Abstract
Vitamin B12 deficiency has been shown to affect bone mass in rodents and negatively impact bone formation in humans. In this study using mouse models, we define the effect of B12 supplementation in the wild-type mother and B12 deficiency in a mouse genetic model (Gif−/− mice) during gestation on bone and muscle architecture and mechanical properties in the offspring. Analysis of bones from 4-wk-old offspring of the wild-type mother following vehicle or B12 supplementation during gestation (from embryonic day 0.5 to 20.5) showed an increase in bone mass caused by an isolated increase in bone formation in the B12-supplemented group compared with vehicle controls. Analysis of the effect of B12 deficiency in the mother in a mouse genetic model (Gif−/− mice) on the long bone architecture of the offspring showed a compromised cortical and trabecular bone mass, which was completely prevented by a single injection of B12 in the B12-deficient Gif−/− mothers. Biomechanical analysis of long bones of the offspring born from B12-supplemented wild-type mothers showed an increase in bone strength, and conversely, offspring born from B12-deficient Gif−/− mothers revealed a compromised bone strength, which could be rescued by a single injection of B12 in the B12-deficient Gif−/− mother. Muscle structure and function analysis however revealed no significant effect on muscle mass, structure, and grip strength of B12 deficiency or supplementation in Gif−/− mice compared with littermate controls. Together, these results demonstrate the beneficial effect of maternally derived B12 in the regulation of bone structure and function in the offspring.
Highlights
Mammalian bone and skeletal muscles are intricately connected and coordinate locomotion [1]
We showed that F2 GifÀ/À mice have normal bone length, bone weight, calcium levels, skeletal mineralization at birth, and normal growth up until 21 days of age, but after that, they develop low bone mass due to an abrogation in the B12-taurine-bone pathway that operates through the liver [17]
Bone histological and histomorphometric analysis in the vertebra showed a dose-dependent increase in bone volume/total volume (BV/TV)% in offspring born from B12-treated mother [11.2 ± 0.4 (B20) and 14.3 ± 0.6 (B200)] compared with control offspring born from vehicle-treated mothers (8.1 ± 0.2) (Fig. 1, E and F)
Summary
Mammalian bone and skeletal muscles are intricately connected and coordinate locomotion [1]. The biomechanical strength of the vertebrate skeleton is determined by the changes in structure and functional properties of either bone or skeletal muscle or both [1]. Healthy bone strength depends on the overall geometry, thickness, and porosity of the bone tissue [2]. These structural changes in the bone tissue are coordinated by the localized changes in the bone remodeling happening throughout the skeleton [3]. A healthy bone structure depends on the changes in the structure and mass of the skeletal muscles that surround the bone [4]. Deterioration in the quality of bone and skeletal muscle tissues of the skeleton results in an increased risk of fractures, yet the factors regulating this process are still not fully understood [7]
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