Anthony M Belenchia1, Karen L Jones2,3, Matthew Will4,5, David Q Beversdorf6, Victoria Vieira-Potter1, Cheryl S Rosenfeld4,7, Catherine A Peterson8. 1. Department of Nutrition and Exercise Physiology, University of Missouri, 204 Gwynn Hall, Columbia, MO, 65211, USA. 2. MIND Institute, University of California, Davis, 2825 50th St, Sacramento, CA, 95817, USA. 3. Division of Rheumatology, Allergy, and Clinical Immunology, Department of Internal Medicine, University of California-Davis, Davis, CA, USA. 4. Bond Life Sciences Center, University of Missouri, 1201 Rollins St, Columbia, MO, 65201, USA. 5. Department of Psychological Sciences, University of Missouri, 1020 Hitt Street, Columbia, MO, 65212-0001, USA. 6. Thompson Autism Center for Neurodevelopmental Disorders, University of Missouri, 205 Portland St, Columbia, MO, 65201-6521, USA. 7. Department Biomedical Sciences, University of Missouri, 440F Life Sciences Center, Columbia, MO, 65211, USA. 8. Department of Nutrition and Exercise Physiology, University of Missouri, 204 Gwynn Hall, Columbia, MO, 65211, USA. petersonca@missouri.edu.
Abstract
PURPOSE: Maternal vitamin D deficiency during pregnancy is a widespread issue that may have long-lasting consequences on offspring adiposity. We sought to determine how maternal vitamin D deficiency during the perinatal period would affect offspring adipose tissue development and gene expression. METHODS: Female C57BL/6 J mice were fed either a vitamin D deficient (VDD) or control diet from 4 weeks before pregnancy (periconception) until 7 days postparturition. Male offspring were weighed and euthanized at 75 days of age (early adult period), at which point serum was collected for biochemical analyses, and perigonadal and subcutaneous white adipose tissue (PGAT and SQAT, respectively) were excised, weighed, then flash-frozen for later histology and analyses of adipogenic gene expression. RESULTS: All adult male offspring were nonobese; there were no significant differences in body weight, adipose pad weight, or adipocyte size. However, VDD-exposed offspring had greater expression of the adipogenic-regulating genes peroxisome proliferator-activated receptor gamma (Pparg) and vitamin D receptor (Vdr). CONCLUSIONS: This study suggests that exposure to vitamin D deficiency during the perinatal period can directly affect genes involved in the development of adipose tissue in nonobese offspring. These novel findings invite further investigation into the mechanisms by which maternal vitamin D status during pregnancy affects adipose development and metabolic health of offspring.
PURPOSE: Maternal vitamin D deficiency during pregnancy is a widespread issue that may have long-lasting consequences on offspring adiposity. We sought to determine how maternal vitamin D deficiency during the perinatal period would affect offspring adipose tissue development and gene expression. METHODS: Female C57BL/6 J mice were fed either a vitamin D deficient (VDD) or control diet from 4 weeks before pregnancy (periconception) until 7 days postparturition. Male offspring were weighed and euthanized at 75 days of age (early adult period), at which point serum was collected for biochemical analyses, and perigonadal and subcutaneous white adipose tissue (PGAT and SQAT, respectively) were excised, weighed, then flash-frozen for later histology and analyses of adipogenic gene expression. RESULTS: All adult male offspring were nonobese; there were no significant differences in body weight, adipose pad weight, or adipocyte size. However, VDD-exposed offspring had greater expression of the adipogenic-regulating genes peroxisome proliferator-activated receptor gamma (Pparg) and vitamin D receptor (Vdr). CONCLUSIONS: This study suggests that exposure to vitamin D deficiency during the perinatal period can directly affect genes involved in the development of adipose tissue in nonobese offspring. These novel findings invite further investigation into the mechanisms by which maternal vitamin D status during pregnancy affects adipose development and metabolic health of offspring.
Entities:
Keywords:
Adipogenesis; DOHaD; Fetal programming; Gene expression; Pregnancy; Vitamin D
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