Dual mode of cortisol action on GH/IGF-I/IGF binding proteins in the tilapia, Oreochromis mossambicus

IGF-binding proteins (IGFBPs) modulate the effects of the IGFs, major stimulators of vertebrate growth and development. In mammals, IGFBP-1 inhibits the actions of IGF-I. Rapid increases in circulating IGFBP-1 occur during catabolic states. Insulin and glucocorticoids are the primary regulators of circulating IGFBP-1 in mammals. Insulin inhibits and glucocorticoids stimulate hepatocyte IGFBP-1 gene expression and production. A 22 kDa IGFBP in salmon blood also increases during catabolic states and has recently been identified as an IGFBP-1 homolog. We examined the hormonal regulation of salmon IGFBP-1 mRNA levels and protein secretion in primary cultured salmon hepatocytes. The glucocorticoid agonist dexamethasone progressively increased hepatocyte IGFBP-1 mRNA levels (eightfold) and medium IGFBP-1 immunoreactivity over concentrations comparable with stressed circulating cortisol levels (10 K9-10 K6 M). Triiodothyronine had no effect on hepatocyte IGFBP-1 mRNA, whereas glucagon increased IGFBP-1 mRNA (2 . 2-fold) at supraphysiological concentrations (10 K6 M). This study suggests that the major inhibitory role of insulin in the regulation of liver IGFBP-1 production in mammals is not found in salmon. However, regulation of salmon liver IGFBP-1 production by other metabolic hormones is similar to what is found in mammals.

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Metabolic hormones regulate insulin-like growth factor binding protein-1 mRNA levels in primary cultured salmon hepatocytes; lack of inhibition by insulin

Pierce¹,

Shimizu²,

Felli³

et al. 2006

“…!48 h). Overall, on an acute time scale, cortisol injections or stressors in fish either have no effect or decrease plasma GH levels, reduce liver igf1 gene expression and plasma IGF1 levels, counteract GH stimulation of liver igf1 transcription, and increase the hepatic expression and plasma levels of low molecular weight IGF binding proteins (IGFBPs) (Kelley et al 2001, Kajimura et al 2003, Pierce et al 2005, Wilkinson et al 2006, Leung et al 2008, Saera-Vila et al 2009, Breves et al 2010, Shepherd et al 2011, Nakano et al 2013. In channel catfish (Ictalurus punctatus), chronic dietary cortisol had no effect on liver igf1 mRNA levels, reduced plasma IGF1, and increased the plasma levels of low molecular weight IGFBPs (Peterson & Small 2005).…”

Section: Introductionmentioning

confidence: 99%

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

Madison

Tavakoli

Krämer

et al. 2015

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.

“…However, the endocrine mechanisms leading to GH resistance in fishes are relatively unexplored. Insulin injection increased plasma IGF-I in brown trout (Salmo trutta) (Banos et al 1999), and cortisol injection decreased plasma IGF-I in tilapia (Kajimura et al 2003), suggesting that mechanisms similar to those in mammalian hepatocytes may be operating.…”

Section: Introductionmentioning

confidence: 99%

Metabolic hormones modulate the effect of growth hormone (GH) on insulin-like growth factor-I (IGF-I) mRNA level in primary culture of salmon hepatocytes

Pierce

Fukada²,

Dickhoff³

2005

Liver production of insulin-like growth factor-I (IGF-I) is a major point of control in the growth hormone (GH)/IGF axis, the endocrine system regulating body growth in fishes and other vertebrates. Pituitary GH stimulates hepatocyte production of IGF-I; however, in catabolic states, hepatocyte GH resistance results in decreases in liver IGF-I production. To investigate endocrine mechanisms leading to the development of hepatocyte GH resistance, we examined the regulation of IGF-I mRNA level by GH and metabolic hormones in primary culture of salmon hepatocytes. Cells were cultured in RPMI medium, and exposed to insulin (Ins, 10 6