Regulation of Bone Mineral Density in Morbidly Obese Women: A Cross-sectional Study in Two Cohorts Before and After Bypass Surgery

Gómez, José Manuel; Vilarrasa, Núria; Masdevall, Carlos; Pujol, Jordi; Solano, Esther; Soler, Juan; Elío, Iñaki; Gallart, L.; Vendrell, Joan

doi:10.1007/s11695-008-9529-4

Cited by 37 publications

(43 citation statements)

References 33 publications

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“…Several studies have shown that obesity could increase bone density (Harris et al 1992, Albala et al 1996, Vandewalle et al 2013; however, other studies have found that obesity has either no effect on bone density (Greco et al 2010) or increases bone porosity (Rosen & Bouxsein 2006, Zhao et al 2008, Gó mez et al 2009). The present study, also, found that obese and insulin resistant rats had a decreased Gla/Glu-osteocalcin ratio, decreased osteoblastic proliferation, increased osteoblastic apoptosis, osteoblastic insulin resistance and increased bone porosity.…”

Section: Discussionmentioning

confidence: 99%

Obesity does not aggravate osteoporosis or osteoblastic insulin resistance in orchiectomized rats

Potikanond¹,

Rattanachote²,

Pintana³

et al. 2016

Journal of Endocrinology

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The present study aimed to test the hypothesis that testosterone deprivation impairs osteoblastic insulin signaling, decreases osteoblast survival, reduces bone density, and that obesity aggravates those deleterious effects in testosterone-deprived rats. Twenty four male Wistar rats underwent either a bilateral orchiectomy (O, nZ12) or a sham operation (S, nZ12). Then the rats in each group were further divided into two subgroups fed with either a normal diet (ND) or a high-fat diet (HF) for 12 weeks. At the end of the protocol, blood samples were collected to determine metabolic parameters and osteocalcin ratios. The tibiae were collected to determine bone mass using microcomputed tomography and for osteoblast isolation. The results showed that rats fed with HF (sham-operated HF-fed rats (HFS) and ORX HF-fed rats (HFO)) developed peripheral insulin resistance and had decreased trabecular bone density. In ND-fed rats, only the ORX ND-fed rats (NDO) group had decreased trabecular bone density. In addition, osteoblastic insulin resistance, as indicated by a decrease in tyrosine phosphorylation of the insulin receptor and Akt, were observed in all groups except the sham-operated ND-fed rats (NDS) rats. Those groups, again with the exception of the NDS rats, also had decreased osteoblastic survival. No differences in the levels of osteoblastic insulin resistance and osteoblastic survival were found among the NDO, HFS, and HFO groups. These findings suggest that either testosterone deprivation or obesity alone can impair osteoblastic insulin signaling and decrease osteoblastic survival leading to the development of osteoporosis. However, obesity does not aggravate those deleterious effects in the bone of testosterone-deprived rats.

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Section: Discussionmentioning

confidence: 99%

Obesity does not aggravate osteoporosis or osteoblastic insulin resistance in orchiectomized rats

Potikanond¹,

Rattanachote²,

Pintana³

et al. 2016

Journal of Endocrinology

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“…There is evidence of an inverse relationship between BMI and osteoclast activity in normal postmenopausal women [3] and of an increase in bone resorption following weight loss [4]. A number of mechanisms for this fat-bone relationship have been described and include the effect of soft tissue mass on skeletal loading [5], the association of fat mass with the secretion of active hormones from the pancreatic beta cells such as insulin [6] and amylin [7] which directly stimulate osteoblast proliferation and the secretion of active hormones (estrogens, leptin, adiponectin, and resistin) from the adipocyte [8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Bone Mineral Density Loss in Morbidly Obese Women After Gastric Bypass: 3-Year Follow-Up

et al. 2010

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Studies that evaluate the influence of gastric bypass (RYGP) on bone mass are limited to short-term follow-up. We analysed changes in bone mineral density (BMD) three years after surgery and evaluated the main determinants of the development of bone disease. Prospective study of 59 morbidly obese white women aged 46 ± 8 years. BMD scanning using DEXA and plasma determinations of calcium, parathyroid hormone, 25-hydroxyvitamin D and insulin-like growth factor-I were made prior, at 12 months and 3 years after surgery. In the first postoperative year BMD decreased at femoral neck (FN) 10.2 % and in the lumbar spine (LS) 3.2 %, in the third year it additionally decreased 2.7 % and 3.1 %, respectively. BMD at both sites remained above the values of women of the same age. In the follow-up, 1.7 % developed osteoporosis at FN and 6.8 % at LS. Patients with bone disease were older, the percentage of women with menopause was greater in this group and had lower initial and final values of lean mass. The percentage of BMD loss at FN remained positively associated with the percentage of lean mass loss [β 0.304, p=0.045], and menopause [β 0.337, p=0.025]. Major osteoporotic fracture and hip fracture risk was low even in menopausal patients (3.1 % and 0.40 %, respectively). After RYGP menopausal women and those with greater lean mass loss are at higher risk of BMD loss but progression to osteoporosis is uncommon and the risk of fracture is low.

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“…The mechanisms involved are the increased production of estrogens by adipose tissue aromatase and the gravitational effect caused by increased body weight [5]. Moreover, recent evidence suggests the existence of an adipose tissuebone axis with the participation of hormonal factors such as leptin, adiponectin, and ghrelin in bone integrity [6][7][8]. On the other hand, a decrease in bone mineral content has been described in patients following very-low-calorie diets [9], and epidemiological data, from the population-based Framingham Osteoporosis Study, also revealed that weight loss is an independent risk factor for osteoporosis [10].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Bone Disease in Morbidly Obese Women After Gastric Bypass and Risk Factors Implicated in Bone Loss

et al. 2009

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Regulation of Bone Mineral Density in Morbidly Obese Women: A Cross-sectional Study in Two Cohorts Before and After Bypass Surgery

Abstract: The inverse correlation found between body fat and BMD in the first cohort indicates morbid obesity increases the risk of osteoporosis and we found a positive correlation with lean and fat mass before bariatric surgery and with lean mass after bypass surgery.

Cited by 37 publications

References 33 publications

Obesity does not aggravate osteoporosis or osteoblastic insulin resistance in orchiectomized rats

Obesity does not aggravate osteoporosis or osteoblastic insulin resistance in orchiectomized rats

Evaluation of Bone Mineral Density Loss in Morbidly Obese Women After Gastric Bypass: 3-Year Follow-Up

Evaluation of Bone Disease in Morbidly Obese Women After Gastric Bypass and Risk Factors Implicated in Bone Loss

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