Insulin-like growth factor-1 (Igf1) signaling responses to food consumption after fasting in the Pacific rockfish Sebastes carnatus
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Insulin-like growth factor-1 (Igf1) signaling responses to food consumption after fasting in the Pacific rockfish Sebastes carnatus

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  • Journal Title:
    Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology
  • Personal Author:
  • NOAA Program & Office:
  • Description:
    Fish adjust rates of somatic growth in the face of changing food consumption. As in other vertebrates, growth in fish is regulated by the growth hormone (Gh)/insulin-like growth factor-1 (Igf1) endocrine axis, and changes in food intake impact growth via alterations to Gh/Igf1 signaling. Understanding the time course by which the Gh/Igf1 axis responds to food consumption is crucial to predict how rapidly changes in food abundance might lead to altered growth dynamics. Here, we looked at the response times of plasma Igf1 and liver Igf1 signaling-associated gene expression to refeeding after food deprivation in juvenile gopher rockfish (Sebastes carnatus), one of several species of northern Pacific Ocean Sebastes rockfishes targeted by fisheries or utilized for aquaculture. Gopher rockfish were fasted for 30 d, after which a subset was fed to satiation for 2 h, while other rockfish continued to be fasted. Refed fish exhibited higher hepatosomatic index (HSI) values and increased Igf1 after food consumption. Gene transcripts for Gh receptor 1 (ghr1), but not ghr2, increased in the liver 2-4 d after eating. Transcripts encoding igf1also increased in the liver of refed fish by 4 d after feeding, only to return to levels similar as continually fasted rockfish by 9 d after feeding. Liver mRNA abundances for Igf binding protein (Igfbp) genes igfbp1a, igfbp1b, and igfbp3a declined within 2 d of feeding. These findings provide evidence that circulating Igf1 in rockfish reflects a fish's feeding experience within the previous few days, and suggest that feeding-induced increases in Igf1 are being mediated in part by altered liver sensitivity to Gh due to upregulated Gh receptor 1 expression.
  • Source:
    Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 282, 111444
  • DOI:
  • ISSN:
    1095-6433
  • Format:
    PDF
  • Publisher:
    Elsevier BV
  • Document Type:
    Journal Article
  • License:
  • Rights Information:
    CC BY-NC-ND
  • Compliance:
    Submitted
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