Influence of pre- and peri-natal nutrition on skeletal acquisition and maintenance

Devlin, Maureen J.; Bouxsein, Mary L.

doi:10.1016/j.bone.2011.06.019

Cited by 53 publications

(45 citation statements)

References 157 publications

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“…Suggestive evidence comes from epidemiologic cohort studies, which report correlations between weight at birth and 1 y of age with bone integrity later in life (7,8). In animal models, gestational nutrition and hormone concentrations affect skeletal microarchitecture, bone mineral content, strength, growth plate morphology, and osteoblast differentiation capability (9)(10)(11)(12)(13)(14). However, the mechanisms remain unknown.…”

mentioning

confidence: 99%

Decreasing maternal myostatin programs adult offspring bone strength in a mouse model of osteogenesis imperfecta

Oestreich

Kamp

McCray

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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During fetal development, the uterine environment can have effects on offspring bone architecture and integrity that persist into adulthood; however, the biochemical and molecular mechanisms remain unknown. Myostatin is a negative regulator of muscle mass. Parental myostatin deficiency (Mstn tm1Sjl/+ ) increases muscle mass in wild-type offspring, suggesting an intrauterine programming effect. Here, we hypothesized that Mstn tm1Sjl/+ dams would also confer increased bone strength. In wild-type offspring, maternal myostatin deficiency altered fetal growth and calvarial collagen content of newborn mice and conferred a lasting impact on bone geometry and biomechanical integrity of offspring at 4 mo of age, the age of peak bone mass. Second, we sought to apply maternal myostatin deficiency to a mouse model with osteogenesis imperfecta (Col1a2 oim ), a heritable connective tissue disorder caused by abnormalities in the structure and/or synthesis of type I collagen. Femora of male Col1a2 oim/+ offspring from natural mating of Mstn tm1Sjl/+ dams to Col1a2 oim/+ sires had a 15% increase in torsional ultimate strength, a 29% increase in tensile strength, and a 24% increase in energy to failure compared with age, sex, and genotype-matched offspring from natural mating of Col1a2 oim/+ dams to Col1a2 oim/+ sires. Finally, increased bone biomechanical strength of Col1a2 oim/+ offspring that had been transferred into Mstn tm1Sjl/+ dams as blastocysts demonstrated that the effects of maternal myostatin deficiency were conferred by the postimplantation environment. Thus, targeting the gestational environment, and specifically prenatal myostatin pathways, provides a potential therapeutic window and an approach for treating osteogenesis imperfecta.osteogenesis imperfecta | developmental origins of health and disease | fetal programming | myostatin | bone health O steogenesis imperfecta (OI) is a genetically and clinically heterogeneous heritable connective tissue disorder characterized by anomalies in type I collagen-containing tissues, particularly bone. Clinical manifestations include osteopenia/osteoporosis, fractures, skeletal deformities, short stature, and skeletal muscle weakness. Current therapies entail use of antiresorptive drugs and surgical interventions but have limited success (1). New approaches that decrease fracture risk while minimizing long-term damage to bone integrity are greatly needed. Myostatin, or growth and differentiation factor 8 (GDF8), is a TGF-β family member and negative regulator of muscle growth and development. It is highly conserved across species, primarily expressed in muscle cells, and participates in paracrine and endocrine signaling (2). Recently, we and others have shown that inhibiting myostatin, either genetically or pharmacologically, increases muscle mass and improves bone microarchitecture (3) and mechanical strength (4) in the OI murine (Col1a2 oim ) model. In addition to regulating muscle growth postnatally, myostatin deficiency in the maternal environment increases muscle mass in ...

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mentioning

confidence: 99%

Decreasing maternal myostatin programs adult offspring bone strength in a mouse model of osteogenesis imperfecta

Oestreich

Kamp

McCray

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…ОБЗОРы лИТЕРАТУРы ______________________ * e-mail:cheply@mail.ru иСтОРиЯ ВОПРОСа с 90-х годов обсуждаются различные аспекты влияния питания плода на развитие хронической соматической патологии у человека в постнаталь-ный период [1][2][3][4][5][6]. если плод получает достаточ-ное количество нутриентов и кислорода, то этот процесс протекает физиологически.…”

Section: № 3/2014 остеопороз и остеопатииunclassified

“…существует еще один путь перепрограммирования генетически определенной траектории развития кости. он заключается в том, что повреждающие факторы могут индуцировать более устойчивые изменения экспрессии ге-нов в результате эпигенетической модификации днк, на-пример, вследствие нарушения процессов метилирования днк [4,6,8] во время гестации. Этот молекулярный ме-ханизм, при ряде неблагоприятных условий, может стать фактором, способным стойко нарушать физиологические функции в постнатальный период.…”

Section: № 3/2014 остеопороз и остеопатииunclassified

“…чтобы окон-чательно уточнить этот вопрос, необходимо определить, в чем выражаются клинические последствия перинатально-го программирования скелета [4]. многочисленные иссле-дования в этом направлении в конечном итоге позволили предположить, что в перинатальном периоде формируется костный фенотип человека [6].…”

Section: № 3/2014 остеопороз и остеопатииunclassified

“…при ретроспективном обследовании матерей, которые получали витамин D [10], выявлено, что у них выше ми-неральная плотность кости (мпк) в дистальном отделе при физиологическом течении беременности показате-ли обеспеченности матери кальцием, фосфором, как прави-ло, также взаимосвязаны с соответствующими параметрами новорожденного [6].…”

Section: витамин D рост и минерализация скелетаunclassified

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Programming of Skeletal Development in Children: The Role of Vitamin D

Scheplyagina¹

2014

Osteopor Bone Dis

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Intraspecific variation of long bone cross‐sectional properties in Pan troglodytes troglodytes and Gorilla gorilla gorilla

Cosman,

MacLatchy,

Schlecht

et al. 2023

American Journal of Biological Anthropology

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ObjectivesMorphological intraspecific variation is due to the balance between skeletal plasticity and genetic constraint on the skeleton. Osteogenic responses to external stimuli, such as locomotion, have been well documented interspecifically across the primate order, but less so at the intraspecific level. Here, we examine the differences in cross‐sectional variability of the femur, humerus, radius, and tibia in Pan troglodytes troglodytes versus Gorilla gorilla gorilla. We investigate whether there are sex, species, bone, and trait differences in response to variable body size and locomotion.Materials and MethodsAdult male and female P. t. troglodytes and G. g. gorilla long bones from the Cleveland Museum of Natural History were scanned with a peripheral quantitative computer tomography system. Scans were taken at the midshaft of each bone according to functional bone length. Coefficients of variation were used to provide a size‐independent measure of variation. We applied a Bonferroni correction to account for the multiple pairwise tests.ResultsThere were limited significant differences between males and females, however, females tended to be more variable than males. Variation in Gorilla, when significant, was greater than in Pan, although significant differences were limited. There were no differences between bone variability in male and female Gorilla, and female Pan.DiscussionIncreased female variability may be due to more variable locomotor behavior, particularly during periods of pregnancy, lactation, and caring for an offspring compared to consistent locomotion over the life course by males. Body size may be a contributing factor to variability; more work is needed to understand this relationship.

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Influence of pre- and peri-natal nutrition on skeletal acquisition and maintenance

Cited by 53 publications

References 157 publications

Decreasing maternal myostatin programs adult offspring bone strength in a mouse model of osteogenesis imperfecta

Decreasing maternal myostatin programs adult offspring bone strength in a mouse model of osteogenesis imperfecta

Programming of Skeletal Development in Children: The Role of Vitamin D

Intraspecific variation of long bone cross‐sectional properties in Pan troglodytes troglodytes and Gorilla gorilla gorilla

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