Pub Date : 2025-07-01Epub Date: 2025-07-04DOI: 10.1016/j.obmed.2025.100627
Halil Çolak
This study aims to forecast the prevalence of obesity among the elderly population (aged 65 and over) in the United States through 2035 using time series forecasting techniques. Obesity data from 2013 to 2022 were analysed using six models: Autoregressive Integrated Moving Average (ARIMA), Long-Short Term Memory (LSTM), Gated Recurrent Units GRU, Random Forest (RF), Vector autoregression model (VAR), and eXtreme Gradient Boosting (XGBoost). The primary goal is to inform future public health strategies and optimize healthcare resource allocation for the aging population. The results indicate a consistent rise in obesity rates. ARIMA predicted an increase from 30.6 % in 2022 to 35.0 % in 2035, while VAR estimated 37.9 %. Machine learning models forecasted sharper growth: RF projected 40.6 %, LSTM 41.3 %, and GRU 39.8 %. XGBoost anticipated the highest rate, reaching 44.3 % in 2035. Model performances were evaluated using coefficient of determination (R2), mean square error, root mean square error, and sum of squares error. VAR and XGBoost achieved the best results (R2 = 0.9995 and 0.9993, respectively), while LSTM (R2 = 0.9004) and GRU (R2 = 0.8648) showed moderate predictive power. ARIMA also performed well with R2 = 0.9420. The findings reveal that ensemble and multivariate models, particularly XGBoost and VAR, offer higher forecasting accuracy. This study fills a gap in the literature by focusing on elderly obesity projections and offers valuable insights for developing targeted intervention policies and health programme.
{"title":"Future projections of elderly obesity in the United States using time series models","authors":"Halil Çolak","doi":"10.1016/j.obmed.2025.100627","DOIUrl":"10.1016/j.obmed.2025.100627","url":null,"abstract":"<div><div>This study aims to forecast the prevalence of obesity among the elderly population (aged 65 and over) in the United States through 2035 using time series forecasting techniques. Obesity data from 2013 to 2022 were analysed using six models: Autoregressive Integrated Moving Average (ARIMA), Long-Short Term Memory (LSTM), Gated Recurrent Units GRU, Random Forest (RF), Vector autoregression model (VAR), and eXtreme Gradient Boosting (XGBoost). The primary goal is to inform future public health strategies and optimize healthcare resource allocation for the aging population. The results indicate a consistent rise in obesity rates. ARIMA predicted an increase from 30.6 % in 2022 to 35.0 % in 2035, while VAR estimated 37.9 %. Machine learning models forecasted sharper growth: RF projected 40.6 %, LSTM 41.3 %, and GRU 39.8 %. XGBoost anticipated the highest rate, reaching 44.3 % in 2035. Model performances were evaluated using coefficient of determination (R<sup>2</sup>), mean square error, root mean square error, and sum of squares error. VAR and XGBoost achieved the best results (R<sup>2</sup> = 0.9995 and 0.9993, respectively), while LSTM (R<sup>2</sup> = 0.9004) and GRU (R<sup>2</sup> = 0.8648) showed moderate predictive power. ARIMA also performed well with R<sup>2</sup> = 0.9420. The findings reveal that ensemble and multivariate models, particularly XGBoost and VAR, offer higher forecasting accuracy. This study fills a gap in the literature by focusing on elderly obesity projections and offers valuable insights for developing targeted intervention policies and health programme.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"56 ","pages":"Article 100627"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144556924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-01Epub Date: 2025-06-11DOI: 10.1016/j.obmed.2025.100623
Esther Ugo Alum , Regina Idu Ejemot-Nwadiaro , Peter A. Betiang , Mariam Basajja , Daniel Ejim Uti
Obesity and climate change are critical global challenges of the 21st century, with shared drivers and far-reaching impacts on public health, environmental sustainability, and socioeconomic equity. Both crises are fueled by factors such as unsustainable food systems, urbanization, and systemic inequities. Industrialized food production contributes to greenhouse gas emissions, deforestation, and resource depletion while promoting calorie-dense, nutrient-poor diets that exacerbate obesity rates. Climate-induced food insecurity further intensifies the malnutrition paradox, where undernutrition and obesity coexist, disproportionately affecting vulnerable populations. This short communication explores the complex connections between obesity and climate change, examining their mutual drivers, public health implications, and role in food systems. The novelty of this communication lies in its amalgamation of emerging, underexplored bidirectional mechanisms, including thermoregulatory effects and differential emissions contributions, supported by recent evidence. Rather than serving as a comprehensive review, this paper aims to offer a concise yet policy-relevant perspective that emphasizes overlooked linkages and actionable solutions. By clearly framing the scope and contribution of this short communication, we aim to distinguish our work from broader literature reviews and highlight its relevance for integrated health-environment policy development. Recommendations include leveraging technology, fostering global collaboration, and advancing interdisciplinary research to address these intersecting crises holistically. Aligning with public health and environmental goals is essential for creating a resilient and equitable future for both human and planetary well-being. This short communication was developed through an extensive review of scholarly articles, policy reports, and case studies addressing the intersections of obesity and climate change. Sources were identified via databases such as PubMed, Scopus, and Google Scholar, with keywords including “obesity,” “climate change,” “food systems,” and “public health policies.” The analysis focused on identifying shared drivers, mutual impacts, and actionable strategies. Emphasis was placed on evidence-based insights and multidisciplinary approaches to propose integrated solutions that address both crises.
{"title":"Obesity and Climate Change: A Two-way Street with Global Health Implications","authors":"Esther Ugo Alum , Regina Idu Ejemot-Nwadiaro , Peter A. Betiang , Mariam Basajja , Daniel Ejim Uti","doi":"10.1016/j.obmed.2025.100623","DOIUrl":"10.1016/j.obmed.2025.100623","url":null,"abstract":"<div><div>Obesity and climate change are critical global challenges of the 21st century, with shared drivers and far-reaching impacts on public health, environmental sustainability, and socioeconomic equity. Both crises are fueled by factors such as unsustainable food systems, urbanization, and systemic inequities. Industrialized food production contributes to greenhouse gas emissions, deforestation, and resource depletion while promoting calorie-dense, nutrient-poor diets that exacerbate obesity rates. Climate-induced food insecurity further intensifies the malnutrition paradox, where undernutrition and obesity coexist, disproportionately affecting vulnerable populations. This short communication explores the complex connections between obesity and climate change, examining their mutual drivers, public health implications, and role in food systems. The novelty of this communication lies in its amalgamation of emerging, underexplored bidirectional mechanisms, including thermoregulatory effects and differential emissions contributions, supported by recent evidence. Rather than serving as a comprehensive review, this paper aims to offer a concise yet policy-relevant perspective that emphasizes overlooked linkages and actionable solutions. By clearly framing the scope and contribution of this short communication, we aim to distinguish our work from broader literature reviews and highlight its relevance for integrated health-environment policy development. Recommendations include leveraging technology, fostering global collaboration, and advancing interdisciplinary research to address these intersecting crises holistically. Aligning with public health and environmental goals is essential for creating a resilient and equitable future for both human and planetary well-being. This short communication was developed through an extensive review of scholarly articles, policy reports, and case studies addressing the intersections of obesity and climate change. Sources were identified via databases such as PubMed, Scopus, and Google Scholar, with keywords including “obesity,” “climate change,” “food systems,” and “public health policies.” The analysis focused on identifying shared drivers, mutual impacts, and actionable strategies. Emphasis was placed on evidence-based insights and multidisciplinary approaches to propose integrated solutions that address both crises.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"56 ","pages":"Article 100623"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144280456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Insights into Development and Pathogenesis investigates the critical role of epigenetic modifications, such as DNA methylation, histone alterations, and non-coding RNA, in the onset and progression of Type 2 diabetes (T2D). It highlights how environmental factors, lifestyle choices, and genetic predispositions influence these epigenetic changes, contributing to insulin resistance, beta-cell dysfunction, and other key mechanisms of T2D. The review provides a comprehensive understanding of the complex interplay between genetic and epigenetic factors in diabetes pathogenesis.
Aim
The aim of this review is to explore the role of epigenetic modifications in the development and pathogenesis of Type 2 diabetes (T2D). It examines how environmental factors, lifestyle, and genetic predisposition influence epigenetic changes, contributing to key mechanisms such as insulin resistance and beta-cell dysfunction. By providing insights into these interactions, the review aims to enhance understanding of T2D etiology and inform potential therapeutic strategies.
Result
The review reveals that epigenetic modifications, including DNA methylation, histone alterations, and non-coding RNA regulation, significantly contribute to the development and progression of Type 2 diabetes (T2D). It highlights how environmental factors, lifestyle choices, and genetic predisposition lead to changes in these epigenetic marks, driving insulin resistance, impaired beta-cell function, and other aspects of T2D. The findings underscore the potential of targeting epigenetic pathways for novel therapeutic approaches in managing T2D.
Conclusion
The review concludes that epigenetic factors play a crucial role in Type 2 diabetes development, offering promising targets for therapeutic intervention. Understanding these mechanisms may lead to more effective prevention and treatment strategies.
{"title":"The impact of epigenetic factors in type 2 diabetes: Insights into development and pathogenesis","authors":"Thammanna Gowda SS, Shobith Rangappa, Parimala Hanumesh","doi":"10.1016/j.obmed.2025.100635","DOIUrl":"10.1016/j.obmed.2025.100635","url":null,"abstract":"<div><h3>Background</h3><div><em>Insights into Development and Pathogenesis</em> investigates the critical role of epigenetic modifications, such as DNA methylation, histone alterations, and non-coding RNA, in the onset and progression of Type 2 diabetes (T2D). It highlights how environmental factors, lifestyle choices, and genetic predispositions influence these epigenetic changes, contributing to insulin resistance, beta-cell dysfunction, and other key mechanisms of T2D. The review provides a comprehensive understanding of the complex interplay between genetic and epigenetic factors in diabetes pathogenesis.</div></div><div><h3>Aim</h3><div>The aim of this review is to explore the role of epigenetic modifications in the development and pathogenesis of Type 2 diabetes (T2D). It examines how environmental factors, lifestyle, and genetic predisposition influence epigenetic changes, contributing to key mechanisms such as insulin resistance and beta-cell dysfunction. By providing insights into these interactions, the review aims to enhance understanding of T2D etiology and inform potential therapeutic strategies.</div></div><div><h3>Result</h3><div>The review reveals that epigenetic modifications, including DNA methylation, histone alterations, and non-coding RNA regulation, significantly contribute to the development and progression of Type 2 diabetes (T2D). It highlights how environmental factors, lifestyle choices, and genetic predisposition lead to changes in these epigenetic marks, driving insulin resistance, impaired beta-cell function, and other aspects of T2D. The findings underscore the potential of targeting epigenetic pathways for novel therapeutic approaches in managing T2D.</div></div><div><h3>Conclusion</h3><div>The review concludes that epigenetic factors play a crucial role in Type 2 diabetes development, offering promising targets for therapeutic intervention. Understanding these mechanisms may lead to more effective prevention and treatment strategies.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"56 ","pages":"Article 100635"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144611630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-01Epub Date: 2025-07-09DOI: 10.1016/j.obmed.2025.100631
Sobia Hasan , Basit Ansari , Tehreem Anis , Fahad Alanazi , Mehrunnisha Ahmed , Ahmad Alanazi , Faizan Zaffar Kashoo
Background and purpose
Diabetes mellitus, a common disorder of glucose metabolism, affects multiple organ systems and often leads to complications such as diabetic peripheral neuropathy (DPN), which impairs balance and mobility. To manage DPN effectively, understanding the relationships between key markers, such as fasting blood sugar (FBS), glycated hemoglobin (HbA1c), and aerobic capacity (VO2max), and balance-related outcomes is crucial but remains underexplored. This study aimed to investigate the associations between diabetes markers (FBS, HbA1c), physical fitness (VO2max), body mass index (BMI), and balance measures such as One-Leg Stance test (OLS), Berg Balance Scale (BBS), and Timed Up and Go test (TUGT) in adults with type 2 diabetes mellitus (T2DM).
Methods
A cross-sectional correlation analysis was performed using baseline data from a randomized controlled study (n = 90, 67.8 % female, mean age = 55.96 ± 4.61 years). Pearson's correlation and mediation analyses were used to assess relationships between diabetes markers, fitness indicators, and balance measures.
Results
Higher FBS and HbA1c correlated negatively with balance (OLS: r = −0.43 to −0.45, p < 0.01; BBS: r = −0.37 to −0.40, p < 0.05) and positively with mobility impairment (HbA1c-TUG: r = 0.28, p = 0.04). A higher VO2max was correlated with better balance (OLS: r = 0.50, p < 0.01) and faster mobility (TUGT: r = −0.39, p < 0.05). A high BMI negatively impacts balance and slows mobility. Neuropathy severity (Michigan Neuropathy Screening Instrument-MNSI) significantly predicted higher HbA1c (β = 0.106, p < 0.001) and reduced VO2max, OLS, and BBS scores.
Discussion
Poor glycemic control (higher FBS and HbA1c) is linked to poorer balance, whereas higher VO2max and lower BMI are correlated with improved balance in T2DM patients. Exercise and metabolic control strategies are essential for optimizing functional outcomes in diabetes management.
背景和目的糖尿病是一种常见的糖代谢紊乱,可影响多器官系统,并经常导致糖尿病周围神经病变(DPN)等并发症,损害平衡和活动能力。为了有效地管理DPN,了解关键指标(如空腹血糖(FBS)、糖化血红蛋白(HbA1c)和有氧能力(VO2max)与平衡相关结果之间的关系至关重要,但仍未得到充分研究。本研究旨在探讨成人2型糖尿病(T2DM)患者的糖尿病标志物(FBS、HbA1c)、体能(VO2max)、体重指数(BMI)和平衡测量(如单腿站立测试(OLS)、Berg平衡量表(BBS)和定时起床测试(TUGT))之间的关系。方法采用随机对照研究(n = 90,女性67.8%,平均年龄55.96±4.61岁)的基线资料进行横断面相关分析。使用Pearson相关分析和中介分析来评估糖尿病标志物、健康指标和平衡测量之间的关系。结果较高的FBS和HbA1c与平衡呈负相关(OLS: r = - 0.43 ~ - 0.45, p <;0.01;BBS: r = - 0.37至- 0.40,p <;活动能力障碍呈阳性(HbA1c-TUG: r = 0.28, p = 0.04)。较高的VO2max与较好的平衡性相关(OLS: r = 0.50, p <;0.01)和更快的迁移速度(TUGT: r = - 0.39, p <;0.05)。高BMI会对平衡产生负面影响,并减缓行动能力。神经病变严重程度(密歇根神经病变筛查仪器- mnsi)显著预测HbA1c升高(β = 0.106, p <;0.001), VO2max、OLS和BBS评分降低。血糖控制不良(较高的FBS和HbA1c)与较差的平衡有关,而较高的VO2max和较低的BMI与T2DM患者的平衡改善有关。运动和代谢控制策略对于优化糖尿病管理的功能结果至关重要。
{"title":"Association between diabetes markers, physical fitness, and balance among people with type 2 diabetes mellitus","authors":"Sobia Hasan , Basit Ansari , Tehreem Anis , Fahad Alanazi , Mehrunnisha Ahmed , Ahmad Alanazi , Faizan Zaffar Kashoo","doi":"10.1016/j.obmed.2025.100631","DOIUrl":"10.1016/j.obmed.2025.100631","url":null,"abstract":"<div><h3>Background and purpose</h3><div>Diabetes mellitus, a common disorder of glucose metabolism, affects multiple organ systems and often leads to complications such as diabetic peripheral neuropathy (DPN), which impairs balance and mobility. To manage DPN effectively, understanding the relationships between key markers, such as fasting blood sugar (FBS), glycated hemoglobin (HbA1c), and aerobic capacity (VO<sub>2</sub>max), and balance-related outcomes is crucial but remains underexplored. This study aimed to investigate the associations between diabetes markers (FBS, HbA1c), physical fitness (VO<sub>2</sub>max), body mass index (BMI), and balance measures such as One-Leg Stance test (OLS), Berg Balance Scale (BBS), and Timed Up and Go test (TUGT) in adults with type 2 diabetes mellitus (T2DM).</div></div><div><h3>Methods</h3><div>A cross-sectional correlation analysis was performed using baseline data from a randomized controlled study (n = 90, 67.8 % female, mean age = 55.96 ± 4.61 years). Pearson's correlation and mediation analyses were used to assess relationships between diabetes markers, fitness indicators, and balance measures.</div></div><div><h3>Results</h3><div>Higher FBS and HbA1c correlated negatively with balance (OLS: r = −0.43 to −0.45, p < 0.01; BBS: r = −0.37 to −0.40, p < 0.05) and positively with mobility impairment (HbA1c-TUG: r = 0.28, p = 0.04). A higher VO<sub>2</sub>max was correlated with better balance (OLS: r = 0.50, p < 0.01) and faster mobility (TUGT: r = −0.39, p < 0.05). A high BMI negatively impacts balance and slows mobility. Neuropathy severity (Michigan Neuropathy Screening Instrument-MNSI) significantly predicted higher HbA1c (β = 0.106, p < 0.001) and reduced VO<sub>2</sub>max, OLS, and BBS scores.</div></div><div><h3>Discussion</h3><div>Poor glycemic control (higher FBS and HbA1c) is linked to poorer balance, whereas higher VO<sub>2</sub>max and lower BMI are correlated with improved balance in T2DM patients. Exercise and metabolic control strategies are essential for optimizing functional outcomes in diabetes management.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"56 ","pages":"Article 100631"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144605147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Coronavirus disease 2019 (COVID-19) and diabetes seem to have a bidirectional relationship. People suffering from diabetes mellitus (DM) are at higher risk than non-diabetics to contract SARS-CoV-2 infections and acquire COVID-19-related health issues. Diabetes is consistently linked to higher disease risk and death among COVID-19 patients. Data also suggest that multiple phenotypic expression alterations caused by SARS-CoV-2 could complicate the pathogenesis of pre-existing diabetes or result in additional pathological conditions. Clinical research data shows that SARS-CoV-2 infection promotes metabolic abnormalities in humans. Furthermore, recent studies concerning new-onset diabetes (NOD) in COVID-19 affected population, who had previously been infected with the virus, reinforce the notion that SARS-CoV-2 has a direct influence on glucose metabolism. Data from various sources indicated that SARS-CoV-2 infected individuals had a greater prevalence of Diabetic Ketoacidosis (DKA), which might be related to a blatant assault on the beta (β)cells of the pancreas. This virus has also been attributed to binding with the ACE 2 receptors found in critical body tissues as well as organs such as β islet cells of the pancreas, small intestine, kidneys and adipose tissues, causing Ketosis-prone diabetes (KPD), which is a very prevalent form of diabetes in Asia, especially India. It has been observed that despite the lack of autoantibodies, the people so affected experience short, transitory insulin deficit that produces DKA at first, but they recover from this β-cell secretory failure over time. This paper highlights the complex interplay between SARS-CoV-2 and its clinical implications on diabetic pathobiology, emphasizing how the cause-effect relationship operates bidirectionally between the two.
{"title":"Intertwined pathways of SARS-CoV-2 infection and its clinical repercussions on glucose homeostasis: Exploring the rise of new-onset diabetes","authors":"Vertika Awasthi , Rupinder Kaur , Chirag Pasricha, Pratima Kumari, Suruchi Chaubey, Sarita Jangra, Sanjana Mehta, Ravinder Singh","doi":"10.1016/j.obmed.2025.100624","DOIUrl":"10.1016/j.obmed.2025.100624","url":null,"abstract":"<div><div>Coronavirus disease 2019 (COVID-19) and diabetes seem to have a bidirectional relationship. People suffering from diabetes mellitus (DM) are at higher risk than non-diabetics to contract SARS-CoV-2 infections and acquire COVID-19-related health issues. Diabetes is consistently linked to higher disease risk and death among COVID-19 patients. Data also suggest that multiple phenotypic expression alterations caused by SARS-CoV-2 could complicate the pathogenesis of pre-existing diabetes or result in additional pathological conditions. Clinical research data shows that SARS-CoV-2 infection promotes metabolic abnormalities in humans. Furthermore, recent studies concerning new-onset diabetes (NOD) in COVID-19 affected population, who had previously been infected with the virus, reinforce the notion that SARS-CoV-2 has a direct influence on glucose metabolism. Data from various sources indicated that SARS-CoV-2 infected individuals had a greater prevalence of Diabetic Ketoacidosis (DKA), which might be related to a blatant assault on the beta (β)cells of the pancreas. This virus has also been attributed to binding with the ACE 2 receptors found in critical body tissues as well as organs such as β islet cells of the pancreas, small intestine, kidneys and adipose tissues, causing Ketosis-prone diabetes (KPD), which is a very prevalent form of diabetes in Asia, especially India. It has been observed that despite the lack of autoantibodies, the people so affected experience short, transitory insulin deficit that produces DKA at first, but they recover from this β-cell secretory failure over time. This paper highlights the complex interplay between SARS-CoV-2 and its clinical implications on diabetic pathobiology, emphasizing how the cause-effect relationship operates bidirectionally between the two.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"56 ","pages":"Article 100624"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144291208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Obesity significantly contributes to the development of type 2 diabetes mellitus (T2DM). Genetic variations in leptin receptor (LEPR) genes are thought to be influential in the onset of T2DM in patients with kidney malfunction and obesity. This study focused on examining the link between the Gln223Arg polymorphism in the LEPR gene and T2DM in the mid-Black Sea region of the Anatolian Turkish population.
Methodology
In this study, we examined a group of 174 patients with T2DM and compared them to a control group of 30 healthy individuals to explore the relationship involving the leptin receptor gene (Gln223Arg). The T2DM group was divided into 91 patients with macroproteinuria and 46 patients with normoproteinuria subgroups. The genetic analysis was conducted using the polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) technique.
Results
Our data revealed a significant increase in the frequency of gene polymorphism with HbA1c levels.
Conclusion
The Gln223Arg leptin receptor gene mutation may cause an elevation of HbA1c in T2DM patients with chronic kidney disease (CKD) in the mid-Black Sea region of the Anatolian Turkish population.
{"title":"Evaluate the Gln223Arg LEPR genotype variation in T2DM patients with chronic kidney disease","authors":"Shahab Ahmed Salıh Gezh , Figen Guzelgul , Nihan Bozkurt , Hakan Sivgin , Koksal Deveci","doi":"10.1016/j.obmed.2025.100630","DOIUrl":"10.1016/j.obmed.2025.100630","url":null,"abstract":"<div><h3>Background</h3><div>Obesity significantly contributes to the development of type 2 diabetes mellitus (T2DM). Genetic variations in leptin receptor (LEPR) genes are thought to be influential in the onset of T2DM in patients with kidney malfunction and obesity. This study focused on examining the link between the Gln223Arg polymorphism in the LEPR gene and T2DM in the mid-Black Sea region of the Anatolian Turkish population.</div></div><div><h3>Methodology</h3><div>In this study, we examined a group of 174 patients with T2DM and compared them to a control group of 30 healthy individuals to explore the relationship involving the leptin receptor gene (Gln223Arg). The T2DM group was divided into 91 patients with macroproteinuria and 46 patients with normoproteinuria subgroups. The genetic analysis was conducted using the polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) technique.</div></div><div><h3>Results</h3><div>Our data revealed a significant increase in the frequency of gene polymorphism with HbA1c levels.</div></div><div><h3>Conclusion</h3><div>The Gln223Arg leptin receptor gene mutation may cause an elevation of HbA1c in T2DM pat<strong>ients with</strong> chronic kidney disease (CKD) in the mid-Black Sea region of the Anatolian Turkish population.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"56 ","pages":"Article 100630"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144605146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The increasing prevalence of hyperlipidemia has become one of the greatest threats to public health. While pharmacological treatments are effective for the management of hyperlipidemia, alternative approaches like dietary supplements are gaining interest for their natural benefits. The present study aimed to evaluate the safety and efficacy of biozen syrup comprised of garlic, apple-cider vinegar, lemon and honey for controlling patients with hyperlipidemia.
Methods
A prospective, open-label study was conducted on patients who had hyperlipidemia. Patients were given with biozen syrup (15 ml in 100 ml warm water) twice daily for 90 days. Clinical assessments and laboratory findings were compared before (day 0) and after (day 90) starting the treatment.
Results
A total of 60 patients were enrolled in the study. After administration of biozen syrup, serum total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), high-sensitivity C-reactive protein (hs-CRP), homocysteine, and apolipoprotein B levels significantly decreased (p < 0.001). The mean serum apolipoprotein A1, high-density lipoprotein cholesterol (HDL-C) were raised post-treatment (p < 0.001). Treatment with biozen syrup had no significant effects (p > 0.001) on serum biochemical parameters related to liver, kidney functions and hematological parameters. Gastrointestinal disturbances was the most frequently occurred ADR (58 %).
Conclusion
The results demonstrated that the biozen was safe and efficacious in lowering the levels of bad cholesterol and raising the levels of good cholesterol.
{"title":"Clinical evaluation of safety and efficacy of biozen syrup in patients with hyperlipidemia","authors":"Rajappan Chandra Satish Kumar , Subramaniam Nandhini , Bhuvaneshwaran Mothishwaran , Chittaranjan Das , Anavarathan Vallipuram , Muhasaparur Ganesan Rajanandh","doi":"10.1016/j.obmed.2025.100601","DOIUrl":"10.1016/j.obmed.2025.100601","url":null,"abstract":"<div><h3>Background</h3><div>The increasing prevalence of hyperlipidemia has become one of the greatest threats to public health. While pharmacological treatments are effective for the management of hyperlipidemia, alternative approaches like dietary supplements are gaining interest for their natural benefits. The present study aimed to evaluate the safety and efficacy of biozen syrup comprised of garlic, apple-cider vinegar, lemon and honey for controlling patients with hyperlipidemia.</div></div><div><h3>Methods</h3><div>A prospective, open-label study was conducted on patients who had hyperlipidemia. Patients were given with biozen syrup (15 ml in 100 ml warm water) twice daily for 90 days. Clinical assessments and laboratory findings were compared before (day 0) and after (day 90) starting the treatment.</div></div><div><h3>Results</h3><div>A total of 60 patients were enrolled in the study. After administration of biozen syrup, serum total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), high-sensitivity C-reactive protein (hs-CRP), homocysteine, and apolipoprotein B levels significantly decreased (<em>p</em> < 0.001). The mean serum apolipoprotein A1, high-density lipoprotein cholesterol (HDL-C) were raised post-treatment (<em>p</em> < 0.001). Treatment with biozen syrup had no significant effects (<em>p</em> > 0.001) on serum biochemical parameters related to liver, kidney functions and hematological parameters. Gastrointestinal disturbances was the most frequently occurred ADR (58 %).</div></div><div><h3>Conclusion</h3><div>The results demonstrated that the biozen was safe and efficacious in lowering the levels of bad cholesterol and raising the levels of good cholesterol.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"55 ","pages":"Article 100601"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143738016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Obesity is the underlying cause of several metabolic disorders, and regular endurance exercise (EE) is considered one of the main weight loss strategies. Since females have less muscle mass than males, maintaining muscle mass is crucial for them in specific exercise considerations and nutritional strategies designed to produce weight loss. This study aimed to investigate the response of serum levels of glycerol, urea, insulin-like growth factor-1 (IGF-1), and cortisol to performing an EE session following the consumption of animal and plant-based milk in overweight and obese young women.
Methods
After 8 h of overnight fasting, 10 female participants consumed 500 ml of water, low-fat cow's milk (LFCM), and soy milk (SM), randomly in three sessions, then performed 90-min EE at 65 % VO2max. Biochemical parameters were measured immediately before and after and 1 h after each session of EE.
Results
The glycerol level increased immediately after EE in the LFCM and water groups compared to the baseline (P < 0.001), and decreased 1 h after EE in both consumption groups compared to the immediately after EE (P values 0.002, <0.001; respectively). Despite the significant increase in urea level 1 h after EE compared to the baseline level with SM consumption (P < 0.001) and immediately and 1 h after EE compared to the baseline with LFCM consumption (P values 0.001, <0.001; respectively), the urea levels remained unchanged with water consumption. Cortisol level was decreased immediately and 1 h after EE in all three groups compared to the baseline (P < 0.001).
Conclusions
Drinking LFCM and water before the EE under overnight fasting conditions similarly stimulates lipolysis, as evidenced by comparable increases in glycerol level. Additionally, SM consumption appears to enhance anti-degradation pathways of muscle proteins compared to LFCM, based on lower urea levels post-exercise.
{"title":"The acute effects of animal and plant-based milk intake before endurance exercise in overweight and obese women: Interplay between lipolysis and proteolysis","authors":"Soheila Moghaddam Eftekhari , Marziyeh Saghebjoo , Fatemeh Islami , Fereshteh Ahmadabadi","doi":"10.1016/j.obmed.2025.100603","DOIUrl":"10.1016/j.obmed.2025.100603","url":null,"abstract":"<div><h3>Aims</h3><div><em>Obesity is</em> the underlying cause of several <em>metabolic disorders, and regular endurance exercise (EE) is considered one of the main weight loss strategies. Since females have less muscle mass than males, maintaining muscle mass is crucial for them in specific exercise considerations and nutritional strategies designed to produce weight loss.</em> This study aimed to investigate the response of serum levels of glycerol, urea, insulin-like growth factor-1 (IGF-1), and cortisol to performing an EE session following the consumption of animal and plant-based milk in overweight and obese young women.</div></div><div><h3>Methods</h3><div>After 8 h of overnight fasting, 10 female participants consumed 500 ml of water, low-fat cow's milk (LFCM), and soy milk (SM), randomly in three sessions, then performed 90-min EE at 65 % VO2max. Biochemical parameters were measured immediately before and after and 1 h after each session of EE.</div></div><div><h3>Results</h3><div>The glycerol level increased immediately after EE in the LFCM and water groups compared to the baseline (P < 0.001), and decreased 1 h after EE in both consumption groups compared to the immediately after EE (P values 0.002, <0.001; respectively). Despite the significant increase in urea level 1 h after EE compared to the baseline level with SM consumption (P < 0.001) and immediately and 1 h after EE compared to the baseline with LFCM consumption (P values 0.001, <0.001; respectively), the urea levels remained unchanged with water consumption. Cortisol level was decreased immediately and 1 h after EE in all three groups compared to the baseline (P < 0.001).</div></div><div><h3>Conclusions</h3><div>Drinking LFCM and water before the EE under overnight fasting conditions similarly stimulates lipolysis, as evidenced by comparable increases in glycerol level. Additionally, SM consumption appears to enhance anti-degradation pathways of muscle proteins compared to LFCM, based on lower urea levels post-exercise.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"55 ","pages":"Article 100603"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143777566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01Epub Date: 2025-04-17DOI: 10.1016/j.obmed.2025.100611
Rambu L.N.K.R. Triandhini , Ahmad Hamim Sadewa , Siti Helmiyati
Diabetes mellitus is a metabolic disorder and a major global health concern. This scoping review aimed to systematically map current data that describe the relationship between genetic variant interactions related to insulin secretion and diet with the incidence of type 2 diabetes mellitus. A literature search was conducted through PubMed, Cochrane, EBSCO, ProQuest, and hand searching. Thirteen eligible articles were obtained from 1375 searches in the database; TCF7L2 variants were the most frequently examined and demonstrated interactions with fiber, followed by the CDKAL1 gene variant, which showed interactions mainly with dietary components, such as fats, proteins, and coffee. Statistically significant findings were also reported for IGFBP2, NOTCH2, KCNJ11, GIPR, HFE, and ZBED3 variants. Nevertheless, most of these studies are yet to be replicated, and some findings indicated inconsistencies. Gene interactions related to insulin secretion and diet play important roles in the risk of type 2 diabetes, although further research is required to validate these findings.
{"title":"Exploring genes related to impaired insulin secretion and the interaction with diet in type 2 diabetes mellitus: A scoping review of observational studies","authors":"Rambu L.N.K.R. Triandhini , Ahmad Hamim Sadewa , Siti Helmiyati","doi":"10.1016/j.obmed.2025.100611","DOIUrl":"10.1016/j.obmed.2025.100611","url":null,"abstract":"<div><div>Diabetes mellitus is a metabolic disorder and a major global health concern. This scoping review aimed to systematically map current data that describe the relationship between genetic variant interactions related to insulin secretion and diet with the incidence of type 2 diabetes mellitus. A literature search was conducted through PubMed, Cochrane, EBSCO, ProQuest, and hand searching. Thirteen eligible articles were obtained from 1375 searches in the database; TCF7L2 variants were the most frequently examined and demonstrated interactions with fiber, followed by the CDKAL1 gene variant, which showed interactions mainly with dietary components, such as fats, proteins, and coffee. Statistically significant findings were also reported for IGFBP2, NOTCH2, KCNJ11, GIPR, HFE, and ZBED3 variants. Nevertheless, most of these studies are yet to be replicated, and some findings indicated inconsistencies. Gene interactions related to insulin secretion and diet play important roles in the risk of type 2 diabetes, although further research is required to validate these findings.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"55 ","pages":"Article 100611"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143859917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01Epub Date: 2025-05-13DOI: 10.1016/j.obmed.2025.100618
Fahad Alkhalfan , Naseer Sangwan , Anu Aggarwal , Alliefair Scalise , José O. Alemán , Bhairavi Rajasekar , Douglas Joseph , Kimberly Peterson , Annelise Hamer , Mariya Ali , John R. Bartholomew , Scott J. Cameron
Aims
Lipedema is a condition often mistaken for other causes of limb swelling including lymphedema and obesity. Lipedema may have a unique metabolic profile. Interrogation of the metabolome is a strategy that could reveal unique biomarkers to distinguish lipedema from lymphedema and obesity.
Methods
Unbiased metabolomics was utilized to examine 38 BMI-matched overweight patients compared with patients with lipedema, lymphedema, and lipolymphedema. Machine learning identified biomarkers to distinguish diseases, and further examined in a validation cohort of 198 patients with each disorders. Adjustments were made for baseline clinical and demographic variables.
Results
Plasma metabolomics firstly revealed uric acid as a biomarker that performs well to distinguish between phenotypically similar diseases in patients with elevated BMI. In a validation cohort of 64 patients with lipedema, uric acid (5.05 mg/dL) was compared with 64 patients with lymphedema (5.4 mg/dl), and 70 overweight patients without these conditions (4.6 mg/dL, p < 0.05). Uric acid-to-cystatin c ratio distinguished between all three groups (Lipedema: 5.2; Lymphedema: 6.3; overweight: 4.0, p < 0.01); however, significance was lost after adjustment for renal function.
Conclusion
Metabolomic analysis revealed uric acid may differentiate between lipedema, lymphedema, lipolymphedema and obese individuals without those conditions. In a validation cohort, while uric acid was higher in lipedema and lymphedema, uric acid adjusted by cystatin c clearance revealed uric acid to be a less useful marker to distinguish lipedema from lymphedema in the context of renal insufficiency.
目的:肢体水肿是一种经常被误认为肢体肿胀的其他原因,包括淋巴水肿和肥胖。脂水肿可能具有独特的代谢特征。代谢组的询问是一种策略,可以揭示独特的生物标志物,以区分脂水肿、淋巴水肿和肥胖。方法采用偏倚代谢组学方法对38例bmi匹配的超重患者与脂性水肿、淋巴水肿和脂性水肿患者进行比较。机器学习识别生物标志物以区分疾病,并在每种疾病的198名患者的验证队列中进一步检查。对基线临床和人口统计学变量进行了调整。结果血浆代谢组学首次揭示了尿酸作为一种生物标志物,能够很好地区分BMI升高患者的表型相似疾病。在64例脂水肿患者的验证队列中,尿酸(5.05 mg/dL)与64例淋巴水肿患者(5.4 mg/dL)和70例没有这些情况的超重患者(4.6 mg/dL, p <;0.05)。尿酸与胱抑素c比值在三组之间的差异(脂水肿:5.2;淋巴水肿:6.3;超重:4.0,p <;0.01);然而,在调整肾功能后,其意义就失去了。结论代谢组学分析显示尿酸可区分脂肪水肿、淋巴水肿、脂肪水肿和肥胖个体。在一个验证队列中,虽然尿酸在脂水肿和淋巴水肿中较高,但通过胱抑素c清除调节的尿酸显示,在肾功能不全的情况下,尿酸作为区分脂水肿和淋巴水肿的一个不太有用的标志物。
{"title":"Exploring uric acid as a biomarker in lipedema and lymphedema: A metabolomics study with prospective validation","authors":"Fahad Alkhalfan , Naseer Sangwan , Anu Aggarwal , Alliefair Scalise , José O. Alemán , Bhairavi Rajasekar , Douglas Joseph , Kimberly Peterson , Annelise Hamer , Mariya Ali , John R. Bartholomew , Scott J. Cameron","doi":"10.1016/j.obmed.2025.100618","DOIUrl":"10.1016/j.obmed.2025.100618","url":null,"abstract":"<div><h3>Aims</h3><div>Lipedema is a condition often mistaken for other causes of limb swelling including lymphedema and obesity. Lipedema may have a unique metabolic profile. Interrogation of the metabolome is a strategy that could reveal unique biomarkers to distinguish lipedema from lymphedema and obesity.</div></div><div><h3>Methods</h3><div>Unbiased metabolomics was utilized to examine 38 BMI-matched overweight patients compared with patients with lipedema, lymphedema, and lipolymphedema. Machine learning identified biomarkers to distinguish diseases, and further examined in a validation cohort of 198 patients with each disorders. Adjustments were made for baseline clinical and demographic variables.</div></div><div><h3>Results</h3><div>Plasma metabolomics firstly revealed uric acid as a biomarker that performs well to distinguish between phenotypically similar diseases in patients with elevated BMI. In a validation cohort of 64 patients with lipedema, uric acid (5.05 mg/dL) was compared with 64 patients with lymphedema (5.4 mg/dl), and 70 overweight patients without these conditions (4.6 mg/dL, p < 0.05). Uric acid-to-cystatin c ratio distinguished between all three groups (Lipedema: 5.2; Lymphedema: 6.3; overweight: 4.0, p < 0.01); however, significance was lost after adjustment for renal function.</div></div><div><h3>Conclusion</h3><div>Metabolomic analysis revealed uric acid may differentiate between lipedema, lymphedema, lipolymphedema and obese individuals without those conditions. In a validation cohort, while uric acid was higher in lipedema and lymphedema, uric acid adjusted by cystatin c clearance revealed uric acid to be a less useful marker to distinguish lipedema from lymphedema in the context of renal insufficiency.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"55 ","pages":"Article 100618"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144123719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}