The influence of first-feeding diet on the Atlantic cod Gadus morhua phenotype: survival, development and long-term consequences for growth.

Atlantic cod Gadus morhua larvae reached four-fold (at low larval density) to 11 fold higher body mass (high larval density) at 50 days post hatch (dph) when fed zooplankton rather than enriched rotifers. A short period (22-36 dph) of dietary change affected larval growth positively if changed from enriched rotifers to natural zooplankton and negatively if prey type changed vice versa. Overall survival did not differ between the two larval groups at low larval density, but at high density the rotifer group had a higher overall survival (10.8% v. 8.9%). Long-term growth was affected significantly by larval diet in favour of the zooplankton diet; juveniles reached a 23% higher mass in a 12 week growth period. No difference in growth performance was found between juveniles fed natural zooplankton during the larval period for 36, 22 or 14 days, but all these juveniles performed significantly better compared with the rotifer-fed group. These findings suggest that optimal diet during a short period in the larval period can result in improved growth in both the larval and juvenile period. Improved rotifer quality may, therefore, hold a large potential for growth improvement in this species.

Distribution of cholecystokinin-immunoreactive cells in the gut of developing Atlantic cod Gadus morhua L. larvae fed zooplankton or rotifers.

One of the main gastrointestinal hormones, cholecystokinin (CCK), was studied in order to advance understanding of the control of the digestive process in Atlantic cod Gadus morhua larvae after onset of first feeding. Larvae were fed either natural zooplankton or enriched rotifers in similar rearing systems and sampled from hatching to 22 days post-hatch (dph). CCK was visualized by immunohistochemistry and the first CCK-immunoreactive (IR) cells were detected at 8 dph corresponding to 6 days after first feeding. The CCK-IR cells were mostly found in the anterior midgut, and the number of CCK-IR cells was lower in the posterior midgut. They were also present in the hindgut of some of the larvae, but not in the foregut. No clear differences were found in the ontogenetic appearance and the distribution pattern of CCK-IR cells between the two dietary treatments. This indicates that the onset of CCK production in the gut as well as the spatial distribution of the CCK-IR cells is not differentially affected by these diets. To what extent the hormone production itself is influenced by dietary factors needs to be studied by more sensitive methods.