Marie Juul Ornstrup1, Thomas Nordstrøm Kjær2, Torben Harsløf2, Hans Stødkilde-Jørgensen2, David Michael Hougaard2, Arieh Cohen2, Steen Bønløkke Pedersen3, Bente Lomholt Langdahl3. 1. Department of EndocrinologyAarhus University Hospital, Tage-Hansens Gade 2, Entrance 3C, DK-8000 Aarhus C, DenmarkDepartment of Clinical MedicineAarhus University, Nordre Ringgade 1, DK-8000 Aarhus, DenmarkThe MR Research CenterAarhus University Hospital, Skejby, Brendstrupgaardsvej 100, DK-8200 Aarhus N, DenmarkDepartment of Clinical BiochemistryImmunology and Genetics, Statens Serum Institut, Artillerivej 5, DK-2300 Copenhagen S, Denmark Department of EndocrinologyAarhus University Hospital, Tage-Hansens Gade 2, Entrance 3C, DK-8000 Aarhus C, DenmarkDepartment of Clinical MedicineAarhus University, Nordre Ringgade 1, DK-8000 Aarhus, DenmarkThe MR Research CenterAarhus University Hospital, Skejby, Brendstrupgaardsvej 100, DK-8200 Aarhus N, DenmarkDepartment of Clinical BiochemistryImmunology and Genetics, Statens Serum Institut, Artillerivej 5, DK-2300 Copenhagen S, Denmark marie.juul.ornstrup@clin.au.dk. 2. Department of EndocrinologyAarhus University Hospital, Tage-Hansens Gade 2, Entrance 3C, DK-8000 Aarhus C, DenmarkDepartment of Clinical MedicineAarhus University, Nordre Ringgade 1, DK-8000 Aarhus, DenmarkThe MR Research CenterAarhus University Hospital, Skejby, Brendstrupgaardsvej 100, DK-8200 Aarhus N, DenmarkDepartment of Clinical BiochemistryImmunology and Genetics, Statens Serum Institut, Artillerivej 5, DK-2300 Copenhagen S, Denmark. 3. Department of EndocrinologyAarhus University Hospital, Tage-Hansens Gade 2, Entrance 3C, DK-8000 Aarhus C, DenmarkDepartment of Clinical MedicineAarhus University, Nordre Ringgade 1, DK-8000 Aarhus, DenmarkThe MR Research CenterAarhus University Hospital, Skejby, Brendstrupgaardsvej 100, DK-8200 Aarhus N, DenmarkDepartment of Clinical BiochemistryImmunology and Genetics, Statens Serum Institut, Artillerivej 5, DK-2300 Copenhagen S, Denmark Department of EndocrinologyAarhus University Hospital, Tage-Hansens Gade 2, Entrance 3C, DK-8000 Aarhus C, DenmarkDepartment of Clinical MedicineAarhus University, Nordre Ringgade 1, DK-8000 Aarhus, DenmarkThe MR Research CenterAarhus University Hospital, Skejby, Brendstrupgaardsvej 100, DK-8200 Aarhus N, DenmarkDepartment of Clinical BiochemistryImmunology and Genetics, Statens Serum Institut, Artillerivej 5, DK-2300 Copenhagen S, Denmark.
Abstract
OBJECTIVE:Visceral adipose tissue (VAT) is associated with an increased risk of metabolic syndrome (MetS). Recent studies have suggested that VAT negatively affects bone. However, MetS has also been associated with higher estradiol (E2) levels, which is bone protective. We therefore investigated the impact of VAT and E2 levels on bone density, structural parameters, and strength estimates. DESIGN: A cross-sectional study was conducted in 72 obese men with MetS to investigate the impact of VAT and E2 levels on bone. METHODS: Bone parameters were assessed by dual-energy X-ray absorptiometry (DXA), quantitative computed tomography (QCT), and high-resolution peripheral QCT (HRpQCT) at lumbar spine, proximal femur, radius, and tibia. VAT volume was measured by magnetic resonance imaging (MRI) and sexual hormones were measured in blood samples. RESULTS: Men with high VAT had a lower bone density at the hip (P<0.05), lower cortical thickness, and higher buckling ratio at femoral neck (FN) (P=0.008 and P=0.02), compared with men with low VAT, despite a similar body weight and BMI. Generally, E2 levels were low (median 43 pmol/l), and men with E2 levels below median had reduced bone density at lumbar spine (P=0.04), and impaired structural parameters at radius and tibia, compared with men with E2 levels above median. At the hip, VAT volume and E2 levels affected bone density independently and additively, and 50% of men with high VAT and low E2 levels had osteopenia with significantly lower T-score at FN (P=0.004). CONCLUSIONS: High VAT and low E2 negatively affect bone in obese men with MetS. VAT and E2 affect bone density at the hip independently and additively, revealing an unexpected high prevalence of osteopenia in middle-aged men with MetS.
RCT Entities:
OBJECTIVE: Visceral adipose tissue (VAT) is associated with an increased risk of metabolic syndrome (MetS). Recent studies have suggested that VAT negatively affects bone. However, MetS has also been associated with higher estradiol (E2) levels, which is bone protective. We therefore investigated the impact of VAT and E2 levels on bone density, structural parameters, and strength estimates. DESIGN: A cross-sectional study was conducted in 72 obesemen with MetS to investigate the impact of VAT and E2 levels on bone. METHODS: Bone parameters were assessed by dual-energy X-ray absorptiometry (DXA), quantitative computed tomography (QCT), and high-resolution peripheral QCT (HRpQCT) at lumbar spine, proximal femur, radius, and tibia. VAT volume was measured by magnetic resonance imaging (MRI) and sexual hormones were measured in blood samples. RESULTS:Men with high VAT had a lower bone density at the hip (P<0.05), lower cortical thickness, and higher buckling ratio at femoral neck (FN) (P=0.008 and P=0.02), compared with men with low VAT, despite a similar body weight and BMI. Generally, E2 levels were low (median 43 pmol/l), and men with E2 levels below median had reduced bone density at lumbar spine (P=0.04), and impaired structural parameters at radius and tibia, compared with men with E2 levels above median. At the hip, VAT volume and E2 levels affected bone density independently and additively, and 50% of men with high VAT and low E2 levels had osteopenia with significantly lower T-score at FN (P=0.004). CONCLUSIONS: High VAT and low E2 negatively affect bone in obesemen with MetS. VAT and E2 affect bone density at the hip independently and additively, revealing an unexpected high prevalence of osteopenia in middle-aged men with MetS.
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