High vitamin D and calcium intakes increase bone mineral (Ca and P) content in high-fat diet-induced obese mice

Song, Qingming; Сергеев, И. Н.

doi:10.1016/j.nutres.2014.11.003

Cited by 13 publications

(10 citation statements)

References 45 publications

(52 reference statements)

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“…Although the diets were not high in fat (16.3% calories from fat), the high carbohydrate content (65% calories from carbohydrates) may have caused excessive weight gain. Adding Ca supplements to high-fat diets prevents loss of cortical bone mineral content in obese mice [ 32 ]. If the diets used in this study did induce obesity, causing negative effects on bone mass and bone strength, the supplemented diet may have helped to prevent or attenuate some of the detrimental effects.…”

Section: Discussionmentioning

confidence: 99%

Combined mineral-supplemented diet and exercise increases bone mass and strength after eight weeks and maintains increases after eight weeks detraining in adult mice

2018

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Exercise has long-lasting benefits to bone mass and structural strength even after cessation. Combining exercise with a calcium- and phosphorus-supplemented diet increases cortical bone mineral content (BMC), area, and yield force more than exercise alone in adult mice. These increases could also be maintained after stopping exercise if the modified diet is maintained. It was hypothesized that combining exercise with a mineral-supplemented diet would lead to greater cortical BMC, area, and yield force immediately after a lengthy exercise program and after an equally long period of non-exercise (detraining) in adult mice. Male, 16-week old C57Bl/6 mice were assigned to 9 weight-matched groups–a baseline group, exercise and non-exercise groups fed a control or mineral-supplemented diet for 8 weeks, exercise + detraining and non-exercise groups fed a control or mineral-supplemented diet for 16 weeks. Exercise + detraining consisted of 8 weeks of exercise followed by 8 weeks without exercise. The daily exercise program consisted of running on a treadmill at 12 m/min, 30 min/day. After 8 weeks, mice fed the supplemented diet had greater tibial cortical BMC and area, trabecular bone volume/tissue volume (BV/TV), bone mineral density (vBMD), yield force, and ultimate force than mice fed the control diet. Exercise increased cortical BMC and area only when coupled with the supplemented diet. After 16 weeks, both exercised and non-exercised mice fed the supplemented diet maintained greater tibial cortical BMC and area, trabecular BV/TV, vBMD, yield force, and ultimate force than mice fed the control diet. Combining exercise with a mineral-supplemented diet leads to greater bone mass and structural strength than exercise alone. These benefits remain after an equally long period of detraining. Long-term use of dietary mineral supplements may help increase and maintain bone mass with aging in adult mice.

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Section: Discussionmentioning

confidence: 99%

Combined mineral-supplemented diet and exercise increases bone mass and strength after eight weeks and maintains increases after eight weeks detraining in adult mice

2018

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“…A high-fat-diet-induced obesity (DIO) mouse model is characterized by obese phenotype, increased blood glucose concentration, and development of adiposity [6,13]. We have shown that DIO mice fed a diet with high vitamin D 3 content demonstrate a decreased weight of adipose tissue and improved biomarkers of adiposity and vitamin D status [38,39]. The glucose and insulin concentrations in the blood of those mice were significantly decreased (to the levels measured in the non-obese control), whereas the concentration of adiponectin (an insulin-sensitizing adipokine) was increased.…”

Section: Vitamin D and Diet-induced Obesitymentioning

confidence: 99%

Vitamin D Status and Vitamin D-Dependent Apoptosis in Obesity

Сергеев

2020

Nutrients

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The role of vitamin D in obesity appears to be linked to vitamin D insufficient/deficient status. However, mechanistic understanding of the role of vitamin D in obesity is lacking. We have shown earlier that the vitamin D hormonal form, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), induces cell death by apoptosis in mature adipocytes. This effect of the hormone is mediated by the cellular Ca2+ signaling pathway: a sustained increase of intracellular (cytosolic) Ca2+ concentration followed by activation of Ca2+-dependent initiators and effectors of apoptosis. In recent animal studies, we demonstrated that low vitamin D status is observed in diet-induced obesity (DIO). High intake of vitamin D3 in DIO decreased the weight of white adipose tissue and improved biomarkers related to adiposity and Ca2+ regulation. The anti-obesity effect of vitamin D (1,25(OH)2D3) in DIO was determined by the induction of Ca2+-mediated apoptosis in mature adipocytes executed by Ca2+-dependent apoptotic proteases (calpains and caspases). Thus, a high intake of vitamin D in obesity increases vitamin D nutritional status and normalizes vitamin D hormonal status that is accompanied by the reduction of adiposity. Overall, our findings imply that vitamin D may contribute to the prevention of obesity and obesity-related diseases and that the mechanism of the anti-obesity effect of 1,25(OH)2D3 includes induction of Ca2+-mediated apoptosis in adipocytes.

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“…1,25(OH) 2 D 3 induces apoptosis in mature adipocytes via Ca 2+ -mediated mechanism: activation of Ca 2+ -dependent calpain and Ca 2+ /calpain-dependent caspase-12 [19,22,25]. High vitamin D 3 intake was also effective in normalization (an increase) of the mineral (Ca and P) content of growing bone in obese mice via regulatory effects mediated by 1,25(OH) 2 D 3 -PTH axis [40]. These findings demonstrate that high vitamin D intake is effective in decreasing blood glucose and insulin in DIO and that the hormonal mechanism of this effect can involve 1,25(OH) 2 D 3 .…”

Section: 25(oh) 2 D 3 -Mediated Apoptosis In Adipocytesmentioning

confidence: 99%

“…It is also necessary to note that, from a mechanistic point of view, the circulating concentration of the hormone 1,25(OH) 2 D 3 is maintained at the precise, narrow level within a broad range of concentrations of 25(OH)D 3 to allow 1,25(OH) 2 D 3 to mediate, via VDRs, the cellular responses (genomic and nongenomic) and perform its physiological functions in a fashion similar to that of other steroid hormones [5]. For example, as discussed in Section 2, it has been demonstrated in a mouse model of diet-induced obesity that normalization (an increase) in concentration of 1,25(OH) 2 D 3 can prevent an increase of body fat and normalize glucose, insulin, and adiponectin levels in blood [3,39,40]. The rational design of vitamin D analogs selectively interacting with membrane VDRs and capable of regulating Ca 2+ signaling in adipocytes and pancreatic β-cells could lead to a more positive clinical outcome in obesity and T2D.…”

Section: Vitamin D Status In Obesity and Diabetesmentioning

confidence: 99%

Vitamin D—Cellular Ca2+ link to obesity and diabetes

Сергеев

2016

The Journal of Steroid Biochemistry and Molecular Biology

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The vitamin D hormone 1,25-Dihydroxyvitamin D (1,25(OH)D)-induced cellular Ca signals regulate apoptosis in adipocytes and insulin secretion from pancreatic β-cells, and low vitamin D status is considered a risk factor for obesity and type 2 diabetes. The anti-obesity effects of 1,25(OH)D in mature adipocytes are determined by its activity to generate, via multiple Ca signaling pathways, a sustained increase in intracellular Ca followed by activation of the Ca-dependent initiators and effectors of apoptosis. In pancreatic β-cells, 1,25(OH)D induces synchronous Ca oscillations, which pattern pulsatile insulin secretion from these cells. An increased intake of vitamin D in a high fat diet-induced obesity mouse model is associated with a decreased weight of white adipose tissue due to induction of apoptosis and the improved blood markers related to adiposity, diabetes, and vitamin D status (plasma concentrations of glucose, insulin, adiponectin, 25-hydroxyvitamin D, and 1,25(OH)D). High vitamin D intake is also effective in increasing the mineral content of growing bone in obese mice via regulatory effects mediated by 1,25(OH)D-parathyroid hormone axis. The 1,25(OH)D-dependent cellular Ca signaling can be important for maintaining the normal levels of apoptosis in adipose tissue and insulin secretion from pancreatic β-cells. An increased intake of vitamin D may contribute to the prevention of obesity, type 2 diabetes, and bone disorders associated with these diseases.

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High vitamin D and calcium intakes increase bone mineral (Ca and P) content in high-fat diet-induced obese mice

Cited by 13 publications

References 45 publications

Combined mineral-supplemented diet and exercise increases bone mass and strength after eight weeks and maintains increases after eight weeks detraining in adult mice

Combined mineral-supplemented diet and exercise increases bone mass and strength after eight weeks and maintains increases after eight weeks detraining in adult mice

Vitamin D Status and Vitamin D-Dependent Apoptosis in Obesity

Vitamin D—Cellular Ca2+ link to obesity and diabetes

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