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Assimilation efficiency of energy in juvenile harp seals was 92.5–95.0% of gross energy intake when fed Atlantic herring and 72.2% when fed shrimp. Faecal energy losses increased directly with intake. Metabolizable energy (ME) ranged from 85.5 to 88.7% of gross energy intake for a diet of herring. Urinary energy losses increased directly with apparent digestible nitrogen intake. Faecal and urinary losses were not affected significantly by feeding frequency. Urine excretion indicated that feeding causes a diuresis, associated with increased energy, nitrogen, and ash excretion. A significant interaction was found for rate of weight change between feeding frequency and energy intake. Seals lost more weight at energy intakes below their maintenance level when fed four meals rather than two meals per day. Differences in rate of weight change with feeding frequency were not observed at other levels of energy intake. Maintenance energy requirements were estimated at 2658 kcal ME daily for seals fed two meals per day and 3514 kcal ME daily when fed four meals per day. Seals required approximately 3 times as much shrimp as herring of high lipid content to meet their energy requirements.

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Assimilation efficiency of gross energy (±SD) in juvenile and adult grey seals fed Atlantic herring was 92.6 ± 2.1%. Metabolizable energy (ME) was 82.7 ± 4.8% of gross energy intake. Faecal energy losses increased directly with energy intake and urinary energy losses increased directly with apparent digestible nitrogen intake. Maintenance energy requirements were estimated at 4215 kcal (1 cal = 4.1868 J) ME daily for both juvenile and adult seals, equivalent to daily food intakes of 3.0–3.2 and 1.5% of body weight for juvenile and adults, respectively.

Maternal ethanol intake during pregnancy results in impairments in general growth and skeletal development in the offspring. We have previously shown that ethanol retards skeletal ossification at doses lower than those that affect growth. Moreover skeletal sites vary in their sensitivity to ethanol effects, with more severe effects occurring in bones that undergo a greater proportion of their development in utero. Taken together, these data suggest that ethanol has specific effects on bone development, and that later stages in the ossification process may be particularly affected. Such effects could have important implications for the offspring's long-term bone health, as studies suggest that the intrauterine environment can program the skeleton. The present study examined the histological stages of bone development to determine if prenatal ethanol exposure alters the morphological development of the growth plate in the fetal rat. Rats were fed a liquid diet containing ethanol (Ethanol, E group), or without ethanol (Pair-Fed, PF, or Control, C groups) for 6 weeks: 3 weeks prior to breeding and during 3 weeks of pregnancy. Fetal tibiae were fixed, decalcified and stained for histological analysis on day 21 of gestation. Maternal ethanol intake resulted in a significant decrease in fetal total bone and diaphysis lengths, compared with tibiae from PF and C fetuses. Although the lengths of the epiphyses were not affected, ethanol disrupted the organization of the histological zones within the epiphyses. Prenatal ethanol exposure decreased the length of the resting zone, but increased the length of the hypertrophic zone. Enlargement of the hypertrophic zone is consistent with an effect of ethanol on the later stages of bone development; however ethanol's effect on the resting zone indicate that earlier stages of bone development may also be disrupted. The functional significance of these morphological changes to long-term bone health remains to be determined.