Potential role of intelectin-1 in the regulation of feeding of goldfish (Carassius auratus).

Appetite regulation in vertebrates involves central neuropeptides and peripheral metabolic and endocrine signals that act together to maintain energy homeostasis. These include orexigenic (e.g., neuropeptide Y, orexin, ghrelin) and anorexigenic (e.g., cocaine- and amphetamine-regulated transcript, corticotropin-releasing factor, cholecystokinin, leptin) factors coordinate feeding behavior. Intelectin-1 (ITLN1), a protein implicated in innate immunity and metabolic signaling in mammals, has not yet been investigated in the context of fish feeding physiology. This study examined the potential role of ITLN1 in appetite regulation and energy metabolism in goldfish (Carassius auratus). We first determined tissue distribution of itln1, which showed highest mRNA levels in spleen and liver and lower expression in brain, intestine, kidney, and gonads. Short-term fasting reduced itln1 expression in the hypothalamus and intestine, but not in liver. Peripheral administration of recombinant human ITLN1 (250-500 ng/g) significantly reduced food intake without altering blood glucose. At the highest dose (500 ng/g), ITLN1 increased brain expression of anorexigenic neuropeptides cart1, crf, trh, cck and lep2, intestinal expression of cck and inflammatory markers (tnfa, il1b) and hepatic lep2 and glycogen synthase (gs) expressions, with no effect on orexigenic peptides or glucose transporters. These findings suggest that ITLN1 might act as a peripheral satiety signal in goldfish, modulating the expression of anorexigenic neuropeptides, gut hormones, and hepatic metabolic genes. This study provides initial evidence that ITLN1 may contribute to appetite regulation in a teleost, suggesting a potential role in coordinating immunity, nutrient metabolism, and central pathways involved in feeding.