The association of obesity and glucose and insulin concentrations with bone density in premenopausal and postmenopausal women

Haffner, Steven M.; Bauer, Richard L.

doi:10.1016/0026-0495(93)90241-f

Cited by 95 publications

(61 citation statements)

References 10 publications

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“…(2) Although increased weight is expected to mia, which might contribute to the associated increase in bone mass. (3) Both insulin and insulin-like growth factor 1 (IGF-1) exert trophic effects on bone in laboratory studies, (4,5) and in clinical studies, insulin resistance is associated with both increased bone density (6)(7)(8)(9) and reduced fracture risk (10) independent of body mass index (BMI). Leptin and adiponectin, two adipocyte-derived hormones, also could influence skeletal metabolism directly.…”

Section: Introductionmentioning

confidence: 99%

Adiponectin and its association with bone mass accrual in childhood

Sayers

Timpson

Sattar

et al. 2010

Journal of Bone and Mineral Research

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Circulating adiponectin levels are inversely related to bone mineral density (BMD) in humans and animal models. Previous studies in humans have been confined largely to adult populations, and whether adiponectin influences bone mass accrual in childhood is unclear. We examined this question using the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort by investigating relationships between circulating adiponectin levels at a mean age of 9.9 years, indices of bone mass as measured by total-body dualenergy X-ray absorptiometry (DXA) at ages 9.9 and 15.5 years, and cortical bone parameters as measured by peripheral quantitative computed tomography (pQCT) of the midtibia at age 15.5 years. A total of 4927 children were included at age 9.9 years, of whom 97% and 90% of boys and girls, respectively, were in prepuberty or early puberty, as defined by Tanner stage 1-2. A total of 2754 children were included at age 15.5 years, of whom 95% and 97% of boys and girls, respectively, were in late puberty, as defined by Tanner stage 4-5. Circulating adiponectin was found to be related to fat mass, lean mass, and, to a lesser extent, height, so analyses were adjusted for these three variables to identify possible independent effects of adiponectin on bone development. Adiponectin was inversely related to totalbody-less-head bone mineral content (BMC; À3.0%), bone area (BA; À1.8%), BMC divided by BA (BMD; À4.8%), and BMC adjusted for BA by linear regression (aBMC; À5.6%), as measured at age 9.9 years (coefficients show change per doubling in adiponectin concentration, p < .001). Consistent with these results, inverse associations also were seen between adiponectin and cortical BMC (À4.8%) and cortical bone area (À4.7%), as measured by tibial pQCT at age 15.5 years (p < .001). Further pQCT results suggested that this inverse association of adiponectin with skeletal development predominantly involved a negative association with endosteal relative to periosteal expansion, as reflected by cortical thickness (À6.0%, p < .001). We conclude that, independent of fat mass, lean mass, and height, adiponectin is associated with lower bone mass in childhood predominantly owing to an influence on relative endosteal expansion. Since these associations were observed before and after puberty, this suggests that setting of adiponectin levels in midchildhood has the potential to exert long-term effects on bone strength and fracture risk. ß

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Section: Introductionmentioning

confidence: 99%

Adiponectin and its association with bone mass accrual in childhood

Sayers

Timpson

Sattar

et al. 2010

Journal of Bone and Mineral Research

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“…However, the findings are more inconsistent. Researchers have reported lower, equal, and greater bone mass in people with type 2 diabetes relative to diabetes-free control subjects (3)(4)(5)(6)7,10,24,29). Part of the inconsistency could be caused by heterogeneous study groups (for example, premenopausal versus postmenopausal women or different diabetes subsets) or by potential confounding by obesity.…”

Section: Type 2 Diabetesmentioning

confidence: 99%

“…Part of the inconsistency could be caused by heterogeneous study groups (for example, premenopausal versus postmenopausal women or different diabetes subsets) or by potential confounding by obesity. Two studies found that individuals with type 2 diabetes had lower bone density relative to nondiabetic control subjects (3,29). However, one (3) examined people who were using insulin to control their diabetes, whereas the other (29) examined those using dietary or oral diabetes agents.…”

Section: Type 2 Diabetesmentioning

confidence: 99%

Type 1 and Type 2 Diabetes and Incident Hip Fractures in Postmenopausal Women

2001

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OBJECTIVE -To examine whether postmenopausal women with diabetes experienced a higher incidence of hip fracture than women without diabetes. RESEARCH DESIGN AND METHODS-A prospective cohort of 32,089 postmenopausal women residing in Iowa were surveyed by mail in 1986 and followed for 11 years. Diabetes status and other potential risk factors were assessed by questionnaires at baseline; incidence of hip fracture was ascertained by follow-up questionnaires.RESULTS -A total of 490 hip fractures were reported over 306,900 person-years of followup. After adjustment for age, smoking status, estrogen use, BMI, and waist-to-hip ratio, women with type 1 diabetes (n ϭ 47) were 12.25 times (95% CI 5.05-29.73) more likely to report an incident hip fracture than women without diabetes. Women with type 2 diabetes had a 1.70-fold higher risk (1.21-2.38) of incident hip fracture than women without diabetes. Longer duration of type 2 diabetes was associated with higher incidence, as was use of insulin or oral diabetes medications in women with type 2 diabetes. Furthermore, women who were initially free of diabetes but in whom diabetes developed had a relative risk of hip fracture of 1.60 (1.14 -2.25) compared with women who never had diabetes.CONCLUSIONS -Postmenopausal women who have diabetes or in whom diabetes develops are at higher risk for hip fracture than nondiabetic postmenopausal women. Strategies to prevent osteoporosis and/or falling may be especially warranted in women with diabetes.

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“…Several mechanisms seem to be involved, such as the mechanical effect of increased weight bearing on muscle that stimulates bone formation (15), increased aromatization of androgen to estrogen in adipose tissue (16,17), decreased sex-hormone binding globulin with an increase in free sex steroids (14), increased serum leptin (18,19), increased synthesis of insulin-like growth factors in the liver and the skeleton, and also hyperinsulinemia and insulin resistance (20).…”

mentioning

confidence: 99%

Influence of obesity on bone density in postmenopausal women

Silva

Mendonça

Conceição

et al. 2007

Arq Bras Endocrinol Metab

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Objective: To evaluate the influence of obesity, age, and years since menopause on bone density. Methods: A retrospective analysis of bone mineral density (BMD) obtained from 588 women, 41 to 60 years, previously menopaused (1-10 years before). Results: Positive influence of obesity was confirmed by the significant differences in BMD at lumbar spine, femoral neck (FN), and trochanter (TR) between the groups (p < 0.01). Age and years since menopause (YSM) were negatively correlated with BMD at all sites (p = 0.000). Comparing patients within 1 to < 6 YSM versus 6 to 10 YSM, BMD was higher in the former at LS and FN (p < 0.005), despite the higher BMI in the older group (p = 0.01). Obese patients had a lower prevalence of osteoporosis at LS and FN (p = 0.009). Regression analysis identified BMI as the strongest determinant of FN and TR BMD, while YSM was the strongest determinant of LS BMD. Conclusion: The protective effect of obesity is overtaken by age and estradiol deficiency. We recommend that even obese postmenopausal women should be screened for osteoporosis. Objetivo: Avaliar a influência de obesidade, idade e anos de menopausa sobre a densidade óssea. Métodos: Análise retrospectiva da densidade mineral óssea (DMO) obtida em 588 mulheres de 41 a 60 anos, já menopausadas (1-10 anos antes). Resultados: A influência positiva da obesidade foi confirmada através de diferenças significativas da DMO entre os grupos na coluna lombar (CL), colo de fêmur (CF) e trocânter (TR) (p < 0,01). Idade e anos desde a menopausa (ADM) foram correlacionados negativamente com DMO em todos os sítios (p = 0,000). Comparando-se pacientes entre 1 e < 6 ADM vs 6 e 10 AMD, a DMO foi maior no primeiro grupo na CL e CF (p < 0,005), apesar de maior DMO no grupo de mais idade (p = 0,01). Pacientes obesas tiveram uma prevalência mais baixa de osteoporose na CL e CF (p = 0,009). Análise de regressão identificou o IMC como o determinante mais forte da DMO de CF e trocânter, enquanto a ADM foi o determinante mais forte da DMO na CL. Conclusão: O efeito protetor da obesidade é sobrepujado pela deficiência de estradiol. Recomendamos que mesmo mulheres obesas na pós-menopausa devam ser examinadas para osteoporose.

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The association of obesity and glucose and insulin concentrations with bone density in premenopausal and postmenopausal women

Cited by 95 publications

References 10 publications

Adiponectin and its association with bone mass accrual in childhood

Adiponectin and its association with bone mass accrual in childhood

Type 1 and Type 2 Diabetes and Incident Hip Fractures in Postmenopausal Women

Influence of obesity on bone density in postmenopausal women

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