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High Folic Acid Intake during Pregnancy Lowers Body Weight and Reduces Femoral Area and Strength in Female Rat Offspring

DOI: 10.1155/2013/154109

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Abstract:

Rats fed gestational diets high in multivitamin or folate produce offspring of altered phenotypes. We hypothesized that female rat offspring born to dams fed a gestational diet high in folic acid (HFol) have compromised bone health and that feeding the offspring the same HFol diet attenuates these effects. Pregnant rats were fed diets with either recommended folic acid (RFol) or 10-fold higher folic acid (HFol) amounts. Female offspring were weaned to either the RFol or HFol diet for 17 weeks. HFol maternal diet resulted in lower offspring body weights (6%, ) and, after adjusting for body weight and femoral length, smaller femoral area (2%, ), compared to control diet. After adjustments, HFol pup diet resulted in lower mineral content (7%, ) and density (4%, ) of lumbar vertebra 4 without differences in strength. An interaction between folate content of the dam and pup diets revealed that a mismatch resulted in lower femoral peak load strength ( ) and stiffness ( ). However, the match in folate content failed to prevent lower weight gain. In conclusion, HFol diets fed to rat dams and their offspring affect area and strength of femurs and mineral quantity but not strength of lumbar vertebrae in the offspring. 1. Introduction Osteoporosis is a major public health concern in North America and affects as many as 2 million Canadians [1] and 40 million Americans [2]. The financial burden of long-term, hospital, and chronic care of osteoporosis is estimated to be $2.3 billion dollars per year in Canada [3] and greater than $15 billion dollars per year in the United States [4]. Adult bone health and risk of osteoporosis is dictated, in part, by whether individuals achieve peak bone mass by young adulthood [2, 5]. Peak bone mass is controlled by genetics as well as lifestyle factors including diet and physical activity. Epidemiological evidence suggests that many children from families with history of fractures have lower bone mass, and therefore higher risk for fractures [2]. Moreover, appropriate nutrition during pregnancy and in early childhood is essential in maintaining bone health and can alter the trajectory of achieving peak bone mass (as reviewed in [5–7]). The interest in folic acid intake during pregnancy and childhood and its effects on bone health is twofold. First, higher intake of folic acid is associated with higher bone mineral density (BMD) of postmenopausal women older than 50 [8, 9] and is associated with a lower risk of fractures in men and women older than 65 [10, 11]. Second, early diet may modulate the risk of developing diseases in

References

[1]  Osteoporosis Canada, Osteoporosis & You: Facts and Statistics, Osteoporosis Canada, Toronto, Canada, 2011.
[2]  National Institutes of Health Osteoporosis and Related Bone Diseases National Resource Center, Osteoporosis Overview 2012, National Institutes of Health Osteoporosis and Related Bone Diseases National Resource Center, Bethesda, MD, USA.
[3]  J. E. Tarride, R. B. Hopkins, W. D. Leslie, et al., “The burden of illness of osteoporosis in Canada,” Osteoporosis International, vol. 23, no. 11, pp. 2591–2600, 2012.
[4]  National Institutes of Health, “NIH consensus development panel on osteoporosis prevention, diagnosis, and therapy, March 7-29, 2000: highlights of the conference,” Southern Medical Journal, vol. 94, no. 6, pp. 569–573, 2001.
[5]  D. L. Nichols, C. F. Sanborn, and E. V. Essery, “Bone density and young athletic women: an update,” Sports Medicine, vol. 37, no. 11, pp. 1001–1014, 2007.
[6]  S. A. Atkinson and W. E. Ward, “Clinical nutrition: 2. The role of nutrition in the prevention and treatment of adult osteoporosis,” Canadian Medical Association Journal, vol. 165, no. 11, pp. 1511–1514, 2001.
[7]  J. P. Brown, R. G. Josse, and Scientific Advisory Council of the Osteoporosis Society of Canada, “2002 Clinical practice guidelines for the diagnosis and management of osteoporosis in Canada,” Canadian Medical Association Journal, vol. 167, no. 10, supplement, pp. S1–S34, 2002.
[8]  L. Rejnmark, P. Vestergaard, A. P. Hermann, C. Brot, P. Eiken, and L. Mosekilde, “Dietary intake of folate, but not vitamin B2 or B12, is associated with increased bone mineral density 5 years after the menopause: results from a 10-year follow-up study in early postmenopausal women,” Calcified Tissue International, vol. 82, no. 1, pp. 1–11, 2008.
[9]  A. Cagnacci, B. Bagni, A. Zini, M. Cannoletta, M. Generali, and A. Volpe, “Relation of folates, vitamin B12 and homocysteine to vertebral bone mineral density change in postmenopausal women. A five-year longitudinal evaluation,” Bone, vol. 42, no. 2, pp. 314–320, 2008.
[10]  G. Ravaglia, P. Forti, F. Maioli et al., “Folate, but not homocysteine, predicts the risk of fracture in elderly persons,” Journals of Gerontology A, vol. 60, no. 11, pp. 1458–1462, 2005.
[11]  Y. Sato, Y. Honda, J. Iwamoto, T. Kanoko, and K. Satoh, “Effect of folate and mecobalamin on hip fractures in patients with stroke: a randomized controlled trial,” Journal of the American Medical Association, vol. 293, no. 9, pp. 1082–1088, 2005.
[12]  I. M. Y. Szeto, A. Aziz, P. J. Das et al., “High multivitamin intake by Wistar rats during pregnancy results in increased food intake and components of the metabolic syndrome in male offspring,” American Journal of Physiology, vol. 295, no. 2, pp. R575–R582, 2008.
[13]  I. M. Y. Szeto, P. J. Das, A. Aziz, and G. H. Anderson, “Multivitamin supplementation of Wistar rats during pregnancy accelerates the development of obesity in offspring fed an obesogenic diet,” International Journal of Obesity, vol. 33, no. 3, pp. 364–372, 2009.
[14]  C. E. Cho, D. Sanchez-Hernandez, S. A. Reza-Lopez, et al., “Obesogenic phenotype of offspring of dams fed a high multivitamin diet is prevented by a post-weaning high multivitamin or high folate diet,” International Journal of Obesity. In press.
[15]  A. Ly, H. Lee, J. Chen et al., “Effect of maternal and postweaning folic acid supplementation on mammary tumor risk in the offspring,” Cancer Research, vol. 71, no. 3, pp. 988–997, 2011.
[16]  K. K. Y. Sie, J. Chen, K. J. Sohn, R. Croxford, L. U. Thompson, and Y. I. Kim, “Folic acid supplementation provided in utero and during lactation reduces the number of terminal end buds of the developing mammary glands in the offspring,” Cancer Letters, vol. 280, no. 1, pp. 72–77, 2009.
[17]  K. Kordas, A. S. Ettinger, H. Lamadrid-Figueroa et al., “Methylenetetrahydrofolate reductase (MTHFR) C677T, A1298C and G1793A genotypes, and the relationship between maternal folate intake, tibia lead and infant size at birth,” British Journal of Nutrition, vol. 102, no. 6, pp. 907–914, 2009.
[18]  R. M. Nilsen, S. E. Vollset, A. L. B. Monsen et al., “Infant birth size is not associated with maternal intake and status of folate during the second trimester in Norwegian pregnant women,” Journal of Nutrition, vol. 140, no. 3, pp. 572–579, 2010.
[19]  G. L. Wolff, R. L. Kodell, S. R. Moore, and C. A. Cooney, “Maternal epigenetics and methyl supplements affect agouti gene expression in A(vy)/a mice,” FASEB Journal, vol. 12, no. 11, pp. 949–957, 1998.
[20]  I. M. Y. Szeto, P. S. P. Huot, S. A. Reza-Lopez, et al., “The effect of high multivitamin diet during pregnancy on food intake and glucose metabolism in Wistar rat offspring fed low-vitamin diets post weaning,” Journal of Developmental Origins of Health and Disease, vol. 2, no. 5, pp. 302–310, 2011.
[21]  S. A. Reza-López, G. H. Anderson, I. M. Y. Szeto, A. Y. Taha, and D. W. L. Ma, “High vitamin intake by Wistar rats during pregnancy alters tissue fatty acid concentration in the offspring fed an obesogenic diet,” Metabolism, vol. 58, no. 5, pp. 722–730, 2009.
[22]  I. M. Szeto, M. E. Payne, A. Jahan-Mihan, et al., “Multivitamin supplementation during pregnancy alters body weight and macronutrient selection in Wistar rat offspring,” Journal of Developmental Origins of Health and Disease, vol. 1, no. 6, pp. 386–395, 2010.
[23]  A. Ganpule, C. S. Yajnik, C. H. D. Fall et al., “Bone mass in Indian children—relationships to maternal nutritional status and diet during pregnancy: The Pune Maternal Nutrition Study,” Journal of Clinical Endocrinology and Metabolism, vol. 91, no. 8, pp. 2994–3001, 2006.
[24]  C. D. Steer and J. H. Tobias, “Insights into the programming of bone development from the Avon Longitudinal Study of Parents and Children (ALSPAC),” The American Journal of Clinical Nutrition, vol. 94, no. 6, supplement, pp. 1861S–1864S, 2011.
[25]  A. Hossein-Nezhad, K. Mirzaei, Z. Maghbooli, A. Najmafshar, and B. Larijani, “The influence of folic acid supplementation on maternal and fetal bone turnover,” Journal of Bone and Mineral Metabolism, vol. 29, no. 2, pp. 186–192, 2011.
[26]  P. Nguyen, R. Boskovic, P. Yazdani, B. Kapur, H. Vandenberghe, and G. Koren, “Comparing folic acid pharmacokinetics among women of childbearing age: single dose ingestion of 1.1 versus 5 MG folic acid,” The Canadian Journal of Clinical Pharmacology, vol. 15, no. 2, pp. e314–e322, 2008.
[27]  G. Koren, Y. I. Goh, and C. Klieger, “Folic acid: the right dose,” Canadian Family Physician, vol. 54, no. 11, pp. 1545–1547, 2008.
[28]  N. J. Wald, “Folic acid and the prevention of neural-tube defects,” The New England Journal of Medicine, vol. 350, no. 2, pp. 101–103, 2004.
[29]  R. M. Cabrera, D. S. Hill, A. J. Etheredge, and R. H. Finnell, “Investigations into the etiology of neural tube defects,” Birth Defects Research C, vol. 72, no. 4, pp. 330–344, 2004.
[30]  A. E. French, R. Grant, S. Weitzman et al., “Folic acid food fortification is associated with a decline in neuroblastoma,” Clinical Pharmacology and Therapeutics, vol. 74, no. 3, pp. 288–294, 2003.
[31]  A. Marti-Carvajal, G. Pena-Marti, G. Comunian-Carrasco, et al., “Prematurity and maternal folate deficiency: anemia during pregnancy study group results in Valencia, Venezuela,” Archivos Latinoamericanos de Nutrición, vol. 54, no. 1, pp. 45–49, 2004.
[32]  P. D. Gluckman, M. A. Hanson, and H. G. Spencer, “Predictive adaptive responses and human evolution,” Trends in Ecology and Evolution, vol. 20, no. 10, pp. 527–533, 2005.
[33]  P. G. Reeves, “Components of the AIN-93 diets as improvements in the AIN-76A diet,” Journal of Nutrition, vol. 127, no. 5, supplement, pp. 838S–841S, 1997.
[34]  P. E. Wainwright, “Issues of design and analysis relating to the use of multiparous species in developmental nutritional studies,” The Journal of Nutrition, vol. 128, no. 3, pp. 661–663, 1998.
[35]  M. F. W. Festing, “Design and statistical methods in studies using animal models of development,” ILAR Journal, vol. 47, no. 1, pp. 5–14, 2006.
[36]  S. M. Sacco, J. M. Y. Jiang, S. Reza-López, D. W. L. Ma, L. U. Thompson, and W. E. Ward, “Flaxseed combined with low-dose estrogen therapy preserves bone tissue in ovariectomized rats,” Menopause, vol. 16, no. 3, pp. 545–554, 2009.
[37]  B. Iglewicz and D. C. Hoaglin, How To Detect and Handle Outliers, ASQC Quality Press, 1993.
[38]  B. Y. Lau, V. A. Fajardo, L. McMeekin et al., “Influence of high-fat diet from differential dietary sources on bone mineral density, bone strength, and bone fatty acid composition in rats,” Applied Physiology, Nutrition and Metabolism, vol. 35, no. 5, pp. 598–606, 2010.
[39]  O. V. Leppanen, H. Sievanen, J. Jokihaara, et al., “The effects of loading and estrogen on rat bone growth,” Journal of Applied Physiology, vol. 108, no. 6, pp. 1737–1744, 2010.
[40]  S. A. Shapses and M. Cifuentes, “Body weight/composition and weight change: effects on bone health,” in Nutrition and Bone Health, M. F. Holick and B. Dawson-Hughes, Eds., pp. 549–573, Humana Press, Totowa, NJ, USA, 2004.
[41]  A. Goulding, “Risk factors for fractures in normally active children and adolescents,” Medicine and Sport Science, vol. 51, pp. 102–120, 2007.
[42]  J. M. Koh, Y. S. Lee, Y. S. Kim et al., “Homocysteine enhances bone resorption by stimulation of osteoclast formation and activity through increased intracellular ROS generation,” Journal of Bone and Mineral Research, vol. 21, no. 7, pp. 1003–1011, 2006.
[43]  D. Studer, C. Millan, E. Ozturk, et al., “Molecular and biophysical mechanisms regulating hypertrophic differentiation in chondrocytes and mesenchymal stem cells,” European Cells and Materials, vol. 24, pp. 118–135, 2012.
[44]  P. Lagiou, L. Mucci, R. Tamimi et al., “Micronutrient intake during pregnancy in relation to birth size,” European Journal of Nutrition, vol. 44, no. 1, pp. 52–59, 2005.
[45]  C. Hoyo, A. P. Murtha, J. M. Schildkraut et al., “Folic acid supplementation before and during pregnancy in the Newborn Epigenetics Study (NEST),” BMC Public Health, vol. 11, article 46, 2011.

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