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Dose response of bone mass to dietary arachidonic acid in piglets fed cow milk-based formula
Janice L Blanaru1, June R Kohut, Shirley C Fitzpatrick-Wong
1Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Canada.
Insights
Dietary arachidonic acid (AA) supplementation in piglets increased bone mass, particularly at higher doses. Bone modeling was unaffected, but higher AA intake positively influenced bone mineral content.
Area of Science:
- Nutritional Science
- Pediatric Nutrition
- Bone Biology
Background:
- Arachidonic acid (AA) and docosahexaenoic acid (DHA) are now approved for infant formula in North America.
- Previous studies in piglets suggest a link between dietary AA and increased bone mass.
Purpose of the Study:
- To investigate the impact of varying dietary arachidonic acid (AA) levels on bone modeling and bone mass in piglets.
- To establish optimal AA supplementation for infant nutrition using a piglet model.
Main Methods:
- Male piglets (n=32) received formulas with 0.30% to 0.75% AA and 0.1% DHA from day 5 to 20.
- Measurements included bone modeling biomarkers, fatty acid status, and bone mineral content (dual-energy X-ray absorptiometry).
- Statistical analyses included two-factor ANOVA and regression analyses.
Main Results:
- Dietary AA significantly altered AA proportions in plasma, liver, and adipose tissue.
- Bone modeling remained unaffected by dietary treatments.
- Higher dietary AA (0.60% and 0.75%) elevated whole-body bone mineral content, predicted by dietary AA and bone resorption.
Conclusions:
- Dietary AA supplementation positively influences bone mass in term-born pigs.
- Optimal dietary AA levels for bone mass accrual were identified.
- Further research is needed to determine the role of varying docosahexaenoic acid (DHA) levels in bone mass.
Background:
The addition of arachidonic acid (AA) and docosahexaenoic acid (DHA) to infant formula was recently approved in North America. In piglets, dietary AA is linked to elevations in bone mass.
Objective:
The objective was to investigate the effects of varied amounts of dietary AA on bone modeling and bone mass with the use of the piglet model for infant nutrition.
Design:
Male piglets (n = 32) were randomly assigned to receive 1 of 4 formulas supplemented with AA (0.30%, 0.45%, 0.60%, or 0.75% of fat) plus DHA (0.1% of fat) from days 5 to 20 of life. Measurements included biomarkers of bone modeling, fatty acid status, and whole-body and femur bone mineral content; bone area was measured by dual-energy X-ray absorptiometry. Differences among groups were detected with two-factor analysis of variance. Regression analyses were used to determine factors responsible for bone mineral content after dietary AA was accounted for.
Results:
Proportions of AA in plasma, liver, and adipose were modified by the dietary treatments, but bone modeling was not affected. Liver AA was positively related to plasma insulin-like growth factor 1 and calcitriol and urinary N-telopeptide. Whole-body bone mineral content was elevated in the piglets fed 0.60% and 0.75% AA and was best predicted by dietary AA and bone resorption.
Conclusions:
This study confirms that dietary AA alters bone mass and clarifies the best amount of AA to add to the diet of pigs born at term. Because the amount of dietary DHA was held constant, whether other amounts of DHA are related to bone mass requires investigation.
