Limits...
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

Serum biochemical characteristics. The ALP level was higher in APP/PS1 mice than that in C57BL/6 mice, and it was reversed after HFD feeding (A). The serum Ca2+ levels in APP/PS1 mice was not different from that of C57BL/6 or APP/PS1 + HFD mice; however, it was higher in APP/PS1 + HFD mice than that in C57BL/6 mice (B). The serum phosphorus level was higher in APP/PS1 mice than that in C57BL/6 mice, which was not reversed by HFD feeding (C). APP/PS1 mice had a lower estrogen level than C57BL/6 mice, which was also not reversed by HFD feeding (D). The serum leptin level was lower in APP/PS1 mice compared to C57BL/6 mice (p = 0.07), and it was significantly induced after HFD feeding (E). Data were means ± SEM. n = 7 for C57BL/6 mice, n = 9 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 < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4125950&req=5

Figure 7: Serum biochemical characteristics. The ALP level was higher in APP/PS1 mice than that in C57BL/6 mice, and it was reversed after HFD feeding (A). The serum Ca2+ levels in APP/PS1 mice was not different from that of C57BL/6 or APP/PS1 + HFD mice; however, it was higher in APP/PS1 + HFD mice than that in C57BL/6 mice (B). The serum phosphorus level was higher in APP/PS1 mice than that in C57BL/6 mice, which was not reversed by HFD feeding (C). APP/PS1 mice had a lower estrogen level than C57BL/6 mice, which was also not reversed by HFD feeding (D). The serum leptin level was lower in APP/PS1 mice compared to C57BL/6 mice (p = 0.07), and it was significantly induced after HFD feeding (E). Data were means ± SEM. n = 7 for C57BL/6 mice, n = 9 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 < 0.001.

Mentions: Several bone-remodeling-related markers, including serum ALP, calcium (Ca2+), phosphorus (P), circulating leptin and estradiol (Figures 7A–E), were measured in this study. The ALP activity was much higher in the APP/PS1 mice than in the C57BL/6 mice and this increase was significantly reversed by HFD feeding (Figure 7A). We found no significant difference in Ca2+ levels either between APP/PS1 mice and C57BL/6 mice, or between APP/PS1 mice and APP/PS1 + HFD mice, but Ca2+ levels were elevated in the APP/PS1 + HFD group compared with that in the C57BL/6 group (Figure 7B). The P concentration was higher in the APP/PS1 mice than in the C57BL/6 group, but this effect was unchanged by HFD feeding (Figure 7C). We found a lower concentration of estrogen in the APP/PS1 mice relative to the C57BL/6 mice, and the low level remained in the HFD-fed mice (Figure 7D). In contrast, there was a trend toward decreased levels of leptin in the APP/PS1 mice (p = 0.07) compared with the C57BL/6 mice, and this parameter was significantly elevated by the HFD feeding (Figure 7E).


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)

Serum biochemical characteristics. The ALP level was higher in APP/PS1 mice than that in C57BL/6 mice, and it was reversed after HFD feeding (A). The serum Ca2+ levels in APP/PS1 mice was not different from that of C57BL/6 or APP/PS1 + HFD mice; however, it was higher in APP/PS1 + HFD mice than that in C57BL/6 mice (B). The serum phosphorus level was higher in APP/PS1 mice than that in C57BL/6 mice, which was not reversed by HFD feeding (C). APP/PS1 mice had a lower estrogen level than C57BL/6 mice, which was also not reversed by HFD feeding (D). The serum leptin level was lower in APP/PS1 mice compared to C57BL/6 mice (p = 0.07), and it was significantly induced after HFD feeding (E). Data were means ± SEM. n = 7 for C57BL/6 mice, n = 9 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 < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 7: Serum biochemical characteristics. The ALP level was higher in APP/PS1 mice than that in C57BL/6 mice, and it was reversed after HFD feeding (A). The serum Ca2+ levels in APP/PS1 mice was not different from that of C57BL/6 or APP/PS1 + HFD mice; however, it was higher in APP/PS1 + HFD mice than that in C57BL/6 mice (B). The serum phosphorus level was higher in APP/PS1 mice than that in C57BL/6 mice, which was not reversed by HFD feeding (C). APP/PS1 mice had a lower estrogen level than C57BL/6 mice, which was also not reversed by HFD feeding (D). The serum leptin level was lower in APP/PS1 mice compared to C57BL/6 mice (p = 0.07), and it was significantly induced after HFD feeding (E). Data were means ± SEM. n = 7 for C57BL/6 mice, n = 9 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 < 0.001.
Mentions: Several bone-remodeling-related markers, including serum ALP, calcium (Ca2+), phosphorus (P), circulating leptin and estradiol (Figures 7A–E), were measured in this study. The ALP activity was much higher in the APP/PS1 mice than in the C57BL/6 mice and this increase was significantly reversed by HFD feeding (Figure 7A). We found no significant difference in Ca2+ levels either between APP/PS1 mice and C57BL/6 mice, or between APP/PS1 mice and APP/PS1 + HFD mice, but Ca2+ levels were elevated in the APP/PS1 + HFD group compared with that in the C57BL/6 group (Figure 7B). The P concentration was higher in the APP/PS1 mice than in the C57BL/6 group, but this effect was unchanged by HFD feeding (Figure 7C). We found a lower concentration of estrogen in the APP/PS1 mice relative to the C57BL/6 mice, and the low level remained in the HFD-fed mice (Figure 7D). In contrast, there was a trend toward decreased levels of leptin in the APP/PS1 mice (p = 0.07) compared with the C57BL/6 mice, and this parameter was significantly elevated by the HFD feeding (Figure 7E).

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