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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 protected femoral cortical bone from AD-involved impairments. The bone mineral density [BMD, (A)], bone mineral content [BMC, (B)], and mean thickness [Cr.Th (C)] were lower in the APP/PS1 mice compared to the C57BL/6 mice, all of which were reversed by HFD feeding. No significant decrease was found in total area [Tt.Ar (D)] and cortical area [Ct.Ar (E)] in the APP/PS1 mice compared to the C57BL/6 mice, whereas, both of which were elevated by HFD feeding.Marrow area (Ma.Ar) did not vary among the three groups (F). The ratio of Ct.Ar to Tt.Ar was decreased in APP/PS1 mice (G), but not reversed by HFD feeding. Micrographs showed the differences of thickness and inner bone surface among all the groups with arrows indicating the representative part (H). Data were means ± SEM. n = 7 for C57BL/6 mice, n = 8 for APP/PS1 mice, and n = 8 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 5: HFD protected femoral cortical bone from AD-involved impairments. The bone mineral density [BMD, (A)], bone mineral content [BMC, (B)], and mean thickness [Cr.Th (C)] were lower in the APP/PS1 mice compared to the C57BL/6 mice, all of which were reversed by HFD feeding. No significant decrease was found in total area [Tt.Ar (D)] and cortical area [Ct.Ar (E)] in the APP/PS1 mice compared to the C57BL/6 mice, whereas, both of which were elevated by HFD feeding.Marrow area (Ma.Ar) did not vary among the three groups (F). The ratio of Ct.Ar to Tt.Ar was decreased in APP/PS1 mice (G), but not reversed by HFD feeding. Micrographs showed the differences of thickness and inner bone surface among all the groups with arrows indicating the representative part (H). Data were means ± SEM. n = 7 for C57BL/6 mice, n = 8 for APP/PS1 mice, and n = 8 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 determine the structural basis for the alteration in biomechanical properties, we further evaluated the cortical bone in femurs using a micro-CT system. Compared to the C57BL/6 group, the APP/PS1 group had lower values for BMD, BMC, and mean thickness (Ct.Th) of cortical femur but showed no significant decreases in total area (Tt.Ar) and cortical area (Ct.Ar) (Figures 5A–E,H). Ct.Ar/Tt.Ar was decreased in the APP/PS1 mice (Figure 5G) compared with the C57BL/6 mice. HFD feeding resulted in significant increases in BMD, BMC, Ct.Th, Tt.Ar, and Ct.Ar of the measured bone in APP/PS1 mice (Figures 5A–E,H). There were no significant differences in marrow area (Ma.Ar) among the groups (Figure 5F). The micrographs also revealed that the inner bone surface facing the marrow was much smoother in the C57BL/6 and APP/PS1 + HFD groups than in APP/PS1 group (Figure 5H).


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 protected femoral cortical bone from AD-involved impairments. The bone mineral density [BMD, (A)], bone mineral content [BMC, (B)], and mean thickness [Cr.Th (C)] were lower in the APP/PS1 mice compared to the C57BL/6 mice, all of which were reversed by HFD feeding. No significant decrease was found in total area [Tt.Ar (D)] and cortical area [Ct.Ar (E)] in the APP/PS1 mice compared to the C57BL/6 mice, whereas, both of which were elevated by HFD feeding.Marrow area (Ma.Ar) did not vary among the three groups (F). The ratio of Ct.Ar to Tt.Ar was decreased in APP/PS1 mice (G), but not reversed by HFD feeding. Micrographs showed the differences of thickness and inner bone surface among all the groups with arrows indicating the representative part (H). Data were means ± SEM. n = 7 for C57BL/6 mice, n = 8 for APP/PS1 mice, and n = 8 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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Related In: Results  -  Collection

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Figure 5: HFD protected femoral cortical bone from AD-involved impairments. The bone mineral density [BMD, (A)], bone mineral content [BMC, (B)], and mean thickness [Cr.Th (C)] were lower in the APP/PS1 mice compared to the C57BL/6 mice, all of which were reversed by HFD feeding. No significant decrease was found in total area [Tt.Ar (D)] and cortical area [Ct.Ar (E)] in the APP/PS1 mice compared to the C57BL/6 mice, whereas, both of which were elevated by HFD feeding.Marrow area (Ma.Ar) did not vary among the three groups (F). The ratio of Ct.Ar to Tt.Ar was decreased in APP/PS1 mice (G), but not reversed by HFD feeding. Micrographs showed the differences of thickness and inner bone surface among all the groups with arrows indicating the representative part (H). Data were means ± SEM. n = 7 for C57BL/6 mice, n = 8 for APP/PS1 mice, and n = 8 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 determine the structural basis for the alteration in biomechanical properties, we further evaluated the cortical bone in femurs using a micro-CT system. Compared to the C57BL/6 group, the APP/PS1 group had lower values for BMD, BMC, and mean thickness (Ct.Th) of cortical femur but showed no significant decreases in total area (Tt.Ar) and cortical area (Ct.Ar) (Figures 5A–E,H). Ct.Ar/Tt.Ar was decreased in the APP/PS1 mice (Figure 5G) compared with the C57BL/6 mice. HFD feeding resulted in significant increases in BMD, BMC, Ct.Th, Tt.Ar, and Ct.Ar of the measured bone in APP/PS1 mice (Figures 5A–E,H). There were no significant differences in marrow area (Ma.Ar) among the groups (Figure 5F). The micrographs also revealed that the inner bone surface facing the marrow was much smoother in the C57BL/6 and APP/PS1 + HFD groups than in APP/PS1 group (Figure 5H).

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