We hypothesized that peptide YY (PYY) is involved in the metabolic regulation of food intake in fish. Therefore， we assessed in rainbow trout (Oncorhynchus mykiss) the effects of intracerebroventricular treatment with 10?ng/g PYY on food intake， expression of neuropeptides involved in food intake control， and the activity of fatty acid-sensing systems. The administration of PYY caused a significant reduction in food intake up to 24?h post-treatment. This anorectic action was associated with changes 2?h after treatment in mRNA abundance of neuropeptides involved in metabolic regulation of food intake in hypothalamus (decreased NPY and raised CART values) and hindbrain (increased POMCa1 values). We also obs... More
We hypothesized that peptide YY (PYY) is involved in the metabolic regulation of food intake in fish. Therefore， we assessed in rainbow trout (Oncorhynchus mykiss) the effects of intracerebroventricular treatment with 10?ng/g PYY on food intake， expression of neuropeptides involved in food intake control， and the activity of fatty acid-sensing systems. The administration of PYY caused a significant reduction in food intake up to 24?h post-treatment. This anorectic action was associated with changes 2?h after treatment in mRNA abundance of neuropeptides involved in metabolic regulation of food intake in hypothalamus (decreased NPY and raised CART values) and hindbrain (increased POMCa1 values). We also observed that PYY treatment induced changes in mRNA abundance of parameters related to fatty acid sensing and metabolism in hypothalamus (decreased values of ACLY， PPARγ， and SREBP1c) and hindbrain (increased values of LPL， FAT/CD36， PPARα， PPARγ， and SREBP1c and decreased values of UCP2a). PYY treatment also increased mRNA abundance of mTOR. In general， it seems that mRNAs encoding some components of the machinery required for fatty acid sensing and metabolism are activated by PYY. The response observed was higher in the hindbrain than in the hypothalamus， supporting the greater importance of this brain area in mediating the modulatory effects of gastrointestinal hormones on feeding regulation.
