Nutrition-regulated lipolysis in rainbow trout (Oncorhynchus mykiss) is associated with alterations in the ERK, PI3K-Akt, JAK-STAT, and PKC signaling pathways

Bergan, Heather E.; Kittilson, Jeffrey D.; Sheridan, Mark A.

doi:10.1016/j.ygcen.2011.12.013

Cited by 24 publications

(19 citation statements)

References 41 publications

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“…Our specific hypothesis was that ERK and PKC mediate GH-stimulated lipolysis. The rationale for this hypothesis extends from our previous observations that hepatic lipolysis and plasma GH levels increased during periods of food deprivation (Norbeck et al 2007) and that fasting-induced lipolysis in trout liver was accompanied by the deactivation of Akt, JAK2, and STAT5 and by the activation of ERK and PKC (Bergan et al 2012). …”

Section: Introductionmentioning

confidence: 75%

“…Fish were fed twice daily to satiety with AquaMax Grower (PMI Nutrition International, Brentwood, MO, USA), except 7 days prior to the experiments. Seven-day fasted fish were used because we had shown previously that they were in a catabolic state and capable of undergoing lipolysis (Bergan et al 2012). Fish were acclimatized to laboratory conditions for at least 4 weeks.…”

Section: Experimental Animals and Conditionsmentioning

confidence: 99%

“…The protein concentration of the supernatant was determined by the Bio-Rad dye-binding method. Protein (50 mg) was separated by SDS-PAGE (7.5% running gel) and transferred onto 0.45 mm nitrocellulose membranes (Bio-Rad Laboratories) for western blot analysis , Bergan et al 2012. The membranes were washed and visualized with chemiluminescence according to the manufacturer's instructions (GE Healthcare, Buckinghamshire, UK); chemiluminescence was detected directly, and the bands were quantified with a FluorChem FC2 imager (Alpha Innotech Corp., San Leandro, CA, USA).…”

Section: Western Blot Analysismentioning

confidence: 99%

“…The abundance of phosphorylated ERK 1/2, Akt, JAK2, STAT5, and PKCa/b II was normalized to total ERK 1/2, Akt, JAK2, STAT5, and b-actin respectively. The use of these commercial antisera to detect signal elements and of pharmacological pathway inhibitors in rainbow trout has been validated previously , Bergan et al 2012.…”

Section: Western Blot Analysismentioning

confidence: 99%

“…During periods of food deprivation, lipid depletion is accompanied by increases in plasma levels of GH in the face of reduced plasma levels of INS and insulin-like growth factor 1 (IGF1) in mammals and fish (Norbeck et al 2007). We have recently shown that fasting-induced lipolysis in trout liver (as well as in adipose tissue and red and white skeletal muscle) was accompanied by the deactivation of Akt, JAK2, and STAT5 and by the activation of ERK and PKC (Bergan et al 2012). In light of the present findings that GH-stimulated lipolysis was mediated by the activation of PKC and ERK in conjunction with the deactivation of PI3K-Akt and JAK-STAT, it is reasonable to conclude that GH promotes lipolysis during fasting by the activation of PKC and ERK and by the deactivation of PI3K/Akt and JAK2-STAT.…”

Section: Figurementioning

confidence: 99%

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PKC and ERK mediate GH-stimulated lipolysis

Bergan

Kittilson

Sheridan

2013

Journal of Molecular Endocrinology

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GH regulates several physiological processes in vertebrates, including the promotion of growth, an anabolic process, and the mobilization of stored lipids, a catabolic process. In this study, we used hepatocytes isolated from rainbow trout (Oncorhynchus mykiss) as a model to examine the mechanism of GH action on lipolysis. GH stimulated lipolysis as measured by increased glycerol release in both a time-and a concentration-related manner. The promotion of lipolysis was accompanied by GH-stimulated phosphorylation of the lipolytic enzyme hormone-sensitive lipase (HSL). GH-stimulated lipolysis was also manifested by an increased expression of the two HSL-encoding mRNAs, HSL1 and HSL2. The signaling pathways that underlie GH-stimulated lipolysis were also studied. GH resulted in the activation of phospholipase C (PLC)/protein kinase C (PKC) and the MEK/ERK pathway, whereas JAK-STAT and the PI3K-Akt pathway were deactivated. The blockade of PLC/PKC and the MEK/ERK pathway inhibited GH-stimulated lipolysis and GH-stimulated phosphorylation of HSL as well as GH-stimulated HSL mRNA expression, whereas the blockade of JAK-STAT or the PI3K-Akt pathway had no effect on the activation of lipolysis or the expression of HSL stimulated by GH. These results indicate that GH promotes lipolysis by activating HSL and by enhancing the de novo expression of HSL mRNAs via the activation of PKC and ERK. These findings also suggest molecular mechanisms for activating the lipid catabolic actions of GH while simultaneously deactivating anabolic processes such as antilipolysis and the growth-promoting actions of GH.

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Section: Introductionmentioning

confidence: 75%

Section: Experimental Animals and Conditionsmentioning

confidence: 99%

Section: Western Blot Analysismentioning

confidence: 99%

Section: Western Blot Analysismentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

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PKC and ERK mediate GH-stimulated lipolysis

Bergan

Kittilson

Sheridan

2013

Journal of Molecular Endocrinology

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Evolution of the Growth Hormone Receptor Family

Sheridan

2016

Encyclopedia of Life Sciences

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The growth hormone receptor (GHR) family includes receptors for growth hormone and prolactin receptor (PRLR). GHRs and PRLRs are membrane receptors that possess several evolutionarily conserved features: a hormone‐binding extracellular domain, a single‐chain transmembrane domain and an intracellular domain important for activating intracellular signal systems that mediate cell‐specific responses. PRLRs diverged early from a common GHR/PRLR in jawless fish (e.g. Agnathans), followed by subsequent divergence of GHRs in the Actinopterygian lineage that gave rise to teleosts and in the Sarcopterygian lineage that gave rise to tetrapods. Structural heterogeneity of GHRs in teleosts results from the existence of multiple genes that arose through a series of independent gene duplication events during the course of their evolution and from alternative transcripts of a single gene. Differential receptor–ligand interactions, differential receptor–cell signalling system interactions and the differential expression of alternate GHR forms underlie the vast array of functions elicited by GH. Key Concepts Growth hormone regulates many processes, including growth, metabolism, osmoregulation, reproduction and behaviour. Growth hormone receptors are single‐pass membrane‐bound receptors that mediate the actions of growth hormone. The growth hormone receptor family arose through a series of gene duplication events during the course of vertebrate evolution. The multiple actions of growth hormone arise from binding to variant forms of growth hormone receptor and from activation of alternate cell signalling pathways.

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