Margaret A. Stefater-Richards, Courtney Panciotti, Valerie Esteva, Miriam Lerner, Carter R. Petty, William F. Gourash, Anita P. Courcoulas
Objective
We have previously shown that early intestinal adaptation precedes and relates to metabolic improvement in humans after Roux-en-Y gastric bypass surgery (RYGB). We hypothesized that intestinal adaptation would persist at the 1-year postoperative time point and that gene expression (GE) signatures would relate to type 2 diabetes remission, providing insight into potential mechanisms for intestinally mediated metabolic improvement after RYGB.
Methods
We determined GE by RNA sequencing in jejunum (Roux limb [RL]) collected from 28 patients before and 12 months after RYGB.
Results
Global GE from paired baseline and 1-year jejunal samples did not separate according to clinical phenotype (type 2 diabetes remission, sustained weight loss). In general, GE was consistent with persistent RL remodeling, and microvilli were elongated by 39%. Remodeling was not attenuated in patients with lack of diabetes remission or with weight regain. Patients with diabetes remission demonstrated greater jejunal activation of lipogenesis-related pathways driven by RXR, LXR, and SREBP.
Conclusions
RL adaptation is a key feature of RYGB in all patients, likely reflecting the dramatic alterations to gastrointestinal anatomy, but jejunal lipogenesis appears to be more strongly activated in those patients with diabetes remission. Further study is needed to understand whether these pathways may drive metabolic remission after RYGB.
{"title":"Gastric bypass elicits persistent gut adaptation and unique diabetes remission-related metabolic gene regulation","authors":"Margaret A. Stefater-Richards, Courtney Panciotti, Valerie Esteva, Miriam Lerner, Carter R. Petty, William F. Gourash, Anita P. Courcoulas","doi":"10.1002/oby.24135","DOIUrl":"10.1002/oby.24135","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>We have previously shown that early intestinal adaptation precedes and relates to metabolic improvement in humans after Roux-en-Y gastric bypass surgery (RYGB). We hypothesized that intestinal adaptation would persist at the 1-year postoperative time point and that gene expression (GE) signatures would relate to type 2 diabetes remission, providing insight into potential mechanisms for intestinally mediated metabolic improvement after RYGB.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We determined GE by RNA sequencing in jejunum (Roux limb [RL]) collected from 28 patients before and 12 months after RYGB.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Global GE from paired baseline and 1-year jejunal samples did not separate according to clinical phenotype (type 2 diabetes remission, sustained weight loss). In general, GE was consistent with persistent RL remodeling, and microvilli were elongated by 39%. Remodeling was not attenuated in patients with lack of diabetes remission or with weight regain. Patients with diabetes remission demonstrated greater jejunal activation of lipogenesis-related pathways driven by RXR, LXR, and SREBP.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>RL adaptation is a key feature of RYGB in all patients, likely reflecting the dramatic alterations to gastrointestinal anatomy, but jejunal lipogenesis appears to be more strongly activated in those patients with diabetes remission. Further study is needed to understand whether these pathways may drive metabolic remission after RYGB.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"32 11","pages":"2135-2148"},"PeriodicalIF":4.2,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11537825/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142484515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Obesity-associated insulin resistance (IR) is responsible for considerable morbidity and mortality globally. Despite vast genomic data, many areas, from pathogenesis to management, still have significant knowledge gaps. We aimed to characterize visceral adipose tissue (VAT) in obesity and IR through a multi-omics approach.
Methods
We procured data on VAT samples from the Gene Expression Omnibus (GEO) for the following two groups: 1) populations with obesity (n = 34) versus those without (n = 26); and 2) populations with obesity and IR (n = 15) versus those with obesity but without IR (n = 15). Gene set enrichment, protein-protein interaction network construction, hub gene identification, and drug-gene interactions were performed, followed by regulatory network prediction involving transcription factors (TFs) and microRNAs (miRNAs).
Results
Interleukin signaling pathways, cellular differentiation, and regulation of immune response revealed a significant cross talk between VAT and the immune system. Other findings include cancer pathways, neurotrophin signaling, and aging. A total of 10 hub genes, i.e., STAT1, KLF4, DUSP1, EGR1, FOS, JUN, IL2, IL6, MMP9, and FGF9, 24 TFs, and approved hub gene-targeting drugs were obtained. A total of 10 targeting miRNAs (e.g., hsa-miR-155-5p, hsa-miR-34a-5p) were associated with obesity and IR-related pathways.
Conclusions
Our multi-omics integration method revealed hub genes, TFs, and miRNAs that can be potential targets for investigation in VAT-related inflammatory processes and IR, therapeutic management, and risk stratifications.
{"title":"Decoding visceral adipose tissue molecular signatures in obesity and insulin resistance: a multi-omics approach","authors":"Dipayan Roy, Raghumoy Ghosh, Ritwik Ghosh, Manoj Khokhar, Ma Yin Yin Naing, Julián Benito-León","doi":"10.1002/oby.24146","DOIUrl":"10.1002/oby.24146","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Obesity-associated insulin resistance (IR) is responsible for considerable morbidity and mortality globally. Despite vast genomic data, many areas, from pathogenesis to management, still have significant knowledge gaps. We aimed to characterize visceral adipose tissue (VAT) in obesity and IR through a multi-omics approach.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We procured data on VAT samples from the Gene Expression Omnibus (GEO) for the following two groups: 1) populations with obesity (<i>n</i> = 34) versus those without (<i>n</i> = 26); and 2) populations with obesity and IR (<i>n</i> = 15) versus those with obesity but without IR (<i>n</i> = 15). Gene set enrichment, protein-protein interaction network construction, hub gene identification, and drug-gene interactions were performed, followed by regulatory network prediction involving transcription factors (TFs) and microRNAs (miRNAs).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Interleukin signaling pathways, cellular differentiation, and regulation of immune response revealed a significant cross talk between VAT and the immune system. Other findings include cancer pathways, neurotrophin signaling, and aging. A total of 10 hub genes, i.e., <i>STAT1</i>, <i>KLF4</i>, <i>DUSP1</i>, <i>EGR1</i>, <i>FOS</i>, <i>JUN</i>, <i>IL2</i>, <i>IL6</i>, <i>MMP9</i>, and <i>FGF9</i>, 24 TFs, and approved hub gene-targeting drugs were obtained. A total of 10 targeting miRNAs (e.g., hsa-miR-155-5p, hsa-miR-34a-5p) were associated with obesity and IR-related pathways.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our multi-omics integration method revealed hub genes, TFs, and miRNAs that can be potential targets for investigation in VAT-related inflammatory processes and IR, therapeutic management, and risk stratifications.</p>\u0000 \u0000 <div>\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"32 11","pages":"2149-2160"},"PeriodicalIF":4.2,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142484514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The neurobiological mechanisms underpinning binge eating disorder (BED) in children remain largely unclear, as the alterations that have been identified to date may be attributable to BED, obesity, or compound effects. This study aimed to delineate functional connectivity (FC) patterns in inhibitory control and reward networks in preadolescent children with and without BED from the Adolescent Brain Cognitive Development (ABCD) Study according to BMI.
Methods
Resting-state FC was examined in the inhibitory control network by using seeds in the dorsolateral prefrontal cortex, the anterior cingulate cortex, and the posterior cingulate cortex, whereas the reward network included seeds in the orbitofrontal cortex, nucleus accumbens, and amygdala. Seed-to-voxel analyses characterized FC differences between preadolescent children with BED with a high BMI and those with BED with a low BMI.
Results
We identified that BED was characterized by reduced connectivity between the reward network and regions in the default mode network, irrespective of weight status. Participants with BED also presented with hypoconnectivity in fronto-amygdalar circuits, which has been consistently associated with impaired emotion regulation capacity.
Conclusions
Our findings support that FC alterations between the reward network and the default mode network may be specifically impacted by the presence of BED as opposed to weight status.
{"title":"Distinct functional connectivity phenotypes in preadolescent children with binge eating disorder by BMI status","authors":"Trevor Steward, Kay Jann, Stuart B. Murray","doi":"10.1002/oby.24145","DOIUrl":"10.1002/oby.24145","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The neurobiological mechanisms underpinning binge eating disorder (BED) in children remain largely unclear, as the alterations that have been identified to date may be attributable to BED, obesity, or compound effects. This study aimed to delineate functional connectivity (FC) patterns in inhibitory control and reward networks in preadolescent children with and without BED from the Adolescent Brain Cognitive Development (ABCD) Study according to BMI.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Resting-state FC was examined in the inhibitory control network by using seeds in the dorsolateral prefrontal cortex, the anterior cingulate cortex, and the posterior cingulate cortex, whereas the reward network included seeds in the orbitofrontal cortex, nucleus accumbens, and amygdala. Seed-to-voxel analyses characterized FC differences between preadolescent children with BED with a high BMI and those with BED with a low BMI.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We identified that BED was characterized by reduced connectivity between the reward network and regions in the default mode network, irrespective of weight status. Participants with BED also presented with hypoconnectivity in fronto-amygdalar circuits, which has been consistently associated with impaired emotion regulation capacity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our findings support that FC alterations between the reward network and the default mode network may be specifically impacted by the presence of BED as opposed to weight status.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"32 11","pages":"2082-2086"},"PeriodicalIF":4.2,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142402499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gabriela de Souza Bett, Fabiana Schuelter-Trevisol, Daisson José Trevisol
{"title":"Response to “Nutritional considerations with antiobesity medications”","authors":"Gabriela de Souza Bett, Fabiana Schuelter-Trevisol, Daisson José Trevisol","doi":"10.1002/oby.24139","DOIUrl":"10.1002/oby.24139","url":null,"abstract":"","PeriodicalId":215,"journal":{"name":"Obesity","volume":"32 11","pages":"1981"},"PeriodicalIF":4.2,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142383078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zachary J. Ward, Roxanne Dupuis, Michael W. Long, Steven L. Gortmaker
Objective
The objective of this study is to estimate health-related quality of life (HRQoL) by continuous BMI by age, sex, and demographic group in the United States.
Methods
We estimated HRQoL (overall and by domain) by continuous BMI using SF-6D (Short-Form Six-Dimension) data from 182,778 respondents ages 18 years and older from the repeated cross-sectional Medical Expenditure Panel Survey (MEPS) 2008 to 2016. We adjusted for BMI self-report bias and for potential confounding between BMI and HRQoL.
Results
We found an inverse J-shaped curve of HRQoL by BMI, with lower values for female individuals and the highest health utilities occurring at BMI of 20.4 kg/m2 (95% CI: 20.32–20.48) for female individuals and 26.5 kg/m2 (95% CI: 26.45–26.55) for male individuals. By BMI category, excess weight contributed to HRQoL loss of 0.0349 for obesity overall, rising to 0.0724 for class III obesity. By domain, pain was the largest cause of HRQoL loss for obesity (26%), followed by role limitations (22%).
Conclusions
HRQoL is lower for people with excess body weight across a broad range of ages and BMI levels, especially at high levels of BMI, with pain being the largest driver of HRQoL loss. These findings highlight the importance of promoting a healthy weight for the entire population while also targeting efforts to prevent extreme weight gain over the life course.
{"title":"Association of continuous BMI with health-related quality of life in the United States by age and sex","authors":"Zachary J. Ward, Roxanne Dupuis, Michael W. Long, Steven L. Gortmaker","doi":"10.1002/oby.24141","DOIUrl":"10.1002/oby.24141","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The objective of this study is to estimate health-related quality of life (HRQoL) by continuous BMI by age, sex, and demographic group in the United States.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We estimated HRQoL (overall and by domain) by continuous BMI using SF-6D (Short-Form Six-Dimension) data from 182,778 respondents ages 18 years and older from the repeated cross-sectional Medical Expenditure Panel Survey (MEPS) 2008 to 2016. We adjusted for BMI self-report bias and for potential confounding between BMI and HRQoL.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We found an inverse J-shaped curve of HRQoL by BMI, with lower values for female individuals and the highest health utilities occurring at BMI of 20.4 kg/m<sup>2</sup> (95% CI: 20.32–20.48) for female individuals and 26.5 kg/m<sup>2</sup> (95% CI: 26.45–26.55) for male individuals. By BMI category, excess weight contributed to HRQoL loss of 0.0349 for obesity overall, rising to 0.0724 for class III obesity. By domain, pain was the largest cause of HRQoL loss for obesity (26%), followed by role limitations (22%).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>HRQoL is lower for people with excess body weight across a broad range of ages and BMI levels, especially at high levels of BMI, with pain being the largest driver of HRQoL loss. These findings highlight the importance of promoting a healthy weight for the entire population while also targeting efforts to prevent extreme weight gain over the life course.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"32 11","pages":"2198-2206"},"PeriodicalIF":4.2,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142383076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sofia Björkman, Gudrún Höskuldsdóttir, Karin Mossberg, Anna Laurenius, My Engström, Lars Fändriks, Björn Eliasson, Ola Wallengren, Ingrid Larsson
Objective
This study aimed to evaluate the effects of self-reported baseline eating behaviors on 24-month weight change in adults with severe obesity.
Methods
A prospective, nonrandomized clinical cohort study on surgical and medical obesity treatment included 971 adults (75% women) with a mean BMI of 42.0 (SD 4.9) kg/m2. To assess baseline eating behaviors and binge eating disorder, the Questionnaire on Eating and Weight Patterns-Revised and the Three-Factor Eating Questionnaire were used.
Results
In analyses adjusted for treatment, age, sex, baseline weight, and BMI, those with nocturnal eating lost less weight (3.5 kg [95% CI: 0.02–6.9]; p < 0.05) at 24 months compared to those without nocturnal eating. Binge eating disorder was not significantly associated with weight loss over 24 months. Emotional eating was associated with less weight loss at 12 months: 1.16 kg per z score (95% CI: 0.37–1.95; p < 0.05). Compared with completers, dropout from medical obesity treatment was associated with emotional and uncontrolled eating at baseline (both p < 0.001).
Conclusions
The association between pretreatment eating behaviors and weight change was found to be generalizable and not restricted to any specific treatment. Certain eating behaviors may affect weight loss as well as attrition. Identifying eating behaviors that may impair treatment efficacy are suggested in the treatment of severe obesity.
{"title":"Impact of eating behavior on 24-month weight change after treatment of severe obesity—A clinical prospective cohort study","authors":"Sofia Björkman, Gudrún Höskuldsdóttir, Karin Mossberg, Anna Laurenius, My Engström, Lars Fändriks, Björn Eliasson, Ola Wallengren, Ingrid Larsson","doi":"10.1002/oby.24131","DOIUrl":"10.1002/oby.24131","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study aimed to evaluate the effects of self-reported baseline eating behaviors on 24-month weight change in adults with severe obesity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A prospective, nonrandomized clinical cohort study on surgical and medical obesity treatment included 971 adults (75% women) with a mean BMI of 42.0 (SD 4.9) kg/m<sup>2</sup>. To assess baseline eating behaviors and binge eating disorder, the Questionnaire on Eating and Weight Patterns-Revised and the Three-Factor Eating Questionnaire were used.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In analyses adjusted for treatment, age, sex, baseline weight, and BMI, those with nocturnal eating lost less weight (3.5 kg [95% CI: 0.02–6.9]; <i>p</i> < 0.05) at 24 months compared to those without nocturnal eating. Binge eating disorder was not significantly associated with weight loss over 24 months. Emotional eating was associated with less weight loss at 12 months: 1.16 kg per <i>z</i> score (95% CI: 0.37–1.95; <i>p</i> < 0.05). Compared with completers, dropout from medical obesity treatment was associated with emotional and uncontrolled eating at baseline (both <i>p</i> < 0.001).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The association between pretreatment eating behaviors and weight change was found to be generalizable and not restricted to any specific treatment. Certain eating behaviors may affect weight loss as well as attrition. Identifying eating behaviors that may impair treatment efficacy are suggested in the treatment of severe obesity.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"32 11","pages":"2100-2110"},"PeriodicalIF":4.2,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/oby.24131","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142383077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jaime P. Almandoz, Thomas A. Wadden, Colleen Tewksbury, Caroline M. Apovian, Angela Fitch, Jamy D. Ard, Zhaoping Li, Jesse Richards, W. Scott Butsch, Irina Jouravskaya, Kadie S. Vanderman, Lisa M. Neff
<p><b>TO THE EDITOR:</b> We thank Bett and colleagues for their interest in our review, “Nutritional considerations with antiobesity medications” [<span>(1)</span>], and we appreciate the opportunity to respond to their letter.</p><p>Because obesity is a chronic disease, we recognize the importance of long-term data on outcomes of treatment with any antiobesity medication (AOM). A significant body of evidence from randomized controlled trials has supported the efficacy and safety of Food and Drug Administration (FDA)-approved AOMs for chronic weight management, including liraglutide (2014), semaglutide (2021), and tirzepatide (2023). Examples of completed randomized controlled trials of >1 year duration include, but are not limited to, the SCALE trial of liraglutide (NCT01272219; 160 weeks) [<span>(2)</span>], the SELECT trial of semaglutide (NCT03574597; 208 weeks) [<span>(3)</span>], and the SURMOUNT-4 trial of tirzepatide (NCT04660643; 88 weeks) [<span>(4)</span>]. Ongoing trials (e.g., SURMOUNT-MMO; 260 weeks) will provide additional long-term data to help inform clinical decision-making.</p><p>We aimed to present a balanced view of the benefits and potential adverse events (AEs) associated with AOMs, with a focus on common AEs that may impact nutritional status, such as gastrointestinal AEs. We recognize that other AEs, including rare but serious events, can occur during treatment, as has been detailed elsewhere [<span>(5, 6)</span>].</p><p>We agree, as noted in the manuscript, that weight regain is commonly seen on treatment cessation and is observed with various obesity treatments, including intensive lifestyle interventions [<span>(7)</span>] and AOMs [<span>(1)</span>]. This highlights the chronic and relapsing nature of the disease and suggests that chronic treatment may be necessary for maintenance of weight reduction. We recognize that limited access to obesity treatment, including but not limited to AOMs, is a major barrier. Challenges that impact access to medications must be addressed to optimize patient care over the long term.</p><p>We recognize that energy requirements vary based on many factors, including age, sex, body weight, and physical activity. We noted in our review that goals for energy intake should be personalized. However, we felt it was important to provide general guidance on minimum goals for energy intake during obesity treatment in particular. Our review of current evidence from low-calorie diets, bariatric surgery, and dietary guidelines for adults overwhelmingly presented energy intake guidance based on sex rather than weight. By contrast, when weight reduction is not the goal, as in the inpatient setting, energy prescriptions are often based on weight. Additional research may help clarify optimal energy intake during weight reduction. Our review included recommendations for liquid meal replacements and high-quality protein supplementation as needed. Whey was not specifically recommended, but these products
致编辑：感谢贝特及其同事对我们的综述 "抗肥胖药物的营养注意事项"[(1)]的关注，我们很高兴有机会对他们的来信作出回应。由于肥胖是一种慢性疾病，我们认识到任何抗肥胖药物（AOM）治疗结果的长期数据的重要性。来自随机对照试验的大量证据支持了美国食品和药物管理局（FDA）批准的用于慢性体重管理的 AOMs 的疗效和安全性，包括利拉鲁肽（2014 年）、赛马鲁肽（2021 年）和替泽帕肽（2023 年）。已完成的为期1年的随机对照试验包括但不限于利拉鲁肽的SCALE试验（NCT01272219；160周）[(2)]、塞马鲁肽的SELECT试验（NCT03574597；208周）[(3)]和替齐帕肽的SURMOUNT-4试验（NCT04660643；88周）[(4)]。正在进行的试验（如 SURMOUNT-MMO；260 周）将提供更多的长期数据，为临床决策提供参考。我们的目标是平衡地阐述与 AOMs 相关的益处和潜在不良事件 (AEs)，重点关注可能影响营养状况的常见不良事件，如胃肠道不良事件。我们认识到，在治疗过程中还可能出现其他不良反应，包括罕见但严重的不良反应，这在其他文献中也有详细介绍[(5, 6)]。我们同意，正如手稿中指出的那样，体重反弹在停止治疗时很常见，而且在各种肥胖症治疗中都能观察到，包括强化生活方式干预[(7)]和AOMs[(1)]。这凸显了肥胖症的慢性和复发性特点，并表明长期治疗可能是维持体重减轻的必要条件。我们认识到，获得肥胖症治疗（包括但不限于 AOMs）的机会有限是一个主要障碍。我们认识到，能量需求因年龄、性别、体重和体力活动等多种因素而异。我们在综述中指出，能量摄入的目标应该是个性化的。但是，我们认为有必要特别就肥胖症治疗期间能量摄入的最低目标提供一般性指导。我们对低热量饮食、减肥手术和成人膳食指南中的现有证据进行了回顾，绝大多数证据都提出了基于性别而非体重的能量摄入指导。相比之下，当减轻体重不是目标时，如在住院环境中，能量处方通常是基于体重的。更多的研究可能有助于明确减重期间的最佳能量摄入。我们的综述包括关于液体代餐和根据需要补充优质蛋白质的建议。我们同意，如果没有摄入足够的水分，膳食纤维摄入可能会导致便秘，并在我们的综述中指出了同时关注纤维和液体摄入的重要性。我们的综述还强调了膳食纤维食物来源（"水果、蔬菜和全谷物"）的重要性，它们含有可溶性和非可溶性纤维。Jaime P. Almandoz从勃林格殷格翰公司、礼来公司和诺和诺德公司获得了咨询费；从临床护理选择、医学和护理教育研究所以及PeerView获得了讲课费或酬金；并在肥胖协会理事会担任领导或受托职务。Thomas A. Wadden 从诺和诺德公司（Novo Nordisk A/S ）和 WW 国际公司（WW International, Inc.Colleen Tewksbury 曾从营养与饮食科学院 (Academy of Nutrition and Dietetics) 和饮食注册委员会 (Commission on Dietetic Registration) 领取讲座、演讲、发言人、手稿撰写或教育活动的报酬或酬金；从营养与饮食科学院 (Academy of Nutrition and Dietetics) 领取出席会议和/或差旅的资助；在营养与饮食科学院体重管理饮食实践小组执行委员会 (Academy of Nutrition and Dietetics Weight Management Dietetic Practice Group Executive Committee) 担任领导或受托职务；以及担任营养与饮食科学院 (Academy of Nutrition and Dietetics) 的发言人。Caroline M. Apovian 曾获得 GI Dynamics 公司（现为 Morphic Medical）、Novo Nordisk A/S 和以患者为中心的结果研究所的机构资助；获得 Cowen and Company, LLC 的咨询费；获得 Rhythm Pharmaceuticals, Inc 的讲课费或酬金；加入 Altimmune、CinFina Pharma、Currax Pharmaceuticals、EPG Communication Holdings、Form Health、L-Nutra、NeuroBo Pharmaceuticals, Inc、Novo Nordisk A/S 、PainScript、Palatin Technologies, Inc.
{"title":"Response to the Letter to the Editor by Bett et al.","authors":"Jaime P. Almandoz, Thomas A. Wadden, Colleen Tewksbury, Caroline M. Apovian, Angela Fitch, Jamy D. Ard, Zhaoping Li, Jesse Richards, W. Scott Butsch, Irina Jouravskaya, Kadie S. Vanderman, Lisa M. Neff","doi":"10.1002/oby.24140","DOIUrl":"10.1002/oby.24140","url":null,"abstract":"<p><b>TO THE EDITOR:</b> We thank Bett and colleagues for their interest in our review, “Nutritional considerations with antiobesity medications” [<span>(1)</span>], and we appreciate the opportunity to respond to their letter.</p><p>Because obesity is a chronic disease, we recognize the importance of long-term data on outcomes of treatment with any antiobesity medication (AOM). A significant body of evidence from randomized controlled trials has supported the efficacy and safety of Food and Drug Administration (FDA)-approved AOMs for chronic weight management, including liraglutide (2014), semaglutide (2021), and tirzepatide (2023). Examples of completed randomized controlled trials of >1 year duration include, but are not limited to, the SCALE trial of liraglutide (NCT01272219; 160 weeks) [<span>(2)</span>], the SELECT trial of semaglutide (NCT03574597; 208 weeks) [<span>(3)</span>], and the SURMOUNT-4 trial of tirzepatide (NCT04660643; 88 weeks) [<span>(4)</span>]. Ongoing trials (e.g., SURMOUNT-MMO; 260 weeks) will provide additional long-term data to help inform clinical decision-making.</p><p>We aimed to present a balanced view of the benefits and potential adverse events (AEs) associated with AOMs, with a focus on common AEs that may impact nutritional status, such as gastrointestinal AEs. We recognize that other AEs, including rare but serious events, can occur during treatment, as has been detailed elsewhere [<span>(5, 6)</span>].</p><p>We agree, as noted in the manuscript, that weight regain is commonly seen on treatment cessation and is observed with various obesity treatments, including intensive lifestyle interventions [<span>(7)</span>] and AOMs [<span>(1)</span>]. This highlights the chronic and relapsing nature of the disease and suggests that chronic treatment may be necessary for maintenance of weight reduction. We recognize that limited access to obesity treatment, including but not limited to AOMs, is a major barrier. Challenges that impact access to medications must be addressed to optimize patient care over the long term.</p><p>We recognize that energy requirements vary based on many factors, including age, sex, body weight, and physical activity. We noted in our review that goals for energy intake should be personalized. However, we felt it was important to provide general guidance on minimum goals for energy intake during obesity treatment in particular. Our review of current evidence from low-calorie diets, bariatric surgery, and dietary guidelines for adults overwhelmingly presented energy intake guidance based on sex rather than weight. By contrast, when weight reduction is not the goal, as in the inpatient setting, energy prescriptions are often based on weight. Additional research may help clarify optimal energy intake during weight reduction. Our review included recommendations for liquid meal replacements and high-quality protein supplementation as needed. Whey was not specifically recommended, but these products","PeriodicalId":215,"journal":{"name":"Obesity","volume":"32 11","pages":"1982-1984"},"PeriodicalIF":4.2,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/oby.24140","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142373950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Meghan L. Butryn, Nicole A. Miller, Charlotte J. Hagerman, Danielle Arigo, Erica LaFata, Fengqing Zhang, Bonnie Spring, Evan Forman
Objective
This study experimentally tested whether coach access to participants' digital self-monitoring data improved behavioral weight-loss outcomes.
Methods
Participants (N = 322) received 12 weeks of group-based behavioral weight-loss sessions via videoconference and were instructed to engage in daily self-monitoring of weight, physical activity (PA), and dietary intake. For participants who were randomly assigned to Coach Share ON (n = 161), coaches regularly accessed a web-based portal that displayed data from the participants' scale, PA sensor, and food record.
Results
Weight loss at 12 weeks was significantly greater in Coach Share ON versus OFF (6.2% vs. 5.3%; p = 0.04). Self-monitoring of PA (98.70% vs. 97.40% of days; p = 0.006) and eating (98.05% vs. 93.51% of days; p = 0.007) was more frequent in Coach Share ON versus OFF. There were no significant differences by condition in PA (p = 0.57), attendance (p = 0.42), working alliance (p = 0.62), or self-monitoring of weight (p = 0.12). Perceived supportive accountability was significantly greater in Coach Share ON versus OFF (p < 0.001).
Conclusions
The short-term efficacy of behavioral weight loss was greater when coaches had direct access to self-monitoring device data. Notably, there also was no evidence of iatrogenic effects of data sharing.
{"title":"Coach access to digital self-monitoring data: an experimental test of short-term effects in behavioral weight-loss treatment","authors":"Meghan L. Butryn, Nicole A. Miller, Charlotte J. Hagerman, Danielle Arigo, Erica LaFata, Fengqing Zhang, Bonnie Spring, Evan Forman","doi":"10.1002/oby.24138","DOIUrl":"10.1002/oby.24138","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study experimentally tested whether coach access to participants' digital self-monitoring data improved behavioral weight-loss outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Participants (<i>N</i> = 322) received 12 weeks of group-based behavioral weight-loss sessions via videoconference and were instructed to engage in daily self-monitoring of weight, physical activity (PA), and dietary intake. For participants who were randomly assigned to Coach Share ON (<i>n</i> = 161), coaches regularly accessed a web-based portal that displayed data from the participants' scale, PA sensor, and food record.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Weight loss at 12 weeks was significantly greater in Coach Share ON versus OFF (6.2% vs. 5.3%; <i>p</i> = 0.04). Self-monitoring of PA (98.70% vs. 97.40% of days; <i>p</i> = 0.006) and eating (98.05% vs. 93.51% of days; <i>p</i> = 0.007) was more frequent in Coach Share ON versus OFF. There were no significant differences by condition in PA (<i>p</i> = 0.57), attendance (<i>p</i> = 0.42), working alliance (<i>p</i> = 0.62), or self-monitoring of weight (<i>p</i> = 0.12). Perceived supportive accountability was significantly greater in Coach Share ON versus OFF (<i>p</i> < 0.001).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The short-term efficacy of behavioral weight loss was greater when coaches had direct access to self-monitoring device data. Notably, there also was no evidence of iatrogenic effects of data sharing.</p>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"32 11","pages":"2111-2119"},"PeriodicalIF":4.2,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142368101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Michael Zhong, Ebuka Onyenobi, Ayo Duomatey, Guanjie Chen, James Perry, Zhenyao Ye, ACCME Research Group as part of the H3Africa Consortium, Charles Rotimi, Clement A. Adebamowo, Adebowale Adeyemo, Sally N. Adebamowo
<div> <section> <h3> Objective</h3> <p>Understanding the genetic underpinnings of anthropometric traits in diverse populations is crucial for gaining insights into their biological mechanisms and potential implications for health.</p> </section> <section> <h3> Methods</h3> <p>We conducted a genome-wide association study, meta-analysis, and gene set analysis of waist-hip ratio (WHR), WHR adjusted for BMI (WHRadjBMI), waist circumference, BMI, and height using the African Collaborative Center for Microbiome and Genomics Research (ACCME) cohort (<i>n</i> = ~11,000) for discovery and polygenic score target analyses and the Africa America Diabetes Mellitus (AADM) study (<i>n</i> = ~5200) for replication and polygenic score validation. We generated and compared polygenic scores from European, African, Afro-Caribbean, and multiethnic ancestry populations.</p> </section> <section> <h3> Results</h3> <p>The top loci associated with each trait in the meta-analysis were in <i>CD36</i> (rs3211826 [<i>p</i> = 5.90 × 10<sup>−12</sup>] for WHR and rs73709003 [<i>p</i> = 1.75 × 10<sup>−13</sup>] for WHRadjBMI), <i>IFI27L1</i> (rs59775050 [<i>p</i> = 2.66 × 10<sup>−08</sup>] for waist circumference), <i>INPP4B</i> (rs2636629 [<i>p</i> = 1.44 × 10<sup>−09</sup>] for BMI), and <i>HMGA1</i> (rs6937622 [<i>p</i> = 1.40 × 10<sup>−15</sup>] for height) gene regions. A novel variant rs7797157, near <i>GNAT3</i>, was also significantly associated with WHR (<i>p</i> = 2.50 × 10<sup>−10</sup>) and WHRadjBMI (<i>p</i> = 2.66 × 10<sup>−11</sup>). The ancestry-specific parameters for the best predictive polygenic scores were European ancestry (<i>R</i><sup><i>2</i></sup> = 0.68%; <i>p</i> = 1.63 × 10<sup>−16</sup>) and multiethnic ancestry (<i>R</i><sup><i>2</i></sup> = 0.06%; <i>p</i> = 1.29 × 10<sup>−02</sup>) for WHR; European ancestry (<i>R</i><sup><i>2</i></sup> = 1.36%; <i>p</i> = 2.94 × 10<sup>−31</sup>) and multiethnic ancestry (<i>R</i><sup><i>2</i></sup> = 1.12%; <i>p</i> = 3.52 × 10<sup>−25</sup>) for BMI; and European ancestry (<i>R</i><sup><i>2</i></sup> = 3.16%; <i>p</i> = 2.95 × 10<sup>−73</sup>), African ancestry (<i>R</i><sup><i>2</i></sup> = 4.16%; <i>p</i> = 1.75 × 10<sup>−96</sup>), and African and Afro-Caribbean ancestry (<i>R</i><sup><i>2</i></sup> = 2.67%; <i>p</i> = 4.35 × 10<sup>−62</sup>) for height.</p> </section> <section> <h3> Conclusions</h3> <p>The discovery of a novel locus for WHR and genetic signals for each trait and the assessment of polygenic score performance underscore the importance of conducting well-powered studies in diverse populations
{"title":"A meta-analysis and polygenic score study identifies novel genetic markers for waist-hip ratio in African populations","authors":"Michael Zhong, Ebuka Onyenobi, Ayo Duomatey, Guanjie Chen, James Perry, Zhenyao Ye, ACCME Research Group as part of the H3Africa Consortium, Charles Rotimi, Clement A. Adebamowo, Adebowale Adeyemo, Sally N. Adebamowo","doi":"10.1002/oby.24123","DOIUrl":"10.1002/oby.24123","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Understanding the genetic underpinnings of anthropometric traits in diverse populations is crucial for gaining insights into their biological mechanisms and potential implications for health.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a genome-wide association study, meta-analysis, and gene set analysis of waist-hip ratio (WHR), WHR adjusted for BMI (WHRadjBMI), waist circumference, BMI, and height using the African Collaborative Center for Microbiome and Genomics Research (ACCME) cohort (<i>n</i> = ~11,000) for discovery and polygenic score target analyses and the Africa America Diabetes Mellitus (AADM) study (<i>n</i> = ~5200) for replication and polygenic score validation. We generated and compared polygenic scores from European, African, Afro-Caribbean, and multiethnic ancestry populations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The top loci associated with each trait in the meta-analysis were in <i>CD36</i> (rs3211826 [<i>p</i> = 5.90 × 10<sup>−12</sup>] for WHR and rs73709003 [<i>p</i> = 1.75 × 10<sup>−13</sup>] for WHRadjBMI), <i>IFI27L1</i> (rs59775050 [<i>p</i> = 2.66 × 10<sup>−08</sup>] for waist circumference), <i>INPP4B</i> (rs2636629 [<i>p</i> = 1.44 × 10<sup>−09</sup>] for BMI), and <i>HMGA1</i> (rs6937622 [<i>p</i> = 1.40 × 10<sup>−15</sup>] for height) gene regions. A novel variant rs7797157, near <i>GNAT3</i>, was also significantly associated with WHR (<i>p</i> = 2.50 × 10<sup>−10</sup>) and WHRadjBMI (<i>p</i> = 2.66 × 10<sup>−11</sup>). The ancestry-specific parameters for the best predictive polygenic scores were European ancestry (<i>R</i><sup><i>2</i></sup> = 0.68%; <i>p</i> = 1.63 × 10<sup>−16</sup>) and multiethnic ancestry (<i>R</i><sup><i>2</i></sup> = 0.06%; <i>p</i> = 1.29 × 10<sup>−02</sup>) for WHR; European ancestry (<i>R</i><sup><i>2</i></sup> = 1.36%; <i>p</i> = 2.94 × 10<sup>−31</sup>) and multiethnic ancestry (<i>R</i><sup><i>2</i></sup> = 1.12%; <i>p</i> = 3.52 × 10<sup>−25</sup>) for BMI; and European ancestry (<i>R</i><sup><i>2</i></sup> = 3.16%; <i>p</i> = 2.95 × 10<sup>−73</sup>), African ancestry (<i>R</i><sup><i>2</i></sup> = 4.16%; <i>p</i> = 1.75 × 10<sup>−96</sup>), and African and Afro-Caribbean ancestry (<i>R</i><sup><i>2</i></sup> = 2.67%; <i>p</i> = 4.35 × 10<sup>−62</sup>) for height.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The discovery of a novel locus for WHR and genetic signals for each trait and the assessment of polygenic score performance underscore the importance of conducting well-powered studies in diverse populations","PeriodicalId":215,"journal":{"name":"Obesity","volume":"32 11","pages":"2175-2185"},"PeriodicalIF":4.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/oby.24123","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142335393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gabriela Neira, Ana Wenting Hernández-Pardos, Sara Becerril, Beatriz Ramírez, Víctor Valentí, Rafael Moncada, Victoria Catalán, Javier Gómez-Ambrosi, María A. Burrell, Camilo Silva, Javier Escalada, Gema Frühbeck, Amaia Rodríguez
Objective
Fibronectin type III domain-containing protein 5 (FNDC5) modulates adipocyte metabolism by increasing white and brown adipose tissue (WAT and BAT) browning and activity, respectively. We investigated whether FNDC5 can regulate visceral WAT and BAT adaptive thermogenesis by improving mitochondrial homeostasis in response to cold and obesity.
Methods
Adipose tissue expression of FNDC5 and factors involved in mitochondrial homeostasis were determined in patients with normal weight and obesity (n = 159) and in rats with diet-induced obesity after 1 week of cold exposure (n = 61). The effect of different FNDC5 concentrations on mitochondrial biogenesis, dynamics, and mitophagy was evaluated in vitro in human adipocytes.
Results
In human visceral adipocytes, FNDC5/irisin triggered mitochondrial biogenesis (TFAM) and fusion (MFN1, MFN2, and OPA1) while inhibiting peripheral fission (DNM1L and FIS1) and mitophagy (PINK1 and PRKN). Circulating and visceral WAT expression of FNDC5 was decreased in patients and experimental animals with obesity, whereas its receptor, integrin αV, was upregulated. Obesity increased mitochondrial fusion while decreasing mitophagy in visceral WAT from patients and rats. By contrast, in rat BAT, an upregulation of Fndc5 and genes involved in mitochondrial biogenesis and fission was observed. Cold exposure promoted mitochondrial biogenesis and healthy peripheral fission while repressing Fndc5 expression and mitophagy in BAT from rats.
Conclusions
Depot differences in FNDC5 production and mitochondrial adaptations in response to obesity and cold might indicate a self-regulatory mechanism to control thermogenesis in response to energy needs.
{"title":"Differential mitochondrial adaptation and FNDC5 production in brown and white adipose tissue in response to cold and obesity","authors":"Gabriela Neira, Ana Wenting Hernández-Pardos, Sara Becerril, Beatriz Ramírez, Víctor Valentí, Rafael Moncada, Victoria Catalán, Javier Gómez-Ambrosi, María A. Burrell, Camilo Silva, Javier Escalada, Gema Frühbeck, Amaia Rodríguez","doi":"10.1002/oby.24132","DOIUrl":"10.1002/oby.24132","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Fibronectin type III domain-containing protein 5 (FNDC5) modulates adipocyte metabolism by increasing white and brown adipose tissue (WAT and BAT) browning and activity, respectively. We investigated whether FNDC5 can regulate visceral WAT and BAT adaptive thermogenesis by improving mitochondrial homeostasis in response to cold and obesity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Adipose tissue expression of FNDC5 and factors involved in mitochondrial homeostasis were determined in patients with normal weight and obesity (<i>n</i> = 159) and in rats with diet-induced obesity after 1 week of cold exposure (<i>n</i> = 61). The effect of different FNDC5 concentrations on mitochondrial biogenesis, dynamics, and mitophagy was evaluated in vitro in human adipocytes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In human visceral adipocytes, FNDC5/irisin triggered mitochondrial biogenesis (<i>TFAM</i>) and fusion (<i>MFN1</i>, <i>MFN2</i>, and <i>OPA1</i>) while inhibiting peripheral fission (<i>DNM1L</i> and <i>FIS1</i>) and mitophagy (<i>PINK1</i> and <i>PRKN</i>). Circulating and visceral WAT expression of FNDC5 was decreased in patients and experimental animals with obesity, whereas its receptor, integrin αV, was upregulated. Obesity increased mitochondrial fusion while decreasing mitophagy in visceral WAT from patients and rats. By contrast, in rat BAT, an upregulation of <i>Fndc5</i> and genes involved in mitochondrial biogenesis and fission was observed. Cold exposure promoted mitochondrial biogenesis and healthy peripheral fission while repressing <i>Fndc5</i> expression and mitophagy in BAT from rats.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Depot differences in FNDC5 production and mitochondrial adaptations in response to obesity and cold might indicate a self-regulatory mechanism to control thermogenesis in response to energy needs.</p>\u0000 \u0000 <div>\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":215,"journal":{"name":"Obesity","volume":"32 11","pages":"2120-2134"},"PeriodicalIF":4.2,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/oby.24132","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142335396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号