Abstract
Rainbow trout (Oncorhynchus mykiss) is considered a “glucose-intolerant” species. With the aim of programming trout to improve their metabolic use of dietary carbohydrates, we hypothesised that a hypoxic stimulus applied during embryogenesis could later affect glucose metabolism at the first-feeding stage. An acute hypoxic stimulus (2.5 or 5.0 mg·L−1 O2) was applied for 24 h to non-hatched embryos or early hatched alevins followed by a challenge test with a high carbohydrate diet at first-feeding. The effectiveness of the early hypoxic stimulus was confirmed by the induction of oxygen-sensitive markers such as egln3. At first-feeding, trout previously subjected to the 2.5 mg·L−1 O2 hypoxia displayed a strong induction of glycolytic and glucose transport genes, whereas these glucose metabolism-related genes were affected much less in trout subjected to the less severe (5.0 mg·L−1 O2) hypoxia. Our results demonstrate that an acute hypoxic stimulus during early development can affect glucose metabolism in trout at first-feeding.
Highlights
4.5 ± 1.6%b to be atypically up-regulated by dietary carbohydrates[14, 15], and this phenotype was demonstrated to take place as soon as the first-feeding stages[15]. These results suggest that applying a stimulus at first-feeding, as Geurden et al did[12], may be too late to programme glucose metabolism in trout for the long-term
No data relating to programming assays with hypoxia in trout are available, previous studies of mammals have found that intra-uterine hypoxia could inhibit gluconeogenesis and alter plasma glucose content in offspring[6, 27], demonstrating that hypoxia has a long-lasting programming effect on glucose metabolism
We hypothesise that an early exposure to hypoxia in trout may modulate glucose metabolism and that such a modification could be recorded as a “physiological memory” and reveal itself later in life when fish are challenged with a high carbohydrate diet
Summary
4.5 ± 1.6%b to be atypically up-regulated by dietary carbohydrates[14, 15], and this phenotype was demonstrated to take place as soon as the first-feeding stages[15]. No data relating to programming assays with hypoxia in trout are available, previous studies of mammals have found that intra-uterine hypoxia could inhibit gluconeogenesis and alter plasma glucose content in offspring[6, 27], demonstrating that hypoxia has a long-lasting programming effect on glucose metabolism. Such a stimulus is easy to apply on a large scale to individuals compared to microinjections performed directly in the yolk as previously tested in zebrafish[28]. As transcriptional modification is the first step to mediate metabolic programming, we mainly focus on the programming effects at the transcriptional level, i.e., alteration in mRNA levels of critical genes involved in glycolysis, gluconeogenesis and the glucose transport pathway
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