Bone mass loss after sleeve gastrectomy: A prospective comparative study with gastric bypass

Bone mass loss (osteoporosis) seen in postmenopausal women is an adverse factor for implant denture. Using an ovariectomized rat model, we studied the mechanism of estrogen-deficiency-caused bone loss and the therapeutic effect of Zoledronic acid. We observed that ovariectomized-caused resorption of bone tissue in the mandible was evident at four weeks and had not fully recovered by 12 weeks post-ovariectomized compared with the sham-operated controls. Further evaluation with a TUNEL assay showed ovariectomized enhanced apoptosis of osteoblasts but inhibited apoptosis of osteoclasts in the mandible. Zoledronic acid given subcutaneously as a single low dose was shown to counteract both of these ovariectomized effects. Immunohistochemical staining showed that ovariectomized induced the protein levels of RANKL and the 65-kD subunit of the NF-κB complex mainly in osteoclasts, as confirmed by staining for TRAP, a marker for osteoclasts, whereas zoledronic acid inhibited these inductions. Western blotting showed that the levels of RANKL, p65, as well as the phosphorylated form of p65, and IκB-α were all higher in the ovariectomized group than in the sham and ovariectomized + zoledronic acid groups at both the 4th- and 12th-week time points in the mandible. These data collectively suggest that ovariectomized causes bone mass loss by enhancing apoptosis of osteoblasts and inhibiting apoptosis of osteoclasts. In osteoclasts, these cellular effects may be achieved by activating RANKL-NF-κB signalling. Moreover, zoledronic acid elicits its therapeutic effects in the mandible by counteracting these cellular and molecular consequences of ovariectomized.

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Ipriflavone effect on prevention and treatment of postmenopausal bone mass loss. Relation to estrogen replacement therapy

Osteoporosis International ◽

10.1007/bf02500477 ◽

1996 ◽

Vol 6 (S1) ◽

pp. 235-235

Author(s):

M. R. Ulla ◽

R. Díaz

Keyword(s):

Bone Mass ◽

Mass Loss ◽

Replacement Therapy ◽

Estrogen Replacement Therapy ◽

Estrogen Replacement ◽

Bone Mass Loss ◽

Prevention And Treatment

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HORMONE REPLACEMENT THERAPY AND CALCITONIN IN WOMEN WITH BONE MASS LOSS

Bone ◽

10.1016/j.bone.2010.01.035 ◽

2010 ◽

Vol 46 ◽

pp. S20

Author(s):

Antonio Bazarra-Fernandez

Keyword(s):

Hormone Replacement Therapy ◽

Bone Mass ◽

Mass Loss ◽

Replacement Therapy ◽

Hormone Replacement ◽

Bone Mass Loss

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Long-Term Effects of Laparoscopic Sleeve Gastrectomy and Roux-en-Y Gastric Bypass on Body Composition and Bone Mass Density

Obesity Facts ◽

10.1159/000512450 ◽

2020 ◽

pp. 1-10

Author(s):

Julian Bühler ◽

Silvan Rast ◽

Christoph Beglinger ◽

Ralph Peterli ◽

Thomas Peters ◽

...

Keyword(s):

Vitamin D ◽

Gastric Bypass ◽

Body Composition ◽

Sleeve Gastrectomy ◽

Bone Mass ◽

Laparoscopic Sleeve Gastrectomy ◽

Mass Density ◽

Bone Mass Density

Background: Currently, the two most common bariatric procedures are laparoscopic sleeve gastrectomy (LSG) and laparoscopic Roux-en-Y gastric bypass (LRYGB). Long-term data comparing the two interventions in terms of their effect on body composition and bone mass density (BMD) are scarce. Objective: The aim of this study was to assess body composition and BMD at least 5 years after LSG and LRYGB. Setting: Department of Endocrinology and Nutrition, St. Claraspital Basel and St. Clara Research Ltd., Basel, Switzerland. Methods:Bariatric patients at least 5 years after surgery (LSG or LRYGB) were recruited, and body composition and BMD were measured by means of dual-energy X-ray absorptiometry. Data from body composition before surgery were included in the analysis. Blood samples were taken for determination of plasma calcium, parathyroid hormone, vitamin D3, alkaline phosphatase, and C-terminal telopeptide, and the individual risk for osteoporotic fracture assessed by the Fracture Risk Assessment Tool score was calculated. After surgery, all patients received multivitamins, vitamin D3, and zinc. In addition, LRYGB patients were prescribed calcium. Results: A total of 142 patients were included, 72 LSG and 70 LRYGB, before surgery: median body mass index 43.1, median age 45.5 years, 62.7% females. Follow-up after a median of 6.7 years. For LRYGB, the percentage total weight loss at follow-up was 26.3% and for LSG 24.1% (p = 0.243). LRYGB led to a slightly lower fat percentage in body composition. At follow-up, 45% of both groups had a T score at the femoral neck below –1, indicating osteopenia. No clinically relevant difference in BMD was found between the groups. Conclusions:At 6.7 years after surgery, no difference in body composition and BMD between LRYGB and LSG was found. Deficiencies and bone loss remain an issue after both interventions and should be monitored.

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The Short-Term Renal Effects of Bariatric Surgery: A Comparative Study Between Sleeve Gastrectomy and One Anastomosis Gastric Bypass Operations Among Egyptian Patients With Severe Obesity

Obesity Surgery ◽

10.1007/s11695-020-04841-5 ◽

2020 ◽

Vol 30 (11) ◽

pp. 4494-4504

Author(s):

Amir I. Bassiony ◽

Alaa Sabry ◽

Osama Shiha ◽

Ahmed ElGeidie ◽

Mohammed K. Nassar

Keyword(s):

Bariatric Surgery ◽

Gastric Bypass ◽

Sleeve Gastrectomy ◽

Comparative Study ◽

Severe Obesity ◽

One Anastomosis Gastric Bypass ◽

Short Term ◽

Renal Effects ◽

Egyptian Patients

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Bromodomain Protein BRD4 Accelerates Glucocorticoid Dysregulation of Bone Mass and Marrow Adiposis by Modulating H3K9 and Foxp1

Cells ◽

10.3390/cells9061500 ◽

2020 ◽

Vol 9 (6) ◽

pp. 1500

Author(s):

Feng-Sheng Wang ◽

Yu-Shan Chen ◽

Jih-Yang Ko ◽

Chung-Wen Kuo ◽

Huei-Jing Ke ◽

...

Keyword(s):

Bone Mass ◽

Mass Loss ◽

Osteogenic Differentiation ◽

Progenitor Cells ◽

Mesenchymal Progenitor Cells ◽

Marrow Fat ◽

Bone Mass Loss ◽

Brd4 Inhibition ◽

The Cost

Glucocorticoid provokes bone mass loss and fatty marrow, accelerating osteoporosis development. Bromodomain protein BRD4, an acetyl–histone-binding chromatin reader, regulates stem cell and tissue homeostasis. We uncovered that glucocorticoid inhibited acetyl Lys-9 at the histone 3 (H3K9ac)-binding Runx2 promoter and decreased osteogenic differentiation, whereas bromodomain protein 4 (BRD4) and adipocyte formation were upregulated in bone-marrow mesenchymal progenitor cells. BRD4 knockdown improved H3K9ac occupation at the Runx2 promoter and osteogenesis, but attenuated glucocorticoid-mediated adipocyte formation together with the unaffected H3K9ac-binding PPARγ2 promoter. BRD4 regulated epigenome related to fatty acid metabolism and the forkhead box P1 (Foxp1) pathway, which occupied the PPARγ2 promoter to modulate glucocorticoid-induced adipocytic activity. In vivo, BRD4 inhibitor JQ-1 treatment mitigated methylprednisolone-induced suppression of bone mass, trabecular microstructure, mineral acquisition, and osteogenic differentiation. Foxp1 signaling, marrow fat, and adipocyte formation in glucocorticoid-treated skeleton were reversed upon JQ-1 treatment. Taken together, glucocorticoid-induced H3K9 hypoacetylation augmented BRD4 action to Foxp1, which steered mesenchymal progenitor cells toward adipocytes at the cost of osteogenic differentiation in osteoporotic skeletons. BRD4 inhibition slowed bone mass loss and marrow adiposity. Collective investigations convey a new epigenetic insight into acetyl histone reader BRD4 control of osteogenesis and adipogenesis in skeleton, and highlight the remedial effects of the BRD4 inhibitor on glucocorticoid-induced osteoporosis.

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