Maternal high-fat diet: effects on offspring bone structure

Lanham, Stuart; Roberts, Carol A.; Hollingworth, Tony; Sreekumar, R.; Elahi, Maqsood M.; Cagampang, Felino R.; Hanson, Mark A.; Oreffo, Richard O.C.

doi:10.1007/s00198-009-1118-4

Cited by 38 publications

(41 citation statements)

References 41 publications

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“…Both parameters were restored with additional vitamin K supplementation. In our previous study (32), we also observed femoral bone volume loss in male high fat fed offspring (although not to a significant level), but a femoral bone volume increase in high fat fed female offspring. These results again, suggest potential sex differences in vitamin K utilization.…”

Section: Discussionsupporting

confidence: 59%

“…In these mice, a combination of a high fat maternal diet and a high fat offspring diet produced greater effects on offspring VKDP expression levels than each high fat diet period alone. This dietary synergy was still evident in parameters such as female femur length and bone marrow adiposity measured in 30 week old mice using this high fat model (32). Vitamin K is fat soluble, hence, increasing levels of adiposity with increasing age may reduce serum levels of vitamin K, and therefore reduce levels of VKDPs produced by organs other than the liver (eg, bone specific osteocalcin) as the liver could be prioritised for the utilization of vitamin K for clotting fac- levels of Gas6 were associated with obesity (which displayed increased blood pressure (BP)) and insulin resistance in adolescents (34), and Gas6 levels were increased in the secretome from atherosclerotic plaques (35).…”

Section: Discussionmentioning

confidence: 80%

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Maternal High-Fat Diet and Offspring Expression Levels of Vitamin K–Dependent Proteins

2014

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Studies suggest that bone growth and development and susceptibility to vascular disease in later life are influenced by maternal nutrition during intrauterine and early postnatal life. There is evidence for a role of vitamin K-dependent proteins (VKDPs) including osteocalcin, matrix Gla protein, periostin, and growth-arrest specific- protein 6, in both bone and vascular development. We have examined whether there are alterations in these VKDPs in bone and vascular tissue from offspring of mothers subjected to a nutritional challenge: a high-fat diet during pregnancy and postnatally, using 6-week-old mouse offspring. Bone site-specific and sex-specific differences across femoral and vertebral bone in male and female offspring were observed. Overall a high-fat maternal diet and offspring diet exacerbated the bone changes observed. Sex-specific differences and tissue-specific differences were observed in VKDP levels in aorta tissue from high-fat diet-fed female offspring from high-fat diet-fed mothers displaying increased levels of Gas6 and Ggcx compared with those of female controls. In contrast, differences were seen in VKDP levels in femoral bone of female offspring with lower expression levels of Mgp in offspring of mothers fed a high-fat diet compared with those of controls. We observed a significant correlation in Mgp expression levels within the femur to measures of bone structure of the femur and vertebra, particularly in the male offspring cohort. In summary, the current study has highlighted the importance of maternal nutrition on offspring bone development and the correlation of VKDPs to bone structure.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 80%

Maternal High-Fat Diet and Offspring Expression Levels of Vitamin K–Dependent Proteins

2014

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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.…”

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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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“…Lanham et al [37] used a mouse model of highfat intake, both during pregnancy and/or for the offspring. Offspring samples were taken at 30 weeks of age.…”

Section: Bone Development Studies Using the Mousementioning

confidence: 99%

Prenatal and Nutritional Influences on Skeletal Development: Lessons from Animal Studies

Lanham

Roach

Cooper

et al. 2009

Clinic Rev Bone Miner Metab

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It is now well established that the onset of adult diseases such as heart disease, stroke, type 2 diabetes and hypertension are linked to an adverse uterine growth environment, in particular through maternal nutrition, during development of the individual. The geographical distribution of the incidence rate of heart disease is similar to that of osteoporosis. This may indicate a link between maternal nutrition during pregnancy and the subsequent risk of developing osteoporosis in the offspring. This review summarises what we know to date, from animal models, about maternal nutrition and the subsequent alterations in the offspring's skeletal structure.

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Maternal high-fat diet: effects on offspring bone structure

Abstract: A maternal HF diet during pregnancy increases bone marrow adiposity and alters bone structure in their offspring.

Cited by 38 publications

References 41 publications

Maternal High-Fat Diet and Offspring Expression Levels of Vitamin K–Dependent Proteins

Maternal High-Fat Diet and Offspring Expression Levels of Vitamin K–Dependent Proteins

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

Prenatal and Nutritional Influences on Skeletal Development: Lessons from Animal Studies

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