽  
Liver Glycogen ◽  
Mrna Levels ◽  
Muscle Lipid ◽  
Glucose Levels ◽  
Treated Fish ◽  
Plasma Gh ◽  
Post Implantation

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.

Changes in plasma insulin and carbohydrate metabolism of zinc-stressed rainbow trout, Salmo gairdneri

1982 ◽  
Vol 60 (9) ◽  
pp. 2079-2084 ◽  
Author(s):  
G. F. Wagner ◽  
B. A. McKeown
Keyword(s):  
Rainbow Trout ◽  
Pancreatic Beta Cells ◽  
Plasma Insulin ◽  
Zinc Sulphate ◽  
Liver Glycogen ◽  
Salmo Gairdneri ◽  
Control Group ◽  
Exposed Fish ◽  
Glucose Levels ◽  
Insulin Radioimmunoassay

An experiment was conducted to determine if the hyperglycemia that is observed in zinc-stressed fish is also accompanied by changes in the levels of plasma insulin and liver glycogen. Juvenile rainbow trout were exposed to three concentrations of zinc sulphate along with a control group over 31 days. Plasma glucose levels were monitored in each group over the course of the experiment. The group demonstrating the most acute and sustained hyperglycemia (0.352 ppm zinc) was then analyzed along with the controls for changes in plasma insulin (using a teleost insulin radioimmunoassay) and liver glycogen levels. Significant depressions in plasma insulin and liver glycogen levels were observed in the zinc-exposed fish when compared with the controls. These changes are discussed with respect to possible influences of epinephrine, which is elevated in stressed fish, and (or) a direct effect of zinc metal on the pancreatic beta cells.

scholarly journals Link between lipid metabolism and voluntary food intake in rainbow trout fed coconut oil rich in medium-chain TAG

2011 ◽  
Vol 107 (11) ◽  
pp. 1714-1725 ◽  
Author(s):  
A. Cláudia Figueiredo-Silva ◽  
Sadasivam Kaushik ◽  
Frédéric Terrier ◽  
Johan W. Schrama ◽  
Françoise Médale ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Rainbow Trout ◽  
Food Intake ◽  
Fatty Acid Synthase ◽  
Lipid Level ◽  
Coconut Oil ◽  
Mrna Levels ◽  
Medium Chain ◽  
Nutrient Utilisation ◽  
Voluntary Food Intake

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.

Additive effects of lactation and food restriction to increase hypothalamic neuropeptide Y mRNA in rats

1997 ◽  
Vol 152 (3) ◽  
pp. 365-369 ◽  
Author(s):  
J P H Wilding ◽  
M O Ajala ◽  
P D Lambert ◽  
S R Bloom
Keyword(s):  
Food Intake ◽  
Neuropeptide Y ◽  
Food Restriction ◽  
Mrna Levels ◽  
Additive Effects ◽  
Daily Food Intake ◽  
Glucose Levels ◽  
Daily Food ◽  
Pregnancy And Lactation ◽  
Effect Of Food

Neuropeptide Y (NPY) is the most powerful appetite stimulant known, and rates of synthesis and release in the hypothalamus correlate closely with nutritional status. Pregnancy and lactation provide an excellent model of physiological hyperphagia. In this study the authors measured food intake, plasma glucose, insulin and luteinizing hormone (LH) and hypothalamic NPY mRNA in rats during pregnancy and in early and late lactation. The effect of food restriction (to 80% of control) during lactation was also studied. Pregnancy resulted in a modest increase in daily food intake over non-lactating controls (controls: 15·6±0·6 g, pregnant: 19·8±1·1 g, P<0·01) During lactation food intake increased dramatically to 355% of non-lactating levels by the 12th day. Insulin and glucose levels were unchanged in lactation, except in the food-restricted animals, when insulin levels were reduced to 49·5±18·4 pmol/l compared with 215±55 pmol/l (P<0·01) in lactating, non-restricted animals, and glucose was reduced to 3·7±0·2 mmol/l compared with 5·1 ± 0·2 mmol/l in non-restricted lactating animals. Hypothalamic NPY mRNA was unchanged in pregnancy, moderately increased after 5 days lactation (130±6·2% of control, P<0·01) and increased further at 14 days lactation (179 ± 14%, P<0·001). The greatest changes occurred in the animals who were food-deprived during lactation, when hypothalamic NPY mRNA levels reached 324 ± 44% (P<0·001) of non-lactating levels. Increases in hypothalamic NPY synthesis may be partly responsible for the increase in food intake seen in lactation, but unlike in food deprivation, the increase is not related to circulating insulin, suggesting involvement of other regulatory factors. Journal of Endocrinology (1997) 152, 365–369

CRF-related peptides contribute to stress response and regulation of appetite in hypoxic rainbow trout

2005 ◽  
Vol 289 (4) ◽  
pp. R982-R990 ◽  
Author(s):  
Nicholas J. Bernier ◽  
Paul M. Craig
Keyword(s):  
Rainbow Trout ◽  
Food Intake ◽  
Plasma Cortisol ◽  
Preoptic Area ◽  
Physiological Role ◽  
Corticotropin Releasing Factor ◽  
Stress Axis ◽  
Mrna Levels ◽  
Hypoxic Conditions ◽  
Hpi Axis

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.

Insulin suppression is associated with hypersomatostatinemia and hyperglucagonemia in glucose-injected rainbow trout

1991 ◽  
Vol 261 (3) ◽  
pp. R609-R613 ◽  
Author(s):  
J. S. Harmon ◽  
C. D. Eilertson ◽  
M. A. Sheridan ◽  
E. M. Plisetskaya
Keyword(s):  
Rainbow Trout ◽  
Plasma Levels ◽  
Liver Glycogen ◽  
Plasma Metabolites ◽  
Lipolytic Enzyme ◽  
Pancreatic Hormones ◽  
Glucose Administration ◽  
Glucose Levels ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Glucose Injection

Rainbow trout, Oncorhynchus mykiss, were used to evaluate the effects of carbohydrate loading on plasma levels of pancreatic hormones and associated changes in metabolic indexes in a carnivorous fish. Glucose (3,000 mg/dl, 10 microliters/g body wt) was injected intraperitoneally into fish (mean wt 54 +/- 5 g) that were killed 0.5-24 h after administration. Glucose injection resulted in hyperglycemia with maximum glucose levels of 306 +/- 13 mg/dl observed 60 min after injection. Glucose administration also resulted in hyperlipidemia. Plasma fatty acids increased twofold in glucose-injected animals. Alterations in plasma metabolites reflected changes in energy stores. Although total lipid concentration was unaffected by glucose injection, lipolytic enzyme activity in the liver was enhanced. Biosynthetic capacity, as indicated by NADPH production from glucose-6-phosphate dehydrogenase, was decreased by glucose injection. Liver glycogen content was reduced in glucose-injected animals 1 h after injection. Glucose injection was attended by increases in the plasma levels of gene II somatostatin-25 (predominant form of pancreatic somatostatin in salmonids) and of glucagon. Insulin levels were initially suppressed after glucose injection. These results indicate that metabolic adjustments caused by glucose administration can be related to the regulatory action of pancreatic hormones. Furthermore, these results suggest that the somatostatin-secreting cells of the trout are sensitive to glucose and that somatostatin-suppressed insulin secretion contributes to the glucose intolerance of trout.

scholarly journals Differential Increase in Forebrain and Caudal Neurosecretory System Corticotropin-Releasing Factor and Urotensin I Gene Expression Associated with Seawater Transfer in Rainbow Trout

Endocrinology ◽  
2005 ◽  
Vol 146 (9) ◽  
pp. 3851-3860 ◽  
Author(s):  
Paul M. Craig ◽  
Haider Al-Timimi ◽  
Nicholas J. Bernier
Keyword(s):  
Rainbow Trout ◽  
Food Intake ◽  
Preoptic Area ◽  
Plasma Osmolality ◽  
Corticotropin Releasing Factor ◽  
Neurosecretory System ◽  
Mrna Levels ◽  
Caudal Neurosecretory System ◽  
Differential Increase ◽  
Crf System

Abstract Transfer to seawater (SW) in rainbow trout elicits an increase in plasma cortisol and a bout of anorexia. Although the corticotropin-releasing factor (CRF) system has known hypophysiotropic and anorexigenic properties, it is not known whether CRF-related peptides originating from either the forebrain or the caudal neurosecretory system (CNSS) play a role during SW acclimation. Therefore, we examined the effects of SW transfer on food intake, plasma osmolality, hypothalamic-pituitary-interrenal axis activity, and the expression of CRF and urotensin I (UI) in the forebrain and the CNSS. While SW transfer chronically suppressed food intake over a 2-wk period, it transiently increased plasma osmolality, ACTH, and cortisol. Similarly, 24 h after SW transfer, hypothalamic and preoptic area CRF mRNA levels were significantly increased but recovered to pretransfer levels within 7 d. Conversely, SW transfer elicited a delayed increase in hypothalamic UI mRNA levels and had no effect on preoptic area UI expression. In the CNSS, SW exposure was associated with parallel increases in CRF and UI mRNA levels from 24 h post transfer through 7 d. Finally, in situ hybridization demonstrated an extensive and overlapping pattern of CNSS CRF and UI expression. These results differentially implicate specific neuronal populations of the CRF system in the acute and chronic responses to a hyperosmotic stress and suggest that forebrain and CNSS CRF-related peptides have different roles in the coordinated response to fluid balance disturbances.

Evidence of a metabolic fatty acid-sensing system in the hypothalamus and Brockmann bodies of rainbow trout: implications in food intake regulation

2012 ◽  
Vol 302 (11) ◽  
pp. R1340-R1350 ◽  
Author(s):  
Marta Librán-Pérez ◽  
Sergio Polakof ◽  
Marcos A. López-Patiño ◽  
Jesús M. Míguez ◽  
José L. Soengas
Keyword(s):  
Fatty Acid ◽  
Rainbow Trout ◽  
Food Intake ◽  
Fatty Acid Metabolism ◽  
Fatty Acid Synthase ◽  
Acid Metabolism ◽  
Chain Fatty Acid ◽  
Mrna Levels ◽  
Sensing System ◽  
Fatty Acid Sensing

Enhanced lipid levels inhibit food intake in fish but no studies have characterized the possible mechanisms involved. We hypothesize that the presence of fatty acid (FA)-sensing mechanisms could be related to the control of food intake. Accordingly, we evaluated in the hypothalamus, hindbrain, and Brockmann bodies (BB) of rainbow trout changes in parameters related to fatty acid metabolism, transport of FA, nuclear receptors, and transcription factors involved in lipid metabolism, and components of the KATP channel after intraperitoneal administration of different doses of oleic acid (long-chain fatty acid, LCFA) or octanoic acid (medium-chain fatty acid, MCFA). The increase in circulating LCFA or MCFA levels elicited an inhibition in food intake and induced in the hypothalamus a response compatible with fatty acid sensing in which fatty acid metabolism, binding to cluster of differentiation 36 (CD36), and mitochondrial activity are apparently involved, which is similar to that suggested in mammals except for the apparent capacity of rainbow trout to detect changes in MCFA levels. Changes in those hypothalamic pathways can be related to the control of food intake, since food intake was inhibited when FA metabolism was perturbed (using fatty acid synthase or acetyl-CoA carboxylase inhibitors) and changes in mRNA levels of specific neuropeptides such as neuropeptide Y and proopiomelancortin were also noticed. This response seems to be exclusive for the hypothalamus, since the other center controlling food intake (hindbrain) was unaffected by treatments. The results obtained in BB suggest that at least two of the components of a putative fatty acid-sensing system (based on fatty acid metabolism and binding to CD36) could be present. Therefore, the present study provides, for the first time in fish, evidence for a specific role for FA (MCFA and LCFA) as metabolic signals in hypothalamus and BB, where the detection of those FA can be associated with the control of food intake and hormone release.

Interleukin-6 secretion in mice is associated with reduced glucose-6-phosphatase and liver glycogen levels

1997 ◽  
Vol 273 (2) ◽  
pp. E262-E267 ◽  
Author(s):  
S. Metzger ◽  
N. Goldschmidt ◽  
V. Barash ◽  
T. Peretz ◽  
O. Drize ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Glycogen Content ◽  
Liver Glycogen ◽  
Mrna Levels ◽  
Chronic Effect ◽  
Glucose Levels ◽  
Reduced Body ◽  
Blood Glucose Levels ◽  
Liver Glycogen Content

Mice bearing interleukin-6 (IL-6)-secreting tumor were used to study the chronic effect of IL-6 on carbohydrate metabolism. Mice were injected with allogeneic tumor cells transduced with the murine IL-6 gene. Serum IL-6 levels were correlated exponentially with tumor weight. Secretion of IL-6 from the developed tumors was associated with decreased food consumption, reduced body weight, and reduced blood glucose levels. Insulin levels did not change, and 2-deoxyglucose uptake was not affected in most tissues examined. A significant increase of 2-deoxyglucose uptake was measured in the liver. Glycogen content in the liver determined 0, 6, 12, and 18 days after tumor inoculation was 42, 23, 12, and 3 mg/g, respectively. The activity of phosphoenolpyruvate carboxykinase was not affected. The activity of glucose-6-phosphatase (G-6-Phase) determined 6, 12, and 18 days after tumor injection was 84, 70, and 50% of G-6-Pase activity in pair-fed mice bearing nonsecreting tumors, respectively. G-6-Pase mRNA levels were markedly reduced due to inhibition of G-6-Pase gene transcriptional rate.

Milnacipran, a serotonin and norepinephrine reuptake inhibitor, induces appetite-suppressing effects without inducing hypothalamic stress responses in mice

2007 ◽  
Vol 292 (5) ◽  
pp. R1775-R1781 ◽  
Author(s):  
Katsunori Nonogaki ◽  
Kana Nozue ◽  
Tomifusa Kuboki ◽  
Yoshitomo Oka
Keyword(s):  
Blood Glucose ◽  
Food Intake ◽  
Receptor Antagonist ◽  
Reuptake Inhibitor ◽  
Plasma Corticosterone ◽  
Cytokine Signaling ◽  
Mrna Levels ◽  
Wild Type ◽  
Glucose Levels ◽  
Blood Glucose Levels

Milnacipran, a selective serotonin (5-HT) and norepinephrine (NE) reuptake inhibitor, increases extracellular 5-HT and NA levels equally in the central nervous system. Here, we report that systemic administration of milnacipran (20–60 mg/kg) significantly suppressed food intake after fasting in C57BL6J mice. The appetite-suppressing effects of milnacipran were sustained for 5 h. Neither SB242084, a selective 5-HT2C receptor antagonist, nor SB224289, a selective 5-HT1B receptor antagonist, reversed the appetite-suppressing effects of milnacipran. Milnacipran suppressed food intake and body weight in wild-type mice and in Ay mice, which have ectopic expression of the agouti protein. Moreover, milnacipran significantly increased hypothalamic proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) mRNA levels, while having no effect on hypothalamic neuropeptide Y, ghrelin, corticotropin-releasing hormone (CRH), and suppressor of cytokine signaling-3 mRNA levels. Interestingly, milnacipran did not increase plasma corticosterone and blood glucose levels, whereas fenfluramine, which inhibits 5-HT reuptake and stimulates 5-HT release, significantly increased plasma corticosterone and blood glucose levels in association with increased hypothalamic CRH mRNA levels. The appetite-suppressing effects of milnacipran had no effects on food intake in food-restricted, wild-type mice and Ay mice. On the other hand, fenfluramine suppressed food intake in food-restricted wild-type mice, but it had no effects in food-restricted Ay mice. These results suggest that inhibition of 5-HT and NA reuptake induces appetite-suppressing effects independent of 5-HT2C and 5-HT1B receptors, and increases hypothalamic POMC and CART gene expression without increasing plasma corticosterone and blood glucose levels in mice.

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