scholarly journals Effect of Vitamin E Isoforms on Bone Metabolism in C57BL/6 J Mice Fed a High Fat Diet

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1795-1795
Author(s):  
Chen Du ◽  
Gina Tran ◽  
Victorine Imrhan ◽  
Chandan Prasad ◽  
Parakat Vijayagopal ◽  
...  
Keyword(s):  
Vitamin E ◽  
Bone Loss ◽  
Bone Metabolism ◽  
Bone Mineral ◽  
High Fat Diet ◽  
Alpha Tocopherol ◽  
Type I ◽  
High Fat ◽  
Mineral Density ◽  
Gamma Tocopherol

Abstract Objectives The purpose of this study was to compare the effects of alpha tocopherol, gamma tocopherol, and the combination of alpha and gamma tocopherols on bone mineral density (BMD), bone mineral content (BMC), and bone metabolism in C57BL/6 J mice fed a high-fat diet. Methods A total of 75 male C57BL/6 mice were randomized to either a low fat diet (LFD) with 6% fat, a high fat diet (HFD) with 20% fat, HFD supplemented with alpha tocopherol (AT), gamma tocopherol (GT), or the combination of AT and GT. LFD and HFD were provided to corresponding groups of mice without vitamin E isoform supplements for 15 weeks to induce bone loss. At the end of the 15 weeks, AT, GT, and a combination of AT and GT were added to 3 of the HFD groups and fed for 10 weeks. LFD group and one of the HFD groups were continued on the same diet for another 10 weeks without additional supplements. All mice were euthanized at the end of the 25 weeks period. Left and right fibula bones were excised, cleaned, and scanned using the Lunar PIXImus dual-energy x-ray absorptiometry (DEXA) densitometer to assess BMD, BMC, lean tissue, and fat tissue content. Serum biomarkers of bone metabolism were evaluated post euthanization. Results HFD resulted in significantly lower fibular BMD and higher tibial bone fat content in comparison to LFD. Animals in the HFD supplemented with GT, but not AT, showed significantly reduced effect of HFD in lowering BMD. Additionally, in the group fed HFD supplemented with GT, a significantly higher concentration of alkaline phosphatase (ALP) and N-terminal propeptide of type I procollagen (PINP) were noted, compared to LFD. This may be indicative of increased bone formation resulting from GT incorporated into the HFD diet. Conclusions The findings of the study suggest that different isoforms of vitamin E affect bone density and bone metabolism differently. Within the different isoforms of vitamin E, gamma tocopherol may have protective effects in bone, especially in the situation of high fat diet induced bone loss. Further examination of the mechanistic action of vitamin E isoforms on skeletal health is warranted. Funding Sources Texas Woman's University.

scholarly journals Inulin supplementation reduces the negative effect of a high-fat diet rich in SFA on bone health of growing pigs

2018 ◽  
Vol 119 (10) ◽  
pp. 1111-1118 ◽  
Author(s):  
Monika Sobol ◽  
Stanisława Raj ◽  
Grzegorz Skiba
Keyword(s):  
Bone Mineral Density ◽  
Bone Mineral ◽  
Bone Health ◽  
High Fat Diet ◽  
Growing Pigs ◽  
Whole Body ◽  
Standard Diet ◽  
High Fat ◽  
Mineral Density ◽  
Negative Effect

AbstractConsumption of a high-fat diet, rich in SFA, causes deterioration of bone properties. Some studies suggest that feeding inulin to animals may increase mineral absorption and positively affect bone quality; however, these studies have been carried out only on rodents fed a standard diet. The primary objective of this study was to determine the effect of inulin on bone health of pigs (using it as an animal model for humans) fed a high-fat diet rich in SFA, having an unbalanced ratio of lysine:metabolisable energy. It was hypothesised that inulin reduces the negative effects of such a diet on bone health. At 50 d of age, twenty-one pigs were randomly allotted to three groups: the control (C) group fed a standard diet, and two experimental (T and TI) groups fed a high-fat diet rich in SFA. Moreover, TI pigs consumed an extra inulin supply (7 % of daily feed intake). After 10 weeks, whole-body bone mineral content (P=0·0054) and bone mineral density (P=0·0322) were higher in pigs of groups TI and C compared with those of group T. Femur bone mineral density was highest in pigs in group C, lower in group TI and lowest in group T (P=0·001). Femurs of pigs in groups TI and C had similar, but higher, maximum strength compared with femurs of pigs in group T (P=0·0082). In conclusion, consumption of a high-fat diet rich in SFA adversely affected bone health, but inulin supplementation in such a diet diminishes this negative effect.

scholarly journals Serum Levels of miR-148a and miR-21-5p Are Increased in Type 1 Diabetic Patients and Correlated with Markers of Bone Strength and Metabolism

2018 ◽  
Vol 4 (4) ◽  
pp. 37 ◽  
Author(s):  
Giuseppina E. Grieco ◽  
Dorica Cataldo ◽  
Elena Ceccarelli ◽  
Laura Nigi ◽  
Giovanna Catalano ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Type 1 Diabetes ◽  
Bone Loss ◽  
Bone Metabolism ◽  
Bone Remodeling ◽  
Bone Mineral ◽  
Bone Fragility ◽  
Bone Homeostasis ◽  
Mineral Density

Type 1 diabetes (T1D) is characterized by bone loss and altered bone remodeling, resulting into reduction of bone mineral density (BMD) and increased risk of fractures. Identification of specific biomarkers and/or causative factors of diabetic bone fragility is of fundamental importance for an early detection of such alterations and to envisage appropriate therapeutic interventions. MicroRNAs (miRNAs) are small non-coding RNAs which negatively regulate genes expression. Of note, miRNAs can be secreted in biological fluids through their association with different cellular components and, in such context, they may represent both candidate biomarkers and/or mediators of bone metabolism alterations. Here, we aimed at identifying miRNAs differentially expressed in serum of T1D patients and potentially involved in bone loss in type 1 diabetes. We selected six miRNAs previously associated with T1D and bone metabolism: miR-21; miR-24; miR-27a; miR-148a; miR-214; and miR-375. Selected miRNAs were analyzed in sera of 15 T1D patients (age: 33.57 ± 8.17; BMI: 21.4 ± 1.65) and 14 non-diabetic subjects (age: 31.7 ± 8.2; BMI: 24.6 ± 4.34). Calcium, osteocalcin, parathormone (PTH), bone ALkaline Phoshatase (bALP), and Vitamin D (VitD) as well as main parameters of bone health were measured in each patient. We observed an increased expression of miR-148a (p = 0.012) and miR-21-5p (p = 0.034) in sera of T1D patients vs non-diabetic subjects. The correlation analysis between miRNAs expression and the main parameters of bone metabolism, showed a correlation between miR-148a and Bone Mineral Density (BMD) total body (TB) values (p = 0.042) and PTH circulating levels (p = 0.033) and the association of miR-21-5p to Bone Mineral Content-Femur (BMC-FEM). Finally, miR-148a and miR-21-5p target genes prediction analysis revealed several factors involved in bone development and remodeling, such as MAFB, WNT1, TGFB2, STAT3, or PDCD4, and the co-modulation of common pathways involved in bone homeostasis thus potentially assigning a role to both miR-148a and miR-21-5p in bone metabolism alterations. In conclusion, these results lead us to hypothesize a potential role for miR-148a and miR-21-5p in bone remodeling, thus representing potential biomarkers of bone fragility in T1D.

scholarly journals Sequestration of Vitamin E by Liver Fat in vivo, in vitro and in Women with Hepato-steatosis

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1696-1696
Author(s):  
Pierre-Christian Violet ◽  
Ifechukwude Ebenuwa ◽  
Stacey Chung ◽  
Jeffrey Atkinson ◽  
Danny Manor ◽  
...  
Keyword(s):  
Liver Disease ◽  
Vitamin E ◽  
High Fat Diet ◽  
Alpha Tocopherol ◽  
Liver Fat ◽  
Slight Reduction ◽  
High Fat ◽  
High Vitamin

Abstract Objectives Hepato-steatosis (HS) due to obesity is now the most common cause of chronic liver disease in the Americas and Western Europe. The only means to prevent disease is avoidance of obesity. α-Tocopherol at doses of 800 I.U. daily was reported to have partial treatment effects for NASH. Because alpha tocopherol is a fat-soluble vitamin, we hypothesized that excess fat in liver, as found in HS, could act unintentionally sequester vitamin E, thereby altering its normal physiology and contributing to development of NASH. Using oral and intravenous deuterated tocopherols, evidence showing HS altered a-tocopherol physiology was reported based on pharmacokinetics studies in obese women with HS. Here we further tested the sequestration hypothesis in vitro, and in vivo. Methods In vitro, we investigated effects of fat on intracellular vitamin E localization. Control human and mouse hepatocytes and hepatocytes pre-loaded with fat were incubated with fluorescent α-tocopherol (BDP-α-tocopherol). In vivo experiments were performed using mice fed a high fat diet with different vitamin E doses. Results Compared to controls, fat- loaded cells contained more a-tocopherol, and BDP-a-tocopherol was specifically localized into intracellular fat droplets. In cells incubated with BDP a-tocopherol, we found that fat loading decreased a-tocopherol release. Induced expression of TPP, which mediates vitamin E intracellular disposition under normal conditions, was not observed in fat loaded cells, further confirming vitamin E was trapped in fat. Livers of mice fed high fat diet had more vitamin E compared to controls. By further increasing vitamin E content of the high fat diet, we observed a reduction in liver size and liver fat in the high vitamin E group. Using a mouse metabolic chamber, we observed a slight reduction of oxygen consumption rate in the high vitamin E group compared to controls. Conclusions Considered together, these findings imply that fat in the liver may produce unrecognized hepatic vitamin E sequestration, which could drive liver disease. These results are consistent with the possibility that increased vitamin E intake might, if begun at an early stage, restore vitamin E physiology, potentially decreasing or preventing progression of HS to NASH. Funding Sources NIH intramural program (DK053213–14).

Addition of 2% crushed fenugreek seed to a high-fat diet reduces bone mineral density in C57BL/6J mice

2014 ◽  
Vol 32 (3) ◽  
pp. 146-151
Author(s):  
Simon A. Cichello ◽  
Denovan Begg ◽  
Markendya Jois ◽  
Richard Weisinger
Keyword(s):  
Bone Mineral Density ◽  
Bone Mineral ◽  
High Fat Diet ◽  
High Fat ◽  
Mineral Density ◽  
Fenugreek Seed

scholarly journals Magnesium Picolinate Improves Bone Formation by Regulation of RANK/RANKL/OPG and BMP-2/Runx2 Signaling Pathways in High-Fat Fed Rats

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3353
Author(s):  
Emre Sahin ◽  
Cemal Orhan ◽  
Tansel Ansal Balci ◽  
Fusun Erten ◽  
Kazim Sahin
Keyword(s):  
Bone Loss ◽  
Bone Formation ◽  
High Fat Diet ◽  
Male Rats ◽  
High Fat ◽  
Mineral Density ◽  
Protein Levels ◽  
Prevent Bone Loss ◽  
Osteogenic Protein ◽  
Affect Bone Metabolism

Magnesium (Mg) deficiency may affect bone metabolism by increasing osteoclasts, decreasing osteoblasts, promoting inflammation/oxidative stress, and result in subsequent bone loss. The objective of the present study was to identify the molecular mechanism underlying the bone protective effect of different forms of Mg (inorganic magnesium oxide (MgO) versus organic magnesium picolinate (MgPic) compound) in rats fed with a high-fat diet (HFD). Forty-two Wistar albino male rats were divided into six group (n = 7): (i) control, (ii) MgO, (iii) MgPic, (iv) HFD, (v) HFD + MgO, and (vi) HFD + MgPic. Bone mineral density (BMD) increased in the Mg supplemented groups, especially MgPic, as compared with the HFD group (p < 0.001). As compared with the HFD + MgO group, the HFD + MgPic group had higher bone P (p < 0.05) and Mg levels (p < 0.001). In addition, as compared to MgO, MgPic improved bone formation by increasing the levels of osteogenetic proteins (COL1A1 (p < 0.001), BMP2 (p < 0.001), Runx2 (p < 0.001), OPG (p < 0.05), and OCN (p < 0.001), IGF-1 (p < 0.001)), while prevented bone resorption by reducing the levels of RANK and RANKL (p < 0.001). In conclusion, the present data showed that the MgPic could increase osteogenic protein levels in bone more effectively than MgO, prevent bone loss, and contribute to bone formation in HFD rats.

scholarly journals Alterations of Bone Metabolism in Patients with Diabetes Mellitus

2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Sain S. Safarova
Keyword(s):  
Bone Mineral Density ◽  
Bone Metabolism ◽  
Bone Remodeling ◽  
Bone Mineral ◽  
Type I Collagen ◽  
Bone Microarchitecture ◽  
Type I ◽  
Mineral Density ◽  
Bone Remodeling Markers ◽  
Patients With Diabetes

Aim. The study aims to develop a practical model for screening bone turnover state in patients with diabetes and evaluate its clinical usefulness to identify diabetic osteopathy. Materials. The study was conducted in 2015–2017 in the Endocrinology Department of the Therapeutic Clinic of AM University. A total of 235 patients were assessed in the study (98 with T1DM and 137 with T2DM). 89 nondiabetic subjects served as controls. Bone mineral density (BMD) [by dual energy X-ray absorptiometry (DXA)] and serum markers of bone remodeling [aminoterminal propeptide of procollagen type I (P1NP) and c-terminal telopeptide of type I collagen (CTX)], parathyrin, and 25(OH)D were measured in all 235 patients. Results. Our results show that patients with T2DM have lower b-CTx values and relatively higher levels of P1NP, reflecting less pronounced changes in bone metabolism compared to patients with T1DM, regardless of age or duration of the disease. Osteoporosis was detected in 50% of patients with T1DM, compared to 13% of patients with T2DM. Conclusion. In some cases, bone remodeling markers are useful for improving the assessment of the state of bone tissue in early stages of diabetes, while alterations in bone microarchitecture may not always be captured by bone mineral density measurements.

scholarly journals The influence of habitual salt intake on bone remodelling in young healthy people

2021 ◽  
pp. 1-10
Author(s):  
Erna Davidović-Cvetko ◽  
Anita Matić ◽  
Jasminka Milas-Ahić ◽  
Ines Drenjančević
Keyword(s):  
Bone Mineral Density ◽  
Vitamin D ◽  
Bone Metabolism ◽  
Bone Mineral ◽  
Biochemical Markers ◽  
Bone Remodelling ◽  
Sodium Intake ◽  
Healthy People ◽  
Type I ◽  
Mineral Density

Introduction: Sodium alters calcium metabolism by increasing calcium excretion, thus possibly influencing bone metabolism. The hypothesis of the present study is that amount of dietary sodium intake affects the bone remodelling. This study aimed to assess whether a habitual intake of sodium has an effect on peak bone mass and biochemical indicators of bone metabolism. Subjects and Methods: In a cross-sectional study that involved 41 young men and women, six biochemical markers were assessed from blood samples using ELISA: osteocalcin, C-terminal procollagen type I peptide, receptor activator kappa B ligand, pyridinoline, parathyroid hormone, and osteoprotegerin, while bone mineral density (BMD) and bone mineral content (BMC) were measured by dual x-ray absorptiometry. Subjects were divided into two groups according to habitual sodium intake (low-Na and high-Na group) assessed by questionnaire. Results: No difference was found between groups of low and high Na intake in BMD and BMC, or in biochemical markers of bone metabolism. Since the groups differed in Ca intake, energy and vitamin D, adjustments were made for those cofounders. Regression analysis showed that only the dietary intake of vitamin D was associated with dual femur BMD and BMC, and no correlation was found between bone remodelling indicators and Na intake after adjustment for vitamin D intake. Conclusion: The present results could not confirm that habitual sodium intake above recommended levels affects bone remodelling processes or decreases bone mineral density in young healthy people if combined with adequate calcium intake.

scholarly journals Growth Hormone Replacement Is Important for the Restoration of Parathyroid Hormone Sensitivity and Improvement in Bone Metabolism in Older Adult Growth Hormone-Deficient Patients

2005 ◽  
Vol 90 (6) ◽  
pp. 3371-3380 ◽  
Author(s):  
H. D. White ◽  
A. M. Ahmad ◽  
B. H. Durham ◽  
A. Patwala ◽  
P. Whittingham ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Growth Hormone ◽  
Circadian Rhythm ◽  
Bone Metabolism ◽  
Bone Mineral ◽  
Target Organ ◽  
Type I ◽  
Mineral Density ◽  
Amino Terminal ◽  
Nephrogenous Camp

Alterations in PTH circadian rhythm and PTH target-organ sensitivity exist in adult GH-deficient (AGHD) patients and may underlie the pathogenesis of AGHD-related osteoporosis. GH replacement (GHR) results in increased bone mineral density, but its benefit in AGHD patients over 60 yr old has been debated. To examine the effect of age on changes in PTH circadian rhythm and target-organ sensitivity after GHR, we recruited 22 AGHD patients (12 were &lt;60 yr of age, and 10 were &gt;60 yr of age). Half-hourly blood samples were collected for PTH, calcium, phosphate, nephrogenous cAMP (marker of renal PTH activity), type-I collagenβ C-telopeptide (bone resorption marker), and procollagen type-I amino-terminal propeptide (bone formation marker) before and after 1, 3, 6, and 12 months of treatment with GHR. Significant PTH circadian rhythms were present in both age groups throughout the study. After GHR, PTH decreased and nephrogenous cAMP, adjusted calcium, and bone turnover markers increased in both groups, suggesting increased PTH target-organ sensitivity. In younger patients, the changes were significant after 1 month of GHR, but, in older patients, the changes were delayed until 3 months, with maximal changes at 12 months. Older AGHD patients derive benefit from GHR in terms of improvement in PTH sensitivity and bone metabolism. Their response appears delayed and may explain why previous studies have not shown a positive effect of GHR on bone mineral density in older AGHD patients.

Design of a Torsion Tester for Measuring Murine Bone Properties for Studies on the Effects of Diabetes and Obesity

2013 ◽  
Author(s):  
Brandon Sherrod ◽  
Shawn Gilbert ◽  
Krista Casazza ◽  
Alan Eberhardt
Keyword(s):  
Bone Mineral Density ◽  
Bone Mineral ◽  
Fracture Incidence ◽  
Type I ◽  
Healthy Weight ◽  
High Fat ◽  
Mineral Density ◽  
Body Regions ◽  
Increased Risk ◽  
Diabetes And Obesity

Conditions such as diabetes and obesity have been found to affect the mechanical integrity of bone. Studies have shown that diabetic rodent models exhibit lower levels of new bone formation during fracture healing 1, lower bone mineral density (BMD) 2, and increased risk of fracture 3. There are differences, however, in the bone integrity of bone samples from type I and type II diabetics, which is most likely due to obesity 2. Findings from research on obesity’s effects on bone integrity have been controversial; although there is an increase in bone mineral density (BMD) with increasing body mass index (BMI) and a decrease in fracture incidence in the central body regions in obese women compared to healthy weight women due to soft tissue padding, there is an increase in fracture incidence at extremeties 4. Other studies have shown that while cortical bone strength may not be adversely affected by high-fat diets, cancellous bone BMD and mechanical strength was significantly lower in high-fat diet mice than low-fat diet mice 5. In addition, extreme obesity has been associated with lower BMD despite the general trend of increased BMD with higher BMI 6.

scholarly journals Effects of 1-year anti-TNF-α therapies on bone mineral density and bone biomarkers in rheumatoid arthritis and ankylosing spondylitis

2019 ◽  
Vol 39 (1) ◽  
pp. 167-175 ◽  
Author(s):  
Katalin Gulyás ◽  
Ágnes Horváth ◽  
Edit Végh ◽  
Anita Pusztai ◽  
Ágnes Szentpétery ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Bone Mineral Density ◽  
Ankylosing Spondylitis ◽  
Bone Loss ◽  
Bone Mineral ◽  
Certolizumab Pegol ◽  
Joint Destruction ◽  
Type I ◽  
Mineral Density ◽  
Tnf Α

Abstract Objectives Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) have been associated with generalized and localized bone loss. We conducted a comprehensive study using imaging (dual-energy X-ray absorptiometry, DXA) and laboratory biomarkers in order to determine bone health and to study the effects of anti-tumor necrosis factor (TNF) biologics in RA and AS. Patients and methods Thirty-six RA and 17 AS patients undergoing 1-year etanercept (ETN) or certolizumab-pegol (CZP) therapy were studied. Bone density was assessed by DXA at baseline and after 12 months. Serum C-reactive protein (CRP), calcium, phosphate, parathyroid hormone (PTH), vitamin D3, osteocalcin, procollagen type I N-propeptide (P1NP), C-terminal telopeptide (βCTX), osteoprotegerin, sclerostin (SOST), Dickkopf-1 (DKK-1), soluble receptor activator nuclear kappa B ligand (sRANKL), and cathepsin K (cathK) levels were determined at baseline and after 6 and 12 months. Results TNF-α inhibition was clinically effective. Anti-TNF-α halted further bone loss over 1 year. In general, anti-TNF therapy significantly increased P1NP, SOST levels, and the P1NP/βCTX ratios, while decreased DKK-1 and CathK production at different time points in most patient subsets. In the full cohort and in RA, baseline and/or 12-month bone mineral density (BMD) at multiple sites exerted inverse relationships with CRP and βCTX, and positive correlation with SOST. In AS, L2-4 BMD after 1-year biologic therapy inversely correlated with baseline βCTX, while femoral neck BMD rather showed inverse correlations with CRP. Conclusions Anti-TNF therapy slowed down generalized bone loss, in association with clinical improvements, in both diseases. TNF blockade may enhance bone formation and suppress joint destruction. Anti-TNF therapy may act inversely on DKK-1 and SOST. Independent predictors of BMD were SOST and βCTX in RA, whilst CRP in AS.Key Points• One-year anti-TNF therapy halted generalized bone loss in association with clinical improvement in arthritides.• Anti-TNF therapy may inversely act on DKK-1 and SOST.• Independent predictors of BMD were SOST and βCTX in RA, while CRP in AS.

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