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High-Fat-Diet-Induced Weight Gain Ameliorates Bone Loss without Exacerbating AβPP Processing and Cognition in Female APP/PS1 Mice.

Peng Y, Liu J, Tang Y, Liu J, Han T, Han S, Li H, Hou C, Liu J, Long J - Front Cell Neurosci (2014)

Bottom Line: Given that there is no evidence that being overweight is associated with AD-type cognitive dysfunction, we hypothesized that moderate weight gain might have a protective effect on the bone loss in AD without exacerbating cognitive dysfunction.The bone mineral density, microarchitecture, and biomechanical properties of the femurs were then evaluated.These results suggest that a body weight gain induced by the HFD feeding regimen significantly improved bone mass in female APP/PS1 mice with no detriments to exploration ability and spatial memory, most likely via the action of elevated circulating leptin.

View Article: PubMed Central - PubMed

Affiliation: Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology and Frontier Institute of Science and Technology, Xi'an Jiaotong University , Xi'an , China.

ABSTRACT
Osteoporosis is negatively correlated with body mass, whereas both osteoporosis and weight loss occur at higher incidence during the progression of Alzheimer's disease (AD) than the age-matched non-dementia individuals. Given that there is no evidence that being overweight is associated with AD-type cognitive dysfunction, we hypothesized that moderate weight gain might have a protective effect on the bone loss in AD without exacerbating cognitive dysfunction. In this study, feeding a high-fat diet (HFD, 45% calorie from fat) to female APP/PS1 transgenic mice, an AD animal model, induced weight gain. The bone mineral density, microarchitecture, and biomechanical properties of the femurs were then evaluated. The results showed that the middle-aged female APP/PS1 transgenic mice were susceptible to osteoporosis of the femoral bones and that weight gain significantly enhanced bone mass and mechanical properties. Notably, HFD was not detrimental to brain insulin signaling and AβPP processing, as well as to exploration ability and working, learning, and memory performance of the transgenic mice measured by T maze and Morris water maze, compared with the mice fed a normal-fat diet (10% calorie from fat). In addition, the circulating levels of leptin but not estradiol were remarkably elevated in HFD-treated mice. These results suggest that a body weight gain induced by the HFD feeding regimen significantly improved bone mass in female APP/PS1 mice with no detriments to exploration ability and spatial memory, most likely via the action of elevated circulating leptin.

No MeSH data available.


Related in: MedlinePlus

HFD ameliorated impairments of femoral mechanical properties in APP/PS1 mice. In the three-point bending test, the elastic force (A), ultimate force (B), second moment of inertia (C), elastic stress (D), and energy (E) were all significantly reduced in APP/PS1 mice compared to the age-matched C57BL/6 mice. No difference was found in elastic modulus (F) and stiffness (G) between C57BL/6 and APP/PS1 mice, but HFD significantly increased these two parameters. Ultimate stress did not vary among the three groups (H). Femur length was shorter in APP/PS1 mice but not reversed by HFD (I). Data were means ± SEM. n = 10 for C57BL/6 mice, n = 12 for APP/PS1 mice, and n = 11 for APP/PS1 + HFD mice. The results were analyzed by one-way ANOVA, followed by Newman–Keuls post hoc test. *p < 0.05; **p < 0.01; ***p < 0.001.
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Figure 4: HFD ameliorated impairments of femoral mechanical properties in APP/PS1 mice. In the three-point bending test, the elastic force (A), ultimate force (B), second moment of inertia (C), elastic stress (D), and energy (E) were all significantly reduced in APP/PS1 mice compared to the age-matched C57BL/6 mice. No difference was found in elastic modulus (F) and stiffness (G) between C57BL/6 and APP/PS1 mice, but HFD significantly increased these two parameters. Ultimate stress did not vary among the three groups (H). Femur length was shorter in APP/PS1 mice but not reversed by HFD (I). Data were means ± SEM. n = 10 for C57BL/6 mice, n = 12 for APP/PS1 mice, and n = 11 for APP/PS1 + HFD mice. The results were analyzed by one-way ANOVA, followed by Newman–Keuls post hoc test. *p < 0.05; **p < 0.01; ***p < 0.001.

Mentions: To understand the mechanical effects of AD pathology and HFD-induced body weight gain on bone, we employed the three-point bending test to measure the mechanical properties of the femurs (Figures 4A–H). We found that the elastic force and ultimate force were both significantly reduced in APP/PS1 mice compared to the age-matched C57BL/6 mice and that these effects were completely reversed by the HFD (Figures 4A,B). With respect to the second moment of inertia, which reflects the geometric size of bone, and load-displacement curve, we found that elastic stress and energy absorption decreased in the APP/PS1 mice and were reversed by the HFD (Figures 4C–E). Although no differences in the elastic modulus and stiffness were observed between the C57BL/6 and APP/PS1 mice, HFD significantly increased the values of these two parameters (Figures 4F,G). Ultimate stress was not different among the three groups of mice (Figure 4H). The femur length was shorter in APP/PS1 mice compared to C57BL/6 mice, and this effect was not altered by the HFD (Figure 4I).


High-Fat-Diet-Induced Weight Gain Ameliorates Bone Loss without Exacerbating AβPP Processing and Cognition in Female APP/PS1 Mice.

Peng Y, Liu J, Tang Y, Liu J, Han T, Han S, Li H, Hou C, Liu J, Long J - Front Cell Neurosci (2014)

HFD ameliorated impairments of femoral mechanical properties in APP/PS1 mice. In the three-point bending test, the elastic force (A), ultimate force (B), second moment of inertia (C), elastic stress (D), and energy (E) were all significantly reduced in APP/PS1 mice compared to the age-matched C57BL/6 mice. No difference was found in elastic modulus (F) and stiffness (G) between C57BL/6 and APP/PS1 mice, but HFD significantly increased these two parameters. Ultimate stress did not vary among the three groups (H). Femur length was shorter in APP/PS1 mice but not reversed by HFD (I). Data were means ± SEM. n = 10 for C57BL/6 mice, n = 12 for APP/PS1 mice, and n = 11 for APP/PS1 + HFD mice. The results were analyzed by one-way ANOVA, followed by Newman–Keuls post hoc test. *p < 0.05; **p < 0.01; ***p < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4125950&req=5

Figure 4: HFD ameliorated impairments of femoral mechanical properties in APP/PS1 mice. In the three-point bending test, the elastic force (A), ultimate force (B), second moment of inertia (C), elastic stress (D), and energy (E) were all significantly reduced in APP/PS1 mice compared to the age-matched C57BL/6 mice. No difference was found in elastic modulus (F) and stiffness (G) between C57BL/6 and APP/PS1 mice, but HFD significantly increased these two parameters. Ultimate stress did not vary among the three groups (H). Femur length was shorter in APP/PS1 mice but not reversed by HFD (I). Data were means ± SEM. n = 10 for C57BL/6 mice, n = 12 for APP/PS1 mice, and n = 11 for APP/PS1 + HFD mice. The results were analyzed by one-way ANOVA, followed by Newman–Keuls post hoc test. *p < 0.05; **p < 0.01; ***p < 0.001.
Mentions: To understand the mechanical effects of AD pathology and HFD-induced body weight gain on bone, we employed the three-point bending test to measure the mechanical properties of the femurs (Figures 4A–H). We found that the elastic force and ultimate force were both significantly reduced in APP/PS1 mice compared to the age-matched C57BL/6 mice and that these effects were completely reversed by the HFD (Figures 4A,B). With respect to the second moment of inertia, which reflects the geometric size of bone, and load-displacement curve, we found that elastic stress and energy absorption decreased in the APP/PS1 mice and were reversed by the HFD (Figures 4C–E). Although no differences in the elastic modulus and stiffness were observed between the C57BL/6 and APP/PS1 mice, HFD significantly increased the values of these two parameters (Figures 4F,G). Ultimate stress was not different among the three groups of mice (Figure 4H). The femur length was shorter in APP/PS1 mice compared to C57BL/6 mice, and this effect was not altered by the HFD (Figure 4I).

Bottom Line: Given that there is no evidence that being overweight is associated with AD-type cognitive dysfunction, we hypothesized that moderate weight gain might have a protective effect on the bone loss in AD without exacerbating cognitive dysfunction.The bone mineral density, microarchitecture, and biomechanical properties of the femurs were then evaluated.These results suggest that a body weight gain induced by the HFD feeding regimen significantly improved bone mass in female APP/PS1 mice with no detriments to exploration ability and spatial memory, most likely via the action of elevated circulating leptin.

View Article: PubMed Central - PubMed

Affiliation: Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology and Frontier Institute of Science and Technology, Xi'an Jiaotong University , Xi'an , China.

ABSTRACT
Osteoporosis is negatively correlated with body mass, whereas both osteoporosis and weight loss occur at higher incidence during the progression of Alzheimer's disease (AD) than the age-matched non-dementia individuals. Given that there is no evidence that being overweight is associated with AD-type cognitive dysfunction, we hypothesized that moderate weight gain might have a protective effect on the bone loss in AD without exacerbating cognitive dysfunction. In this study, feeding a high-fat diet (HFD, 45% calorie from fat) to female APP/PS1 transgenic mice, an AD animal model, induced weight gain. The bone mineral density, microarchitecture, and biomechanical properties of the femurs were then evaluated. The results showed that the middle-aged female APP/PS1 transgenic mice were susceptible to osteoporosis of the femoral bones and that weight gain significantly enhanced bone mass and mechanical properties. Notably, HFD was not detrimental to brain insulin signaling and AβPP processing, as well as to exploration ability and working, learning, and memory performance of the transgenic mice measured by T maze and Morris water maze, compared with the mice fed a normal-fat diet (10% calorie from fat). In addition, the circulating levels of leptin but not estradiol were remarkably elevated in HFD-treated mice. These results suggest that a body weight gain induced by the HFD feeding regimen significantly improved bone mass in female APP/PS1 mice with no detriments to exploration ability and spatial memory, most likely via the action of elevated circulating leptin.

No MeSH data available.


Related in: MedlinePlus