Micro-architectural changes in cancellous bone differ in female and male C57BL/6 mice with high-fat diet-induced low bone mineral density

Abstract

The relationship between fat and bone mass at distinct trabecular and cortical skeletal compartments in a high-fat diet (HFD) model was studied. For this, C57BL/6 mice were assigned to four groups of eight animals each. Two groups, each of males and females, received a standard chow diet while the remaining other two groups received the HFD for a period of 10 weeks. Male mice on the HFD were heavier and gained more weight (15·8 %; P, 0·05) v. those on the control diet or when compared with the female rats fed the HFD. We observed an increased lipid profile in both males and females, with significantly higher lipid levels (about 20 -25 %; P, 0·01) in males. However, glucose intolerance was more pronounced in females than males on the HFD (about 30 %; P,0·05). The micro-architectural assessment of bones showed that compared with female mice on the HFD, male mice on the HFD showed more deterioration at the trabecular region. This was corroborated by plasma osteocalcin and carboxy-terminal collagen crosslinks (CTx) levels confirming greater loss in males (about 20 %; P, 0·01). In both sexes cortical bone parameters and strength remained unchanged after 10 weeks of HFD treatment. The direct effect of the HFD on bone at the messenger RNA level in progenitor cells isolated from femoral bone marrow was a significantly increased expression of adipogenic marker genes v. osteogenic genes. Overall, the present data indicate that obesity induced by a HFD aggravates bone loss in the cancellous bone compartment, with a greater loss in males than females, although 10 weeks of HFD treatment did not alter cortical bone mass and strength in both males and females.

MicroRNA 874-3p Exerts Skeletal Anabolic Effects Epigenetically during Weaning by Suppressing Hdac1 Expression

“…Transfections of the agomir and antagomir into mouse osteoblasts were carried out at 50 -60% confluence with reduced-serum and antibiotic-free OptiMEM using the transfection agent Lipofectamine (Invitrogen). Alp activity, mineralization, and qPCR were performed using protocols published previously (19,20). For the reporterpromoter assays, Runx2-Luc and Renilla luciferase vectors (from GeneCopoeia) were co-transfected into osteoblasts, and luciferase activity was determined using a dual assay luciferase kit (19).…”

“…Alp activity, mineralization, and qPCR were performed using protocols published previously (19,20). For the reporterpromoter assays, Runx2-Luc and Renilla luciferase vectors (from GeneCopoeia) were co-transfected into osteoblasts, and luciferase activity was determined using a dual assay luciferase kit (19). The full length of the Runx2 promoter is 1039 bp (catalog no.…”

“…Female BALB/c mice (18 Ϯ 5 g) and female adult SpragueDawley rats (220 Ϯ 30 g) were kept in a 12-h light-dark cycle with controlled temperature (22-24°C) and humidity (50 -60%) and ad libitum access to standard rodent food and water (19). Micro-computed tomography (CT) measurements were carried out on a SkyScan 1076 CT scanner (Aartselaar, Antwerp, Belgium).…”

Fructose Consumption Does Not Worsen Bone Deficits Resulting From High-Fat Feeding in Young Male Rats

“…[5,8,10] In contrast, a combined high-fat/sucrose diet impairs lumbar and femoral neck strength in rodents, likely a result of smaller bone cross-sectional area and/or reduced cortical bone area in comparison to a low-fat/complex carbohydrate diet. [37, 51] Interestingly, we observed that the cortical bone compartments at the distal femur and femoral diaphysis of HF and HF/F animals exhibited increased Ct.Th and Ct.Ar/Tt.Ar and densitometric characteristics, although, these changes did not improve whole bone mechanical characteristics in comparison with Controls.…”

“…[4] Similarly, high-fat [5][6][7][8][9][10] or high fructose diets [11,12] [20] suggesting that increased oxidative stress resulting from ROS generation and/or reduced activity of the antioxidant systems may influence the adverse skeletal development resulting from high-fat or high-fructose diets.…”