Abstract
Nesfatin-1 is an 82 amino acid peptide that has been involved in a wide variety of physiological functions in both mammals and fish. This study aimed to elucidate the role of nesfatin-1 on rainbow trout food intake, and its putative effects on glucose and fatty acid sensing systems. Intracerebroventricular administration of 25 ng/g nesfatin-1 resulted in a significant inhibition of appetite, likely mediated by the activation of central POMC and CART. Nesfatin-1 stimulated the glucosensing machinery (changes in sglt1, g6pase, gsase, and gnat3 mRNA expression) in the hindbrain and hypothalamus. Central fatty acid sensing mechanisms were unaltered by nesfatin-1, but this peptide altered the expression of mRNAs encoding factors regulating lipid metabolism (fat/cd36, acly, mcd, fas, lpl, pparα, and pparγ), suggesting that nesfatin-1 promotes lipid accumulation in neurons. In the liver, intracerebroventricular nesfatin-1 treatment resulted in decreased capacity for glucose use and lipogenesis, and increased the potential of fatty acid oxidation. Altogether, the present results demonstrate that nesfatin-1 is involved in the homeostatic regulation of food intake and metabolism in fish.
Highlights
Food intake in vertebrates is subject to a complex regulation involving both peripheral components in charge of transmitting the metabolic status of the organism, and the central nervous system (CNS), responsible for receiving, processing and responding to this information [1]
Glucosensing in fish is mainly driven by the canonical mechanism based on glucokinase (GCK), glucose facilitative transporter 2 (GLUT2) and ATP-dependent inward rectified potassium channel (KATP) [3,4,5,6], GCK-independent glucosensing mechanisms based on the sodium-glucose linked transporter 1 (SGLT-1), liver X receptor (LXR) and sweet taste receptor have been described in the rainbow trout brain [7, 8]
The present study evaluates the effects of ICV administered nesfatin-1 on food intake, and on the expression of key genes involved in nutrient sensing mechanisms in the brain and liver of rainbow trout
Summary
Food intake in vertebrates is subject to a complex regulation involving both peripheral components in charge of transmitting the metabolic status of the organism, and the central nervous system (CNS), responsible for receiving, processing and responding to this information [1]. Specific hypothalamic nuclei in the CNS are responsive to changes in energy status, and respond with variations in the expression of key neuropeptides (agouti-related protein (AgRP)/neuropeptide Y (NPY), and pro-opio melanocortin (POMC)/cocaine and amphetaminerelated transcript (CART)), leading to changes in food intake [2]. These hypothalamic neurons, together with neurons from the hindbrain possess nutrient sensing mechanisms able to detect the levels of nutrients, glucose, fatty acids and amino acids, as demonstrated in mammals [2] and in fish [3, 4]. Available evidence suggests that comparable signaling pathways and transcription factors might be linking nutrient sensing and the expression of neuropeptides [15,16,17]
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