Hypoxemia-induced leptin secretion: a mechanism for the control of food intake in diseased fish

MacDonald, Lauren E; Alderman, Sarah L.; Krämer, Sarah; Woo, P. T. K.; Bernier, Nicholas J.

doi:10.1530/joe-13-0615

Cited by 26 publications

(11 citation statements)

References 85 publications

(118 reference statements)

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“…Our observations of increased AgRP gene expression during anorexia are reminiscent of findings of studies of the effects of parasitic infection in rats and fish . In rats, NPY gene expression in the arcuate nucleus was increased 8 days after infection, coincident with decreased food intake .…”

Section: Discussionsupporting

confidence: 77%

Hypothalamic Agouti‐Related Peptide mRNA is Elevated During Natural and Stress‐Induced Anorexia

Dunn

Wilson

D’Eath

et al. 2015

J Neuroendocrinology

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This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.As part of their natural lives, animals can undergo periods of voluntarily reduced food intake and body weight (i.e. animal anorexias) that are beneficial for survival or breeding, such as during territorial behaviour, hibernation, migration and incubation of eggs. For incubation, a change in the defended level of body weight or 'sliding set point' appears to be involved, although the neural mechanisms reponsible for this are unknown. We investigated how neuropeptide gene expression in the arcuate nucleus of the domestic chicken responded to a 60-70% voluntary reduction in food intake measured both after incubation and after an environmental stressor involving transfer to unfamiliar housing. We hypothesised that gene expression would not change in these circumstances because the reduced food intake and body weight represented a defended level in birds with free access to food. Unexpectedly, we observed increased gene expression of the orexigenic peptide agouti-related peptide (AgRP) in both incubating and transferred animals compared to controls. Also pro-opiomelanocortin (POMC) mRNA was higher in incubating hens and significantly increased 6 days after exposure to the stressor. Conversely expression of neuropeptide Y and cocaine-and amphetamine-regulated transcript gene was unchanged in both experimental situations. We conclude that AgRP expression remains sensitive to the level of energy stores during natural anorexias, which is of adaptive advantage, although its normal orexigenic effects are over-ridden by inhibitory signals. In the case of stress-induced anorexia, increased POMC may contribute to this inhibitory role, whereas, for incubation, reduced feeding may also be associated with increased expression in the hypothalamus of the anorexigenic peptide vasoactive intestinal peptide.

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Section: Discussionsupporting

confidence: 77%

Hypothalamic Agouti‐Related Peptide mRNA is Elevated During Natural and Stress‐Induced Anorexia

Dunn

Wilson

D’Eath

et al. 2015

J Neuroendocrinology

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“…Consistent with the stimulatory effects of glucocorticoids on the expression and secretion of leptin from adipocytes in mammals (Lee & Fried 2009), our in vitro results demonstrate that physiological concentrations of cortisol directly stimulate lep-a1 mRNA levels through GRs in rainbow trout hepatocytes. Given the anorexigenic effects of leptin (Murashita et al 2008, MacDonald et al 2014 and CRF (Bernier 2006, Ortega et al 2013 in rainbow trout, the inverse relationship between the expression of these genes and food intake during the dosage and recovery periods suggest that liver leptin and POA CRF mediate at least a portion of the appetite-suppressing effects of cortisol in this species. Whether the cortisol-mediated increase in hepatic lep-a1 gene expression translates into an increase in circulating leptin levels, and whether leptin stimulates CRF release in fish as it does in mammals (Roubos et al 2012) remain to be determined.…”

Section: Discussionmentioning

confidence: 99%

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

Madison

Tavakoli

Krämer

et al. 2015

Journal of Endocrinology

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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 w70 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 pituitary gh, liver gh receptor (ghr), liver igfI and igf binding protein (igfbp)-1 and -2 mRNA levels, reduced plasma GH and no change in plasma IGF1. During recovery, while plasma GH and pituitary gh, liver ghr and igfI gene expression did not differ between treatments, the high cortisol-treated fish had lower plasma IGF1 and elevated liver igfbp1 mRNA 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 liver lep-a1 and POA crf mRNA, from sustained increases in hepatic igfbp1 expression that reduce the growth-promoting actions of the GH/IGF axis, and from a mobilization of energy reserves.

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“…Nonetheless, hypoxia and food-deprivation effects on EODa both follow timecourses roughly consistent with the rate at which leptin treatment increased EODa, suggesting the possibility that leptin mediates EODa responses to metabolic state in both cases. Indeed, leptin mediates hypoxia responses in several species of fish (Bernier et al, 2012;Chu et al, 2010;MacDonald et al, 2014), but does so by increasing leptin expression which in turn inhibits feeding. Additional research to determine the endocrine cascades that reduce EODa in hypoxic conditions and during food deprivation will provide a more complete picture of the neuroendocrine mechanisms for managing the energetic costs of EOD production during metabolic stress in E. virescens.…”

Section: Discussionmentioning

confidence: 99%

Food deprivation reduces and leptin increases the amplitude of an active sensory and communication signal in a weakly electric fish

Sinnett

Markham

2015

Hormones and Behavior

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Energetic demands of social communication signals can constrain signal duration, repetition, and magnitude. The metabolic costs of communication signals are further magnified when they are coupled to active sensory systems that require constant signal generation. Under such circumstances, metabolic stress incurs additional risk because energy shortfalls could degrade sensory system performance as well as the social functions of the communication signal. The weakly electric fish Eigenmannia virescens generates electric organ discharges (EODs) that serve as both active sensory and communication signals. These EODs are maintained at steady frequencies of 200-600Hz throughout the lifespan, and thus represent a substantial metabolic investment. We investigated the effects of metabolic stress (food deprivation) on EOD amplitude (EODa) and EOD frequency (EODf) in E. virescens and found that only EODa decreases during food deprivation and recovers after restoration of feeding. Cortisol did not alter EODa under any conditions, and plasma cortisol levels were not changed by food deprivation. Both melanocortin hormones and social challenges caused transient EODa increases in both food-deprived and well-fed fish. Intramuscular injections of leptin increased EODa in food-deprived fish but not well-fed fish, identifying leptin as a novel regulator of EODa and suggesting that leptin mediates EODa responses to metabolic stress. The sensitivity of EODa to dietary energy availability likely arises because of the extreme energetic costs of EOD production in E. virescens and also could reflect reproductive strategies of iteroparous species that reduce social signaling and reproduction during periods of stress to later resume reproductive efforts when conditions improve.

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Hypoxemia-induced leptin secretion: a mechanism for the control of food intake in diseased fish

Cited by 26 publications

References 85 publications

Hypothalamic Agouti‐Related Peptide mRNA is Elevated During Natural and Stress‐Induced Anorexia

Hypothalamic Agouti‐Related Peptide mRNA is Elevated During Natural and Stress‐Induced Anorexia

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

Food deprivation reduces and leptin increases the amplitude of an active sensory and communication signal in a weakly electric fish

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