J Obes Metab Syndr 2025; 34(1): 41-53
Published online January 30, 2025 https://doi.org/10.7570/jomes24009
Copyright © Korean Society for the Study of Obesity.
Myung Jin Kim1,2, Seonok Kim3, Han Na Jung4, Chang Hee Jung1,2, Woo Je Lee1,2, Yun Kyung Cho1,2,*
1Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul; 2Asan Diabetes Center, Asan Medical Center, Seoul; 3Department of Clinical Epidemiology and Biostatistics, Asan Medical Center, University of Ulsan College of Medicine, Seoul; 4Division of Endocrinology and Metabolism, Department of Internal Medicine, Hallym University Sacred Heart Hospital, Anyang, Korea
Correspondence to:
Yun Kyung Cho
https://orcid.org/0000-0002-4089-1376
Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul 05505, Korea
Tel: +82-2-3010-3241
Fax: +82-2-2045-4034
E-mail: yukycyk@gmail.com
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Background: Although an appropriate weight management strategy is essential for obese individuals, weight loss can have adverse effects on bone mineral density (BMD). We conducted a systematic review of randomized controlled trials to evaluate changes in BMD after the implementation of various weight loss strategies.
Methods: The PubMed, Embase, Web of Science, and Cochrane Library databases were searched to find articles published from database inception until June 2023. Randomized controlled trials of various treatments for obese patients that reported changes in BMD were selected. The primary outcome was BMD of the whole body, lumbar spine, and total hip, measured using dual X-ray absorptiometry.
Results: Eighteen randomized controlled trials involving 2,510 participants with obesity were included in the analysis. At follow-up examination, the BMD of the lumbar spine decreased significantly after metabolic surgery (mean difference [MD]=–0.40 g/cm2; 95% confidence interval [CI], –0.73 to –0.07; I2=0%); lifestyle and pharmacological interventions did not result in a significant decrease in BMD at any location. Metabolic surgery also produced the most substantial difference in weight, with an MD of –3.14 (95% CI, –3.82 to –2.47).
Conclusion: This meta-analysis is the first to examine the effects of all categories of anti-obesity strategies, including the use of anti-obesity medications, on BMD. Bariatric metabolic surgery can have adverse effects on BMD. Moreover, medications can be used as a treatment for weight loss without compromising bone quality.
Keywords: Obesity, Bone density, Bariatric surgery, Anti-obesity agents, Randomized controlled trial
The prevalence of overweight and obesity has exhibited a noteworthy increase in the past three decades, accounting for nearly one-third of the world’s population.1 Considering the established association between obesity and high cardiometabolic morbidity2 and mortality,3 a proper weight management strategy is essential for individuals with obesity. The mainstays of weight control in patients with obesity include lifestyle intervention, pharmacotherapy, and metabolic bariatric surgery.4 In the realm of anti-obesity pharmacotherapy, phentermine/topiramate, liraglutide, naltrexone/bupropion, and orlistat are currently approved in Korea.5 The newly developed glucagon-like peptide-1 receptor agonists (GLP-1 RAs), particularly semaglutide, have demonstrated notable effectiveness in promoting weight loss.6
From another perspective, obesity can confer a bone-protective effect through the favorable weight-bearing influence of high body mass on skeletal health.7,8 The Rancho Bernardo study, a large cross-sectional study, confirmed the relationship between weight loss and a decrease in bone mineral density (BMD).9 Significant reductions in BMD at the hip have been observed following various types of metabolic bariatric surgery,10,11 as well as after diet-induced weight loss,11-13 and they could partly be mitigated by adding exercise training.14 Among pharmaceutical interventions, the use of orlistat has shown a decline in forearm BMD from baseline, although the difference between orlistat and placebo was not significant.15
Interestingly, the current literature suggests that GLP-1 RAs do not negatively affect bone integrity beyond that of the associated weight loss. Studies of the GLP-1 RAs exenatide16-18 and liraglutide19 have demonstrated that BMD remains stable or increases in patients with type 2 diabetes mellitus (T2DM), despite weight reduction. If these latest anti-obesity drugs offer benefits in preserving BMD, they might emerge as a compelling weight loss approach. However, results of direct comparisons between novel pharmaceutical approaches and traditional weight loss methods remain inconclusive due to the absence of comprehensive comparative studies and the inconsistent outcomes of previous investigations.
Therefore, we conducted a systematic review of previous studies to elucidate the changes in BMD associated with calorie restriction, exercise, use of anti-obesity medications, and metabolic surgery in obese patients. Ultimately, we aim to guide the selection of weight loss strategies that can actively promote skeletal health, which has been relatively overlooked.
This meta-analysis follows the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement.20 The population, intervention, comparison, and outcome model was used to search the literature. The PubMed, Embase, Web of Science, and Cochrane Library databases were searched for studies published from database inception to June 1, 2023. The search terms used are provided in the Supplementary Methods.
Randomized controlled trials (RCTs) of various treatments for obesity that reported changes in BMD were included in the analysis. By contrast, (1) case series, case reports, and retrospective studies; (2) systematic reviews and meta-analyses; (3) studies written in languages other than English; and (4) studies conducted in patients with underlying malignancies were excluded. Two researchers (MJK and YKC) independently assessed and identified all relevant publications to determine their eligibility. Disagreements regarding eligibility were resolved through consensus.
The primary outcome was the difference in the BMD of the whole body, lumbar spine, and total hip, measured using dual X-ray absorptiometry before and after each anti-obesity treatment. The secondary outcomes were differences in body weight (kg) and the levels of bone turnover markers: osteocalcin, bone-specific alkaline phosphatase (ALP), C-telopeptide, and procollagen type 1 N-terminal propeptide (P1NP).
Two authors (MJK and YKC) independently extracted the data from each study using pre-standardized forms. The following data were collected: name of first author, publication year, country, follow-up duration, number and characteristics of participants, proportion of men, type of weight loss intervention, mean age, and baseline body mass index (BMI). As outcome measurements, information was obtained on changes in BMD, body weight, and bone turnover markers after each intervention. In multi-arm trials, each treatment arm and the control group were compared.
Two authors (MJK and YKC) assessed the quality of the included studies using the Joanna Briggs Institute critical appraisal checklist.21 RCTs that performed randomization, allocation concealment, blinding process, follow-up, comparison of similarities between two groups, reporting of outcome measures, and statistical analysis were included. Each criterion was assessed as having a low, moderate, or high risk of bias by using 13 question codes for RCTs. Supplementary Table 1 shows the risk of bias for all the included RCTs. Discrepancies in the quality assessment were resolved through discussion.
We collected data on the average changes in BMD, body weight, and bone turnover markers between the intervention and control groups. If the standard deviation of the change was not reported, the difference between values was determined assuming a 0.5 correlation between two time points.22 Subsequently, we computed the standardized mean difference (SMD) between the intervention and control groups for each study. Pooled estimates were generated by combining the SMDs from each study using a random-effects model. To assess heterogeneity among the included studies, the I2 statistic and Cochrane Q test were used.23 Based on the I2 cut-off values of 25%, 50%, and 75%, the level of heterogeneity was classified as low, moderate, and high, respectively.23 Heterogeneity between studies was identified when the Q statistic had a P-value of less than 0.1.23 Publication bias was assessed using funnel plots and Egger’s tests. All statistical analyses were carried out using the ‘meta’ package in R statistical software version 4.2.2 (R Foundation for Statistical Computing).
Of the initial 649 citations identified in our literature search, 18 were deemed appropriate for inclusion in our meta-analysis (Fig. 1). During the full-text review, studies were excluded if they did not provide complete articles; included additional interventions alongside weight loss programs, such as different doses of calcium supplements or high-protein meals; or presented only baseline or post-intervention data. In addition, studies related to bariatric surgery were excluded if they compared different surgical procedures without including a control group. The study by Gadde et al.24 generally satisfied the other conditions, but it was excluded because of the absence of BMD results for the placebo group.
In the study conducted by Maghrabi et al.,25 the intensive medical therapy group was categorized as the control group because calorie restriction was not implemented for therapeutic purposes in that context. With regard to the surgical outcomes in Maghrabi et al.’s study,25 the results of the 12-month tests were selected among the multiple follow-up examinations because that aligned with the other bariatric surgery studies. Moreover, the median value between sleeve gastrectomy (SG) and Roux-en-Y gastric bypass was chosen as the representative value for analysis.25 Although Lipkin et al.26 reported separate results for men and women, we opted to examine the outcomes only in women because women were predominantly involved in the other studies. Finally, we analyzed the BMD of only the whole body, lumbar spine, and hip.
Table 1 provides an overview of the characteristics of the studies, which included 2,510 participants with obesity. These studies were categorized as follows: five studies explored the effects of calorie restriction;13,14,27-29 two examined the effects of exercise therapy;14,29 nine compared the effects of combining calorie restriction and exercise with calorie restriction alone28-33 or with no intervention;26,28,29,34,35 three assessed the outcomes of pharmacological treatments;15,36,37 and three evaluated the outcomes of bariatric surgery.25,38,39
Most of the studies were conducted in the United States,40 but some studies were performed in European countries,15,37 Southeast Asia,30,39 and Africa.32 Women were the predominant participants in all studies, with six of them exclusively enrolling women.13,27,30,32,35,36 The average age of the participants ranged from 30 to 50 years, except for the study conducted by Misra et al.,38 which included adolescents aged between 14 and 22 years. The baseline BMI of the participants ranged from 27.5 to 47.0 kg/m2. The follow-up intervals ranged from 3 months to 4 years. Three studies included patients with T2DM,25,26,39 one included patients with schizophrenia,37 one included lactating patients,35 and one included patients with osteoarthritis.33 Each study used a distinct protocol for calcium and vitamin D supplementation (Table 1).
Fig. 2 illustrates the changes in whole-body BMD among obese individuals who underwent a weight loss intervention. In general, no significant changes were observed in whole-body BMD compared with baseline, except for the studies conducted by Ricci et al.27 and Nakata et al.30 Ricci et al. reported a reduction in BMD following calorie restriction (mean difference [MD]=–1.01; 95% confidence interval [CI], –1.82 to –0.20). Alternatively, Nakata et al.30 observed an increase in BMD in the calorie restriction and exercise combination group compared with the calorie restriction alone group (MD=0.98; 95% CI, 0.27 to 1.68). In the analysis of calorie restriction plus exercise compared with calorie restriction alone, a subgroup analysis by country effectively reduced the heterogeneity, yielding an I2 value of 0% in both countries (Supplementary Fig. 1A).
Fig. 3 shows the variations in lumbar spine BMD according to the different weight loss treatments tested. Obese patients who underwent metabolic surgery experienced a significant decrease in lumbar spine BMD (MD=–0.40 g/cm2; 95% CI, –0.73 to –0.07). Conversely, pharmacological interventions did not result in a significant change from baseline, compared with the control (MD=0.04 g/cm2; 95% CI, –0.44 to 0.51). Calorie restriction, exercise, and a combination of calorie restriction and exercise had neutral effects on lumbar BMD. The high heterogeneity observed in the analysis of calorie restriction plus exercise compared with calorie restriction alone was mitigated following a subgroup analysis by country (Supplementary Fig. 1B). When we conducted a subgroup analysis based on the type of surgery, there was a noticeable difference in the degree of decline in lumbar spine BMD depending on the type of surgery, with the SG group showing the greatest decrease in BMD (Supplementary Fig. 2)
As demonstrated in Fig. 4, total hip BMD decreased in individuals who underwent metabolic bariatric surgery (MD=–1.31 g/cm2; 95% CI, –2.63 to 0.01), but the change was not considered significant. By contrast, patients treated with anti-obesity medications did not exhibit a significant decline in total hip BMD compared with the control group, with an MD of –0.08 (95% CI, –0.53 to 0.37). Calorie restriction and the combination of calorie restriction and exercise had no effects on total hip BMD. After a subgroup analysis by country, the heterogeneity observed in the analysis of calorie restriction plus exercise compared with calorie restriction alone improved (Supplementary Fig. 1C). The considerable heterogeneity observed in the analysis of metabolic bariatric surgery could be attributed to the significant decline in BMD observed in the study of Maghrabi et al.25
Overall, all the tested weight loss methods resulted in a reduction in body weight compared with controls, with significant differences observed in the calorie restriction, calorie restriction plus exercise, and metabolic surgery groups (Supplementary Fig. 3). Metabolic surgery exhibited the most substantial difference, with an MD of –3.14 (95% CI, –3.82 to –2.47). The I2 statistic and Cochrane Q test indicated high heterogeneity in the studies on calorie restriction and calorie restriction plus exercise. A subgroup analysis based on study duration (24 weeks vs. 52 weeks) in the calorie restriction groups effectively reduced the heterogeneity, with I2 decreasing from 76% to 0% (Supplementary Fig. 4). However, subgroup analyses of the calorie restriction and exercise groups, considering study duration, age group, men percentage, and baseline body weight, did not reduce heterogeneity (data not shown).
Serum osteocalcin levels significantly increased in studies involving calorie restriction, with an MD of 0.46 (95% CI, 0.09 to 0.82), but no significant changes were observed in the anti-obesity medication groups (Supplementary Fig. 5A). The bone-specific ALP levels in the calorie restriction and medication groups remained unchanged (Supplementary Fig. 5B). Anti-obesity medications did not lead to significant changes in the C-telopeptide and P1NP levels (Supplementary Fig. 5C and D).
Supplementary Table 1 provides a detailed assessment of the quality of all included studies. All of the studies except that conducted by Tangalakis et al.39 exhibited a low-to-moderate risk of bias. Supplementary Figs. 6-8 show funnel plots of the primary outcome analysis results based on the area where BMD was measured. No funnel plot is displayed when the analysis included only two studies because the evaluation of publication bias was challenging in such cases. Overall, the likelihood of publication bias was low, with some variations observed between groups.
We performed a meta-analysis of RCTs conducted among obese patients to comprehensively evaluate and compare the effects of various obesity treatment methods on BMD. Metabolic bariatric surgery led to a significant reduction in the BMD of the lumbar spine. Conversely, other lifestyle and pharmacological interventions did not significantly decrease the BMD in any location. In studies involving calorie restriction, no significant alterations were observed in bone turnover markers, except for an increase in osteocalcin levels.
Adverse skeletal consequences after weight loss have been widely studied, and conflicting findings have been reported depending on the weight loss method used and the specific anatomical site of BMD measurement. Several meta-analyses and review articles available up to 2021 suggest a consistent reduction in hip BMD after diet-induced weight loss and metabolic surgery.11,12,40 The evidence regarding changes in lumbar spine BMD remains less conclusive.12 Exercise-induced weight loss appears to have a neutral effect on overall BMD40 and might mitigate the potential adverse effects of calorie restriction on bone density.12 Notably, none of the previous reviews included anti-obesity pharmaceuticals in their analyses. The results of our study generally agree with those of the previous meta-analyses, though some differences are notable. When we conducted a pooled analysis of the entire group to evaluate changes in BMD irrespective of the specific weight loss approach used, we discovered that weight loss had no significant effect on BMD at any anatomical site (whole body, lumbar spine, and hip) (Supplementary Fig. 9). When considered by weight loss strategy, no significant reduction in BMD was found following diet-induced weight loss, whereas metabolic surgery revealed a significant decrease in lumbar spine BMD. A decreasing trend in hip BMD was observed after metabolic surgery, but the change was not significant.
The mechanism by which BMD decreases with weight loss is multifactorial. The primary factor is likely the reduction in mechanical loading on bone as a consequence of weight loss.41 That process triggers the release of sclerostin by osteocytes, a protein that blocks bone formation.42 Combining calorie restriction with aerobic or resistance training prevented the rise in sclerostin levels. This observation supports sclerostin’s involvement in the effects of mechanical unloading on bone.43 Another potential factor contributing to the reduction in BMD could be diminished dietary intake or problems related to nutrient absorption.12,44 However, we did not assess the effects of supplementation because the protocols for vitamin D and calcium supplementation varied across the studies included in our analysis. Therefore, further research is warranted to provide greater clarity on this matter.
To the best of our knowledge, this systematic review is the first to examine the effects of pharmacological interventions on BMD. Although no studies have yet examined how the recently developed GLP-1 RAs semaglutide and tirzepatide affect BMD, our results suggest that liraglutide and exenatide, in addition to orlistat, can induce weight loss without adversely affecting BMD. However, the reduction in body weight was not considered significant in any of the included studies testing anti-obesity medications,15,36 which might have weakened their effects on BMD. As mentioned in the study by Gotfredsen et al.,15 the difference in the amount of weight loss between the study groups decreased from 4.2 to 3.1 kg after the extraction of a sub-cohort with BMD data from the original trial. If the entire population had been targeted, the results might have been different. In the study by Iepsen et al.,36 the control group underwent a thorough dietary intervention, which might explain why the difference in body weight between the two groups was not significant.
The exact mechanism through which GLP-1 RAs protect bone quality remains unclear, but they might influence the rate of bone turnover45 or reduce bone resorption.46 Those effects could be due to their inhibition of osteoclast production,47 through their influence on the osteoprotegerin (OPG)/receptor activator of nuclear factor κB (RANK) signaling system.48 In that system, receptor activator of nuclear factor κB ligand (RANKL) binds to RANK receptors on osteoclast progenitor cells, leading to their differentiation and activation.48,49 Previous animal studies have shown that treatment with GLP-1 RAs increases the expression of OPG genes,50 which hinders the activation of RANK and thereby hinders osteoclast differentiation.51 Additionally, GLP-1 RAs stimulate calcitonin release, which indirectly inhibits bone resorption.52 However, those findings were primarily observed in animal studies and might not directly apply to humans; clinical data in this regard are limited.
In the context of non-pharmacological interventions, the combination of exercise and calorie restriction tended to slightly increase BMD, compared with calorie restriction alone, although the increase was not significant. When comparing the effects of calorie restriction plus exercise with those of calorie restriction alone, our data showed significant heterogeneity. A subgroup analysis based on country of origin was performed to address that variability (Supplementary Fig. 1). Studies conducted in the United States generally yielded consistent results. Meanwhile, the studies conducted by Nakata et al.30 in Japan and Hosny et al.32 in Egypt demonstrated a more pronounced effect of exercise combined with calorie restriction, despite the absence of significant differences from the studies conducted in the United States in participant characteristics, follow-up duration, dietary interventions, exercise protocols, and calcium/vitamin D supplementation. This observation highlights the need for future analyses that involve more RCTs to explore the potential influence of race on outcomes from combining exercise with calorie restriction.
This study has several limitations. First, the included studies exhibited heterogeneity in various aspects, including country, follow-up interval, sex ratio, underlying disease, and other baseline characteristics. To address this concern, we used random-effects models for our pooled estimates and conducted subgroup analyses. Second, our exclusion of retrospective studies limited the number of included studies, particularly those that used medication and bariatric surgery. Nevertheless, the comparison between treatment groups and a control group inherent in RCTs is the most reliable method. Third, due to the limited number of articles, publication bias was relatively high in some groups, indicating the need for larger-scale prospective studies. Fourth, BMD results measured from certain sites (e.g., the radius and femoral neck) were excluded due to the limited study availability. Consequently, our findings might have been affected by data exclusion and insufficient information. Fifth, although we estimated the changes in BMD following each intervention, the risk of clinical fracture was not assessed.
Despite those limitations, this meta-analysis is the first to examine all categories of anti-obesity strategies (lifestyle interventions, anti-obesity medications, and bariatric surgery) to determine their effects on BMD. Our findings highlight the substantial influence of metabolic surgery on weight loss and its potential adverse effects on BMD, particularly in the lumbar spine, compared with non-surgical interventions. The absence of a significant BMD reduction following the application of pharmaceutical interventions indicates their potential as a strategy for effective weight loss that does not compromise bone health. However, prospective studies conducted in more controlled settings are needed to validate our observations.
Supplementary materials can be found online at https://doi.org/10.7570/jomes24009.
Chang Hee Jung is an associate editor of the journal. But he was not involved in the peer reviewer selection, evaluation, or decision process of this article. No other potential conflicts of interest relevant to this article were reported.
This study was supported by a 2022 JOMES Research Grant (Grant No. KSSO-J-2023002) from the Korean Society for the Study of Obesity.
Study concept and design: YKC; acquisition of data: MJK; analysis and interpretation of data: MJK, SK, HNJ, and YKC; drafting of the manuscript: MJK; critical revision of the manuscript: CHJ, WJL, and YKC; statistical analysis: SK; obtained funding: YKC; administrative, technical, or material support: YKC; and study supervision: YKC.
Characteristics of the included studies
Author (year) | Country | Study participants | Number | Men (%) | F/U | Intervention; control | Baseline data | Calcium and vitamin D supplements | |
---|---|---|---|---|---|---|---|---|---|
Age (yr)* | BMI (kg/m2) | ||||||||
Chao et al. (2000)13 | USA | Overweight women | 67 | 0 | 12 mo | Calorie restriction (n = 27); No intervention (n = 40) | 65.9 ± 5.0 | 30.9 ± 2.9† | Calcium supplements were allowed. |
Gotfredsen et al. (2001)15 | Denmark | Obese men and women older than 18 years | 30 | 13 | 12 mo | Orlistat (n = 16); Placebo (n = 14) | 41.0 ± 11.0 | 36.9 ± 3.7 | Not described |
Ricci et al. (2001)27 | USA | Postmenopausal obese women | 27 | 0 | 25 wk | Calorie restriction (n = 14); No intervention (n = 13) | 55.9 ± 7.9 | 33.0 ± 3.8 | Vitamin and mineral supplements were not permitted. |
Villareal et al. (2006)14 | USA | Healthy men and postmenopausal women | 48 | 37.5 | 12 mo | Calorie restriction (n = 19); Exercise (n = 19); No intervention (n = 10) | 57.0 ± 3.0 | 27.3 ± 2.0 | All participants were given 162 mg/day of calcium and 400 IU/day of cholecalciferol. |
Redman et al. (2008)28 | USA | Overweight men and premenopausal women | 46 | 43.4 | 24 wk | Calorie restriction (n = 24); Calorie restriction+exercise (n = 12); Low-calorie diet+weight maintenance (n = 12); No intervention (n = 11) | 37.0 ± 2.0 | 27.3 ± 0.5 | Vitamin supplements were not permitted. |
Nakata et al. (2008)30 | Japan | Overweight women | 35 | 0 | 14 wk | Calorie restriction+exercise (n = 17); Calorie restriction (n = 10) | 40.3 ± 6.5 | 27.4 ± 2.5 | Vitamins and calcium were supplemented by a balanced food product. |
Villareal et al. (2008)34 | USA | Obese men and women over the age 65 | 27 | 33.3 | 52 wk | Calorie restriction+exercise (n = 17); No intervention (n = 10) | 71.1 ± 5.1 | 39.0 ± 5.0 | Subjects were given a daily multivitamin supplement and were counseled to consume adequate dietary calcium and vitamin D (1,200–1,500 mg/day of calcium and 1,000 IU/day of vitamin D). |
Shah et al. (2011)29 | USA | Obese men and women older than 65 years | 107 | 37.4 | 52 wk | Calorie restriction (n = 26); Exercise (n = 26); Calorie restriction+exercise (n = 28); No intervention (n = 27) | 69.0 ± 4.0 | 37.3 ± 4.7 | All subjects were given supplements to ensure an intake of 1,500 mg/day of calcium and 1,000 IU/day of vitamin D. |
Colleran et al. (2012)35 | USA | Lactating women | 27 | 0 | 16 wk | Calorie restriction+exercise (n = 14); No intervention (n = 13) | 30.3 ± 3.8 | 28.0 ± 3.3 | All participants were provided with a multivitamin supplement. |
Hosny et al. (2012)32 | Egypt | Premenopausal obese women | 40 | 0 | 3 mo | Calorie restriction+exercise (n = 20); Calorie restriction (n = 20) | 35.2 ± 2.9 | 32.9 ± 1.4 | Not described |
Lipkin et al. (2014)26 | USA | Obese men and women with T2DM | 1,309 | 37.5 | 4 yr | Calorie restriction+exercise (women) (n = 415); No intervention (women) (n = 403) | 57.8 ± 6.4 | 36.3 ± 5.5 | No supplements were used. |
Beavers et al. (2014)33 | USA | Obese men and women with knee OA | 454 | 53.9 | 18 mo | Calorie restriction (n = 152); Calorie restriction+exercise (n = 152); Exercise (n = 150) | 66.0 ± 6.2 | 33.4 ± 3.7 | Calcium and vitamin D supplementation were allowed. |
Iepsen et al. (2015)36 | USA | Overweight women | 37 | 0 | 52 wk | Liraglutide (n = 18); Control (n = 19) | 46.0 ± 2.0 | 34.4 ± 0.5 | Not described |
Maghrabi et al. (2015)25 | USA | Obese men and women with T2DM | 54 | 41.7 | 2 yr | RYGB (n = 18); SG (n = 19); Control (n = 17) | 48.0 ± 4.0 | 36.0 ± 1.0 | Calcium and vitamin D supplementation were recommended as per clinical practice guidelines. |
Weiss et al. (2017)31 | USA | Overweight men and postmenopausal women | 52 | 25 | 14 wk | Calorie restriction (n = 17); Exercise (n = 16); Calorie restriction+exercise (n = 19) | 57.0 ± 5.0 | 27.7±1.7 | Calcium and vitamin D supplementation were allowed. |
Eriksson et al. (2018)37 | Denmark | Obese men and women with schizophrenia | 45 | 46.7 | 3 mo | Exenatide (n = 23); Placebo (n = 22) | 34.5 ± 10.1 | 38.4 ± 6.1 | Not described |
Misra et al. (2020)38 | USA | Obese men and women age 14–22 years | 44 | 27.2 | 12 mo | SG (n = 22); Control (n = 22) | 17.0 ± 0.5 | 42.4 ± 1.3 | Not described |
Tangalakis et al. (2020)39 | USA | Obese men and women with T2DM | 61 | 32.8 | 12 mo | RYGB (n = 30); Control (n = 31) | 47.4 ± 1.5 | 40.1 ± 0.9 | Not described |
Values are presented as mean ± standard deviation unless otherwise specified.
*The data are expressed in pounds and converted using a rate of 1 lb=0.454 kg; †If data from the entire cohort were not specified, baseline data from the control group are presented.
F/U, follow-up; BMI, body mass index; T2DM, type 2 diabetes mellitus; OA, osteoarthritis; RYGB, Roux-en-Y gastric bypass; SG, sleeve gastrectomy.
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