Abstract
The growth hormone (GH)–insulin-like growth factor I (IGF-I) system regulates important physiological functions in salmonid fish, including hydromineral balance, growth, and metabolism. While major research efforts have been directed toward this complex endocrine system, understanding of some key aspects is lacking. The aim was to provide new insights into GH resistance and growth hormone-binding proteins (GHBPs). Fish frequently respond to catabolic conditions with elevated GH and depressed IGF-I plasma levels, a condition of acquired GH resistance. The underlying mechanisms or the functional significance of GH resistance are, however, not well understood. Although data suggest that a significant proportion of plasma GH is bound to specific GHBPs, the regulation of plasma GHBP levels as well as their role in modulating the GH–IGF-I system in fish is virtually unknown. Two in vivo studies were conducted on rainbow trout. In experiment I, fish were fasted for 4 weeks and then refed and sampled over 72 h. In experiment II, two lines of fish with different muscle adiposity were sampled after 1, 2, and 4 weeks of fasting. In both studies, plasma GH, IGF-I, and GHBP levels were assessed as well as the hepatic gene expression of the growth hormone receptor 2a (ghr2a) isoform. While most rainbow trout acquired GH resistance within 4 weeks of fasting, fish selected for high muscle adiposity did not. This suggests that GH resistance does not set in while fat reserves as still available for energy metabolism, and that GH resistance is permissive for protein catabolism. Plasma GHBP levels varied between 5 and 25 ng ml−1, with large fluctuations during both long-term (4 weeks) fasting and short-term (72 h) refeeding, indicating differentiated responses depending on prior energy status of the fish. The two opposing functions of GHBPs of prolonging the biological half-life of GH while decreasing GH availability to target tissues makes the data interpretation difficult, but nutritional regulatory mechanisms are suggested. The lack of correlation between hepatic ghr2a expression and plasma GHBP levels indicate that ghr2a assessment cannot be used as a proxy measure for GHBP levels, even if circulating GHBPs are derived from the GH receptor molecule.
Highlights
As in mammals, the growth hormone (GH)–insulin-like growth factor I (IGF-I) system is the major endocrine system simulating growth in salmonids [1], indicating a strong evolutionary conservation
In comparison with the ad lib (AL) fish, the FA fish had elevated plasma GH levels (Figure 1A), suppressed plasma IGF-I (Figure 1B), while plasma growth hormone-binding proteins (GHBPs) levels (Figure 1C) and hepatic ghr2a expression was similar between the groups (Figure 1D)
Plasma GH levels of the FA fish were elevated over the AL fish at 8 h, after which plasma GH levels were similar in both groups (Figure 1A)
Summary
The growth hormone (GH)–insulin-like growth factor I (IGF-I) system is the major endocrine system simulating growth in salmonids [1], indicating a strong evolutionary conservation. GH can stimulate tissue growth directly, but does so indirectly through GH-induced production of IGF-I in most tissues, where it exerts paracrine regulation of growth and metabolism through its IGF-I receptor (IGF-IR) [1, 5]. GH stimulates IGF-I secretion into the circulation, where it acts as an endocrine stimulator, especially of skeletal growth [6] as well as acting as a negative-feedback signal on GH secretion [7]. In mammals as well as fish, both hormones regulate important aspects of metabolism through augmentative effects on protein accretion and counteractive effects on glucose and lipid utilization [1, 8, 9]
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