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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 did not deteriorate the working, learning and memory performance in APP/PS1 mice. In the T-maze spontaneous alternation test, both APP/PS1 group and APP/PS1 + HFD group showed fewer percentages to make the alternative choices (A) and had a longer latency time (B) than C57BL/6 group. APP/PS1 group exhibited significant longer escape latency on days 3, 5, and 6, and longer distance on days 2, 3, 4, and 5, while APP/PS1 + HFD group exhibited significant longer escape latency on days 3, and 6, and longer distance on days 2 and 3 (C,D). The mean crossings of the C57BL/6 group were more frequent than those of APP/PS1 and APP/PS1 + HFD groups (E). Additionally, no difference was found between the APP/PS1 and APP/PS1 + HFD groups. Data were means ± SEM. n = 10 for C57BL/6 mice, n = 12 for APP/PS1 mice, and n = 11 for APP/PS1 + HFD mice. T-maze results were analyzed by one-way ANOVA, followed by Newman–Keuls post hoc test. *p < 0.05; **p < 0.01. The water maze result was analyzed by two-way ANOVA, followed by Bonferroni’s post hoc test. ∧p < 0.05; ∧∧p < 0.01; ∧∧∧p < 0.001, APP/PS1 versus C57BL/6; #p < 0.05; ##p < 0.01; ###p < 0.001, APP/PS1 + HFD versus C57BL/6.
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Figure 2: HFD did not deteriorate the working, learning and memory performance in APP/PS1 mice. In the T-maze spontaneous alternation test, both APP/PS1 group and APP/PS1 + HFD group showed fewer percentages to make the alternative choices (A) and had a longer latency time (B) than C57BL/6 group. APP/PS1 group exhibited significant longer escape latency on days 3, 5, and 6, and longer distance on days 2, 3, 4, and 5, while APP/PS1 + HFD group exhibited significant longer escape latency on days 3, and 6, and longer distance on days 2 and 3 (C,D). The mean crossings of the C57BL/6 group were more frequent than those of APP/PS1 and APP/PS1 + HFD groups (E). Additionally, no difference was found between the APP/PS1 and APP/PS1 + HFD groups. Data were means ± SEM. n = 10 for C57BL/6 mice, n = 12 for APP/PS1 mice, and n = 11 for APP/PS1 + HFD mice. T-maze results were analyzed by one-way ANOVA, followed by Newman–Keuls post hoc test. *p < 0.05; **p < 0.01. The water maze result was analyzed by two-way ANOVA, followed by Bonferroni’s post hoc test. ∧p < 0.05; ∧∧p < 0.01; ∧∧∧p < 0.001, APP/PS1 versus C57BL/6; #p < 0.05; ##p < 0.01; ###p < 0.001, APP/PS1 + HFD versus C57BL/6.

Mentions: To evaluate whether the HFD accelerated the development of AD, the behavioral tests (T-maze and water maze) were conducted in the 9-month-old animals. The APP/PS1 group and APP/PS1 + HFD group exhibited impaired exploration ability, spatial learning and memory abilities, as indicated by fewer alternative choices and longer latency in the T-maze test, and longer escape latency and distance during training phase, and fewer crossings on the platform during probe trial in the water maze test compared to the C57BL/6 mice. Notably, no significant behavioral differences were found between the APP/PS1 and APP/PS1 + HFD groups (Figures 2A–E) in this study, suggesting that feeding a diet at a level of 45% calorie from fat for as long as 6 months does not lead to a detriment of exploration ability, spatial learning and memory in the female transgenic mouse model of AD.


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 did not deteriorate the working, learning and memory performance in APP/PS1 mice. In the T-maze spontaneous alternation test, both APP/PS1 group and APP/PS1 + HFD group showed fewer percentages to make the alternative choices (A) and had a longer latency time (B) than C57BL/6 group. APP/PS1 group exhibited significant longer escape latency on days 3, 5, and 6, and longer distance on days 2, 3, 4, and 5, while APP/PS1 + HFD group exhibited significant longer escape latency on days 3, and 6, and longer distance on days 2 and 3 (C,D). The mean crossings of the C57BL/6 group were more frequent than those of APP/PS1 and APP/PS1 + HFD groups (E). Additionally, no difference was found between the APP/PS1 and APP/PS1 + HFD groups. Data were means ± SEM. n = 10 for C57BL/6 mice, n = 12 for APP/PS1 mice, and n = 11 for APP/PS1 + HFD mice. T-maze results were analyzed by one-way ANOVA, followed by Newman–Keuls post hoc test. *p < 0.05; **p < 0.01. The water maze result was analyzed by two-way ANOVA, followed by Bonferroni’s post hoc test. ∧p < 0.05; ∧∧p < 0.01; ∧∧∧p < 0.001, APP/PS1 versus C57BL/6; #p < 0.05; ##p < 0.01; ###p < 0.001, APP/PS1 + HFD versus C57BL/6.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
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Figure 2: HFD did not deteriorate the working, learning and memory performance in APP/PS1 mice. In the T-maze spontaneous alternation test, both APP/PS1 group and APP/PS1 + HFD group showed fewer percentages to make the alternative choices (A) and had a longer latency time (B) than C57BL/6 group. APP/PS1 group exhibited significant longer escape latency on days 3, 5, and 6, and longer distance on days 2, 3, 4, and 5, while APP/PS1 + HFD group exhibited significant longer escape latency on days 3, and 6, and longer distance on days 2 and 3 (C,D). The mean crossings of the C57BL/6 group were more frequent than those of APP/PS1 and APP/PS1 + HFD groups (E). Additionally, no difference was found between the APP/PS1 and APP/PS1 + HFD groups. Data were means ± SEM. n = 10 for C57BL/6 mice, n = 12 for APP/PS1 mice, and n = 11 for APP/PS1 + HFD mice. T-maze results were analyzed by one-way ANOVA, followed by Newman–Keuls post hoc test. *p < 0.05; **p < 0.01. The water maze result was analyzed by two-way ANOVA, followed by Bonferroni’s post hoc test. ∧p < 0.05; ∧∧p < 0.01; ∧∧∧p < 0.001, APP/PS1 versus C57BL/6; #p < 0.05; ##p < 0.01; ###p < 0.001, APP/PS1 + HFD versus C57BL/6.
Mentions: To evaluate whether the HFD accelerated the development of AD, the behavioral tests (T-maze and water maze) were conducted in the 9-month-old animals. The APP/PS1 group and APP/PS1 + HFD group exhibited impaired exploration ability, spatial learning and memory abilities, as indicated by fewer alternative choices and longer latency in the T-maze test, and longer escape latency and distance during training phase, and fewer crossings on the platform during probe trial in the water maze test compared to the C57BL/6 mice. Notably, no significant behavioral differences were found between the APP/PS1 and APP/PS1 + HFD groups (Figures 2A–E) in this study, suggesting that feeding a diet at a level of 45% calorie from fat for as long as 6 months does not lead to a detriment of exploration ability, spatial learning and memory in the female transgenic mouse model of AD.

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