Pub Date : 2025-09-01Epub Date: 2025-09-05DOI: 10.1016/j.obmed.2025.100644
Beatriz Bobbio de Brito , João Arthur Souza Fiorido , Doglas Gobbi Marchesi , Luís Carlos Lopes Júnior , Luciane Bresciani Salaroli , Blanca Elena Guerrero Daboin , Andressa Bolsoni Lopes , Fabiano Kenji Haraguchi
Aims
Phase angle (PhA), an indicator of cellular integrity and fluid balance, is underexplored in individuals with severe obesity, particularly during postoperative weight loss. This study evaluated PhA trajectories and their body composition determinants over 12 months following Roux-en-Y gastric bypass (RYGB).
Methods
Sixty participants meeting inclusion criteria were assessed at four time points: before surgery, and at 2, 6, and 12 months after RYGB. Body composition and PhA were evaluated at each follow-up. The Friedman test (α = 0.05) was used to examine changes over time. Spearman's correlation and multiple linear regression explored associations between PhA and body composition variables.
Results
PhA declined significantly after surgery and showed a consistent inverse association with the extracellular to intracellular water (ECW:ICW) ratio at all postoperative assessments (p < 0.05). Significant reductions were also observed in weight, BMI, waist circumference, fat mass, fat-free mass, and total body water (p < 0.05).
Conclusion
The ECW:ICW ratio was the primary determinant of PhA decline, reflecting fluid redistribution and early metabolic adaptation during rapid weight loss. PhA may serve as a practical marker for monitoring physiological responses to bariatric surgery.
{"title":"Phase angle decline after Roux-en-Y gastric bypass reflects fluid redistribution during the weight loss: A 12-month follow-up study","authors":"Beatriz Bobbio de Brito , João Arthur Souza Fiorido , Doglas Gobbi Marchesi , Luís Carlos Lopes Júnior , Luciane Bresciani Salaroli , Blanca Elena Guerrero Daboin , Andressa Bolsoni Lopes , Fabiano Kenji Haraguchi","doi":"10.1016/j.obmed.2025.100644","DOIUrl":"10.1016/j.obmed.2025.100644","url":null,"abstract":"<div><h3>Aims</h3><div>Phase angle (PhA), an indicator of cellular integrity and fluid balance, is underexplored in individuals with severe obesity, particularly during postoperative weight loss. This study evaluated PhA trajectories and their body composition determinants over 12 months following Roux-en-Y gastric bypass (RYGB).</div></div><div><h3>Methods</h3><div>Sixty participants meeting inclusion criteria were assessed at four time points: before surgery, and at 2, 6, and 12 months after RYGB. Body composition and PhA were evaluated at each follow-up. The Friedman test (α = 0.05) was used to examine changes over time. Spearman's correlation and multiple linear regression explored associations between PhA and body composition variables.</div></div><div><h3>Results</h3><div>PhA declined significantly after surgery and showed a consistent inverse association with the extracellular to intracellular water (ECW:ICW) ratio at all postoperative assessments (p < 0.05). Significant reductions were also observed in weight, BMI, waist circumference, fat mass, fat-free mass, and total body water (p < 0.05).</div></div><div><h3>Conclusion</h3><div>The ECW:ICW ratio was the primary determinant of PhA decline, reflecting fluid redistribution and early metabolic adaptation during rapid weight loss. PhA may serve as a practical marker for monitoring physiological responses to bariatric surgery.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"57 ","pages":"Article 100644"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145007700","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 role of Very Low-Energy Ketogenic Treatment (VLEKT) in managing type 2 diabetes mellitus (T2DM) remains underexplored. This retrospective, single-center study evaluated the effectiveness of a structured VLEKT protocol in achieving diabetes remission or improving glycemic control (reversal) in overweight and obese T2DM patients in a real-world setting.
Methods
Thirty-eight patients underwent a three-phase VLEKT intervention. The initial phase included three consecutive very low-energy ketogenic stages with calibrated meal replacements, aimed at reducing endogenous insulin secretion, stimulating lipolysis, and promoting fat loss. The second phase involved transitioning to a low-calorie diet and increased physical activity, followed by a maintenance phase to sustain metabolic benefits. Anthropometric data, HbA1c, and medication use were recorded at each visit.
Results
VLEKT significantly improved weight and glycemic control. After 6 months, 47.4 % of patients achieved diabetes remission, with 28.9 % maintaining remission at 2 years. Nearly half of the patients showed a trend toward remission within 3 months, based on early medication discontinuation and normalized glucose values, but this did not meet the formal criteria for remission. Shorter diabetes duration and fewer baseline glucose-lowering drugs predicted remission. The intervention also enabled sustained weight loss and reduced medication reliance over 18 months. Limitations include the retrospective design, small sample size, single-center scope, and potential selection bias due to self-funded participation.
Conclusion
VLEKT is a feasible, safe, and effective non-pharmacological approach to induce T2DM remission in routine clinical practice. These findings support integrating ketogenic nutritional protocols into multidisciplinary diabetes care, offering clinicians valuable alternatives to conventional drug therapies.
{"title":"Type 2 diabetes remission with very low-energy ketogenic treatment: a retrospective real-world study","authors":"Daniela Sofra , Maitane Nuñez-Garcia , Ignacio Sajoux , Massimiliano Caprio , Francesca Amati","doi":"10.1016/j.obmed.2025.100633","DOIUrl":"10.1016/j.obmed.2025.100633","url":null,"abstract":"<div><h3>Aims</h3><div>The role of Very Low-Energy Ketogenic Treatment (VLEKT) in managing type 2 diabetes mellitus (T2DM) remains underexplored. This retrospective, single-center study evaluated the effectiveness of a structured VLEKT protocol in achieving diabetes remission or improving glycemic control (reversal) in overweight and obese T2DM patients in a real-world setting.</div></div><div><h3>Methods</h3><div>Thirty-eight patients underwent a three-phase VLEKT intervention. The initial phase included three consecutive very low-energy ketogenic stages with calibrated meal replacements, aimed at reducing endogenous insulin secretion, stimulating lipolysis, and promoting fat loss. The second phase involved transitioning to a low-calorie diet and increased physical activity, followed by a maintenance phase to sustain metabolic benefits. Anthropometric data, HbA1c, and medication use were recorded at each visit.</div></div><div><h3>Results</h3><div>VLEKT significantly improved weight and glycemic control. After 6 months, 47.4 % of patients achieved diabetes remission, with 28.9 % maintaining remission at 2 years. Nearly half of the patients showed a trend toward remission within 3 months, based on early medication discontinuation and normalized glucose values, but this did not meet the formal criteria for remission. Shorter diabetes duration and fewer baseline glucose-lowering drugs predicted remission. The intervention also enabled sustained weight loss and reduced medication reliance over 18 months. Limitations include the retrospective design, small sample size, single-center scope, and potential selection bias due to self-funded participation.</div></div><div><h3>Conclusion</h3><div>VLEKT is a feasible, safe, and effective non-pharmacological approach to induce T2DM remission in routine clinical practice. These findings support integrating ketogenic nutritional protocols into multidisciplinary diabetes care, offering clinicians valuable alternatives to conventional drug therapies.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"57 ","pages":"Article 100633"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144655871","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 : 2025-09-01Epub Date: 2025-09-09DOI: 10.1016/j.obmed.2025.100647
Brittney J. Palermo , Katherine S. Wilkinson , Timothy B. Plante , Suzanne E. Judd , Debora Kamin Mukaz , D. Leann Long , Nels C. Olson , Melissa J. Smith , Mary Cushman
Background
Diabetes is a leading cause of morbidity and mortality in the United States, affecting Black more than White adults. The soluble receptor for advanced glycation end products (sRAGE) prevents signaling that induces inflammation and is implicated in diabetes pathogenesis. This analysis investigated if low sRAGE is associated with diabetes risk, and if sRAGE mediates the racial disparity in diabetes.
Methods
The REasons for Geographic and Racial Differences in Stroke prospective cohort included 30,239 Black and White adults aged ≥45 with baseline and follow up exam. We studied a 4400 participant sub-cohort with 9.5-year follow-up to classify diabetes, with analyses being survey weighted to the larger cohort. Baseline sRAGE was measured in 3400 at risk for diabetes; modified Poisson regression estimated relative risk (RR) by sRAGE. Inverse odds weighting mediation analysis examined the contribution of sRAGE to the racial disparity in diabetes.
Results
Ten percent of White and 18 % of Black participants experienced incident diabetes. The RR of diabetes was elevated in lower quartiles of sRAGE compared to the fourth quartile. With diabetes risk factor adjustment, the RR was 1.32 (95 % CI 0.97–1.79) in the lowest compared to the highest quartile (p-trend across quartiles 0.06). sRAGE did not mediate any of the racial disparity in diabetes.
Conclusions
Among Black and White Americans, low sRAGE was associated with increased risk of developing diabetes; associations attenuated and became non-significant with covariate adjustment. sRAGE may serve as a marker for diabetes risk, but clinical utility is unlikely given small non-significant associations, and no identified mediation of the association by sRAGE.
背景:糖尿病是美国发病率和死亡率的主要原因,对黑人的影响大于白人。晚期糖基化终产物的可溶性受体(sRAGE)阻止诱导炎症的信号传导,并参与糖尿病的发病机制。该分析调查了低sRAGE是否与糖尿病风险相关,以及sRAGE是否介导了糖尿病的种族差异。方法对30239名年龄≥45岁的黑人和白人进行卒中前瞻性队列研究,并进行基线和随访检查。我们研究了4400名参与者的亚队列,随访9.5年,对糖尿病进行分类,并对更大的队列进行调查加权分析。在3400名有糖尿病风险的患者中测量了基线sRAGE;修正泊松回归用sRAGE估计相对危险度(RR)。反向优势加权中介分析检验了sRAGE对糖尿病种族差异的贡献。结果:10%的白人和18%的黑人参与者经历了偶发性糖尿病。与第四个四分位数相比,低四分位数的sRAGE中糖尿病的RR升高。调整糖尿病危险因素后,与最高四分位数相比,最低四分位数的RR为1.32 (95% CI 0.97-1.79)(四分位数的p趋势为0.06)。sRAGE并没有调节糖尿病的种族差异。结论:在美国黑人和白人中,低sRAGE与患糖尿病的风险增加有关;协变量调整后,相关性减弱并变得不显著。sRAGE可以作为糖尿病风险的标记物,但由于较小的非显著相关性,并且没有确定sRAGE的关联中介,因此临床应用不太可能。
{"title":"Soluble receptor for advanced glycation end products and diabetes in Black and White Americans: the REGARDS study","authors":"Brittney J. Palermo , Katherine S. Wilkinson , Timothy B. Plante , Suzanne E. Judd , Debora Kamin Mukaz , D. Leann Long , Nels C. Olson , Melissa J. Smith , Mary Cushman","doi":"10.1016/j.obmed.2025.100647","DOIUrl":"10.1016/j.obmed.2025.100647","url":null,"abstract":"<div><h3>Background</h3><div>Diabetes is a leading cause of morbidity and mortality in the United States, affecting Black more than White adults. The soluble receptor for advanced glycation end products (sRAGE) prevents signaling that induces inflammation and is implicated in diabetes pathogenesis. This analysis investigated if low sRAGE is associated with diabetes risk, and if sRAGE mediates the racial disparity in diabetes.</div></div><div><h3>Methods</h3><div>The REasons for Geographic and Racial Differences in Stroke prospective cohort included 30,239 Black and White adults aged ≥45 with baseline and follow up exam. We studied a 4400 participant sub-cohort with 9.5-year follow-up to classify diabetes, with analyses being survey weighted to the larger cohort. Baseline sRAGE was measured in 3400 at risk for diabetes; modified Poisson regression estimated relative risk (RR) by sRAGE. Inverse odds weighting mediation analysis examined the contribution of sRAGE to the racial disparity in diabetes.</div></div><div><h3>Results</h3><div>Ten percent of White and 18 % of Black participants experienced incident diabetes. The RR of diabetes was elevated in lower quartiles of sRAGE compared to the fourth quartile. With diabetes risk factor adjustment, the RR was 1.32 (95 % CI 0.97–1.79) in the lowest compared to the highest quartile (p-trend across quartiles 0.06). sRAGE did not mediate any of the racial disparity in diabetes.</div></div><div><h3>Conclusions</h3><div>Among Black and White Americans, low sRAGE was associated with increased risk of developing diabetes; associations attenuated and became non-significant with covariate adjustment. sRAGE may serve as a marker for diabetes risk, but clinical utility is unlikely given small non-significant associations, and no identified mediation of the association by sRAGE.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"57 ","pages":"Article 100647"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145048332","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}
Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder, affecting 5–10 % of women of reproductive age, and is characterized by complex etiology involving reproductive and metabolic disturbances. The core clinical features include anovulation, irregular ovulation, polycystic ovarian morphology, and hyperandrogenism (HA), with frequent accompaniments of metabolic dysfunctions such as dyslipidemia, insulin resistance (IR), abdominal obesity, and impaired glucose metabolism. The available evidence shows significant involvement of gut microbiota in the pathogenesis and progression of PCOS. Alterations in gut, PCOS axis-including changes in gut microbiota composition as contributed by such alterations in the pathogenesis of PCOS and its complications like obesity, IR, and type 2 diabetes mellitus (T2DM), will be discussed in this review. This review covers such aspects that gut dysbiosis, HA, chronic inflammation, and non-alcoholic fatty liver disease are related to the pathology of PCOS, thereby amplifying it. Lifestyle-related interventions include physical activity, yoga, therapeutic strategies in terms of gut microbiota including fecal microbiota transplantation (FMT), prebiotics, probiotics, synbiotics, and psychobiotics, which are reviewed for improving metabolic as well as reproductive outcomes in PCOS. Rather, this review focuses on the pressing need for further research into understanding the roles of gut microbiota in PCOS as well as optimizing gut-targeted therapies aimed at better managing this complex condition.
{"title":"Microbial dysbiosis, obesity, and insulin Resistance: Understanding gut-ovary association in polycystic ovary syndrome","authors":"Suparna Parua , Anukona Hazra , Krishnendu Adhikary , Krishnendu Ganguly , Deepika Ahuja , Rajkumar Maiti , Lipika Das Mukhopadhyay , Sulagna Dutta , Pragati Panda , Koushik Bhattacharya , Pallav Sengupta , Alak Kumar Syamal","doi":"10.1016/j.obmed.2025.100626","DOIUrl":"10.1016/j.obmed.2025.100626","url":null,"abstract":"<div><div>Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder, affecting 5–10 % of women of reproductive age, and is characterized by complex etiology involving reproductive and metabolic disturbances. The core clinical features include anovulation, irregular ovulation, polycystic ovarian morphology, and hyperandrogenism (HA), with frequent accompaniments of metabolic dysfunctions such as dyslipidemia, insulin resistance (IR), abdominal obesity, and impaired glucose metabolism. The available evidence shows significant involvement of gut microbiota in the pathogenesis and progression of PCOS. Alterations in gut, PCOS axis-including changes in gut microbiota composition as contributed by such alterations in the pathogenesis of PCOS and its complications like obesity, IR, and type 2 diabetes mellitus (T2DM), will be discussed in this review. This review covers such aspects that gut dysbiosis, HA, chronic inflammation, and non-alcoholic fatty liver disease are related to the pathology of PCOS, thereby amplifying it. Lifestyle-related interventions include physical activity, yoga, therapeutic strategies in terms of gut microbiota including fecal microbiota transplantation (FMT), prebiotics, probiotics, synbiotics, and psychobiotics, which are reviewed for improving metabolic as well as reproductive outcomes in PCOS. Rather, this review focuses on the pressing need for further research into understanding the roles of gut microbiota in PCOS as well as optimizing gut-targeted therapies aimed at better managing this complex condition.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"56 ","pages":"Article 100626"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144481420","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: 2025-06-09DOI: 10.1016/j.obmed.2025.100622
Esther Ugo Alum , David Chukwu Obasi , Jacinta Nnennaya Abba , Ugonna Cassandra Aniokete , Prince Nkemakolam Okoroh , Ada Ak Akwari
The global prevalence of diabetes is on the rise, necessitating advanced strategies for effective management. Nutrition therapy plays a critical role in managing diabetes, contributing to glycemic control, weight regulation, and complication prevention. Historically centered around carbohydrate counting and standardized meal plans, nutrition strategies have evolved toward more flexible, patient-centered approaches. Emerging evidence underscores the importance of individualized dietary interventions tailored to patients’ cultural preferences, metabolic profiles, and comorbid conditions. Approaches such as the Mediterranean diet, Dietary Approaches to Stop Hypertension (DASH), and plant-based diets have demonstrated significant benefits in both type 1 and type 2 diabetes. The integration of digital tools, behavioral science, and emerging insights from nutrigenomics and the gut microbiome further supports a paradigm shift toward precision nutrition. In this commentary, we highlight the evolution of nutrition therapy in diabetes care, emphasizing the transition from generic recommendations to personalized dietary strategies aimed at improving long-term outcomes. It emphasizes the potential of precision nutrition to optimize glycemic control, mitigate complications, and improve patient adherence. We argue that the future of diabetes care depends on a personalized nutrition model that accounts for metabolic individuality, cultural context, and digital health integration. Our discussion highlights a critical transition in practice and research priorities, offering a timely framework for clinicians and policymakers navigating the evolving landscape of diabetes management. Peer-reviewed articles, clinical guidelines, and systematic reviews were sourced from databases such as PubMed, Scopus, and Google Scholar. The analysis focused on studies evaluating carbohydrate counting, personalized nutrition, and their respective impacts on glycemic control and patient outcomes. Key topics included advancements in nutrigenomics, metabolomics, and the integration of precision medicine in dietary interventions. The findings were synthesized to highlight current challenges, emerging trends, and potential solutions in implementing personalized nutrition strategies for diabetes care.
{"title":"Evolving paradigms in nutrition therapy for Diabetes: From carbohydrate counting to precision diets","authors":"Esther Ugo Alum , David Chukwu Obasi , Jacinta Nnennaya Abba , Ugonna Cassandra Aniokete , Prince Nkemakolam Okoroh , Ada Ak Akwari","doi":"10.1016/j.obmed.2025.100622","DOIUrl":"10.1016/j.obmed.2025.100622","url":null,"abstract":"<div><div>The global prevalence of diabetes is on the rise, necessitating advanced strategies for effective management. Nutrition therapy plays a critical role in managing diabetes, contributing to glycemic control, weight regulation, and complication prevention. Historically centered around carbohydrate counting and standardized meal plans, nutrition strategies have evolved toward more flexible, patient-centered approaches. Emerging evidence underscores the importance of individualized dietary interventions tailored to patients’ cultural preferences, metabolic profiles, and comorbid conditions. Approaches such as the Mediterranean diet, Dietary Approaches to Stop Hypertension (DASH), and plant-based diets have demonstrated significant benefits in both type 1 and type 2 diabetes. The integration of digital tools, behavioral science, and emerging insights from nutrigenomics and the gut microbiome further supports a paradigm shift toward precision nutrition. In this commentary, we highlight the evolution of nutrition therapy in diabetes care, emphasizing the transition from generic recommendations to personalized dietary strategies aimed at improving long-term outcomes. It emphasizes the potential of precision nutrition to optimize glycemic control, mitigate complications, and improve patient adherence. We argue that the future of diabetes care depends on a personalized nutrition model that accounts for metabolic individuality, cultural context, and digital health integration. Our discussion highlights a critical transition in practice and research priorities, offering a timely framework for clinicians and policymakers navigating the evolving landscape of diabetes management. Peer-reviewed articles, clinical guidelines, and systematic reviews were sourced from databases such as PubMed, Scopus, and Google Scholar. The analysis focused on studies evaluating carbohydrate counting, personalized nutrition, and their respective impacts on glycemic control and patient outcomes. Key topics included advancements in nutrigenomics, metabolomics, and the integration of precision medicine in dietary interventions. The findings were synthesized to highlight current challenges, emerging trends, and potential solutions in implementing personalized nutrition strategies for diabetes care.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"56 ","pages":"Article 100622"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144270538","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: 2025-07-11DOI: 10.1016/j.obmed.2025.100632
Reem M. Al Haj Ahmad , Dalia M. Abu Al-Haijaa
Obesity adversely impacts the quality of life; people with obesity are more vulnerable to chronic diseases such as T2DM, insulin resistance, and dementia. Brain-derived neurotrophic factor (BDNF) has a significant role in cognition and brain health; it influences synaptic plasticity and neurogenesis. BDNF has been proposed as mechanistic a modulator to explain the association between peripheral dysmetabolism and cognitive decline. This review highlights the metabolic alterations associated with obesity including, insulin resistance, inflammation, and BDNF levels. It illustrates, as well, the mechanistic crosstalk between adiposity and the decline of brain health and cognition explained by the BDNF alteration. A narrative review of the recent research focusing on BDNF molecular biology and functions, the effect of obesity on its regulation, and neuronal health and cognition during obesity and its allied metabolic changes. Although the results of the related published research were contradicted, obesity was related to BDNF expression and signaling dysregulation. This dysregulation leads to neuroinflammation a condition that impairs synaptic plasticity and neurogenesis, and increases apoptosis. These fluctuations were linked to cognitive decline and different types of neurodegeneration. Insulin resistance and hyperinsulinemia were the main hubs for connecting adiposity, BDNF, and dementia. Correction of BDNF expression and signaling may offer an evolving therapeutic practice for the treatment and prevention of obesity-related cognitive decline. Further longitudinal and clinical trial studies are needed to clarify the causal direction and expand our vision of treatment and prevention regimes for cognitive disorders.
{"title":"Molecular mechanisms underlying obesity-altered brain functions: the alteration of BDNF production","authors":"Reem M. Al Haj Ahmad , Dalia M. Abu Al-Haijaa","doi":"10.1016/j.obmed.2025.100632","DOIUrl":"10.1016/j.obmed.2025.100632","url":null,"abstract":"<div><div>Obesity adversely impacts the quality of life; people with obesity are more vulnerable to chronic diseases such as T2DM, insulin resistance, and dementia. Brain-derived neurotrophic factor (BDNF) has a significant role in cognition and brain health; it influences synaptic plasticity and neurogenesis. BDNF has been proposed as mechanistic a modulator to explain the association between peripheral dysmetabolism and cognitive decline. This review highlights the metabolic alterations associated with obesity including, insulin resistance, inflammation, and BDNF levels. It illustrates, as well, the mechanistic crosstalk between adiposity and the decline of brain health and cognition explained by the BDNF alteration. A narrative review of the recent research focusing on BDNF molecular biology and functions, the effect of obesity on its regulation, and neuronal health and cognition during obesity and its allied metabolic changes. Although the results of the related published research were contradicted, obesity was related to BDNF expression and signaling dysregulation. This dysregulation leads to neuroinflammation a condition that impairs synaptic plasticity and neurogenesis, and increases apoptosis. These fluctuations were linked to cognitive decline and different types of neurodegeneration. Insulin resistance and hyperinsulinemia were the main hubs for connecting adiposity, BDNF, and dementia. Correction of BDNF expression and signaling may offer an evolving therapeutic practice for the treatment and prevention of obesity-related cognitive decline. Further longitudinal and clinical trial studies are needed to clarify the causal direction and expand our vision of treatment and prevention regimes for cognitive disorders.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"56 ","pages":"Article 100632"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144623779","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: 2025-05-24DOI: 10.1016/j.obmed.2025.100621
Momin Aramash , Manisha N. Chalse , Aniroodha V. Pethkar , Urmila M. Aswar
Background and aims
Diabetic nephropathy (DN) is a major disorder of prolonged diabetes mellitus (DM) which ends up in chronic renal failure. Here, we report the beneficial effects of copper oxide nanoparticles loaded with Syzygium aromaticum extract (SaCuONpls) on DN in Wistar rats. Syzygium aromaticum is a spice with numerous therapeutic uses. Altered copper concentration in the blood is responsible for various diseases and affects different organs. Moreover minor copper deficiencies can promote the progression of many pathologies including DM.
Methods
Diabetes induced nephropathy was produced by administration of nicotinamide and streptozotocin. Rats with a blood glucose of more than 250 mg/dL were considered hyperglycemic. Diabetic rats were left untreated for 42 days for the development of nephropathy that was characterized by a marked decline in urine creatinine levels and increased levels of microproteinuria. The nephropathic rats were orally treated with SaCuONpls (2.5, 5, and 10 mg/kg) and the standard drug, glimepiride (10 mg/kg) for 42 days. At the end of the experiment, the serum parameters, urine parameters, oxidative stress, and inflammatory markers were studied and kidneys were removed for histology (H&E, PAS, and MT staining).
Results
Treatment of SaCuONpls significantly improved the serum and urine biochemistry, antioxidant potential by increasing activity of SOD, CAT and GSH and declined the oxidative stress mediated by MDA and NO and the ameliorative effect of proinflammatory mediators (NF-κB, TNF-α, IL-1β and IL-6) was noticed. SaCuONpls mitigated adverse histopathological changes.
Conclusions
The therapeutic potential of SaCuONpls was ascertained by enhanced renal function.
{"title":"Syzygium aromaticum loaded copper oxide nanoparticles ameliorates diabetic nephropathy by diminishing oxidative stress and inflammatory responses in Wistar rats","authors":"Momin Aramash , Manisha N. Chalse , Aniroodha V. Pethkar , Urmila M. Aswar","doi":"10.1016/j.obmed.2025.100621","DOIUrl":"10.1016/j.obmed.2025.100621","url":null,"abstract":"<div><h3>Background and aims</h3><div>Diabetic nephropathy (DN) is a major disorder of prolonged diabetes mellitus (DM) which ends up in chronic renal failure. Here, we report the beneficial effects of copper oxide nanoparticles loaded with <em>Syzygium aromaticum</em> extract (SaCuONpls) on DN in Wistar rats. <em>Syzygium aromaticum</em> is a spice with numerous therapeutic uses. Altered copper concentration in the blood is responsible for various diseases and affects different organs. Moreover minor copper deficiencies can promote the progression of many pathologies including DM.</div></div><div><h3>Methods</h3><div>Diabetes induced nephropathy was produced by administration of nicotinamide and streptozotocin. Rats with a blood glucose of more than 250 mg/dL were considered hyperglycemic. Diabetic rats were left untreated for 42 days for the development of nephropathy that was characterized by a marked decline in urine creatinine levels and increased levels of microproteinuria. The nephropathic rats were orally treated with SaCuONpls (2.5, 5, and 10 mg/kg) and the standard drug, glimepiride (10 mg/kg) for 42 days. At the end of the experiment, the serum parameters, urine parameters, oxidative stress, and inflammatory markers were studied and kidneys were removed for histology (H&E, PAS, and MT staining).</div></div><div><h3>Results</h3><div>Treatment of SaCuONpls significantly improved the serum and urine biochemistry, antioxidant potential by increasing activity of SOD, CAT and GSH and declined the oxidative stress mediated by MDA and NO and the ameliorative effect of proinflammatory mediators (NF-κB, TNF-α, IL-1β and IL-6) was noticed. SaCuONpls mitigated adverse histopathological changes.</div></div><div><h3>Conclusions</h3><div>The therapeutic potential of SaCuONpls was ascertained by enhanced renal function.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"56 ","pages":"Article 100621"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144137885","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: 2025-07-08DOI: 10.1016/j.obmed.2025.100629
Gnanaprakash Jeyaraj
Diabetes mellitus (DM) is a major risk factor for atherosclerotic cardiovascular disease (ASCVD), driven by complex metabolic and inflammatory pathways. Among these, the NLRP3 inflammasome has emerged as a crucial mediator linking hyperglycemia, oxidative stress, and chronic inflammation to vascular dysfunction. Dyslipidemia, endothelial dysfunction, and excessive reactive oxygen species (ROS) production further exacerbate plaque formation and cardiovascular complications. Recent cardiovascular outcome trials (CVOTs) highlight the cardioprotective benefits of sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1 RAs), while novel anti-inflammatory strategies, including IL-1β inhibition and NLRP3-targeting agents, offer promising therapeutic avenues. This review explores the molecular mechanisms underlying diabetic atherosclerosis, with a unique emphasis on the role of the NLRP3 inflammasome in disease progression and how targeted interventions including SGLT2 inhibitors, GLP-1 receptor agonists, and emerging NLRP3-modulating agents can be integrated with precision medicine strategies. Unlike existing reviews, we highlight how genomic, epigenetic, and phenotypic stratification can guide combination therapies to optimize cardiovascular protection. Integrating individualized anti-inflammatory and metabolic interventions may provide tailored cardiovascular care, reducing morbidity and mortality in diabetic patients. Future research should focus on refining these personalized approaches to mitigate diabetes-associated cardiovascular complications.
{"title":"Cardiovascular complications in Diabetes: The role of NLRP3 inflammasome and targeted interventions","authors":"Gnanaprakash Jeyaraj","doi":"10.1016/j.obmed.2025.100629","DOIUrl":"10.1016/j.obmed.2025.100629","url":null,"abstract":"<div><div>Diabetes mellitus (DM) is a major risk factor for atherosclerotic cardiovascular disease (ASCVD), driven by complex metabolic and inflammatory pathways. Among these, the NLRP3 inflammasome has emerged as a crucial mediator linking hyperglycemia, oxidative stress, and chronic inflammation to vascular dysfunction. Dyslipidemia, endothelial dysfunction, and excessive reactive oxygen species (ROS) production further exacerbate plaque formation and cardiovascular complications. Recent cardiovascular outcome trials (CVOTs) highlight the cardioprotective benefits of sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1 RAs), while novel anti-inflammatory strategies, including IL-1β inhibition and NLRP3-targeting agents, offer promising therapeutic avenues. This review explores the molecular mechanisms underlying diabetic atherosclerosis, with a unique emphasis on the role of the NLRP3 inflammasome in disease progression and how targeted interventions including SGLT2 inhibitors, GLP-1 receptor agonists, and emerging NLRP3-modulating agents can be integrated with precision medicine strategies. Unlike existing reviews, we highlight how genomic, epigenetic, and phenotypic stratification can guide combination therapies to optimize cardiovascular protection. Integrating individualized anti-inflammatory and metabolic interventions may provide tailored cardiovascular care, reducing morbidity and mortality in diabetic patients. Future research should focus on refining these personalized approaches to mitigate diabetes-associated cardiovascular complications.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"56 ","pages":"Article 100629"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144605145","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: 2025-07-10DOI: 10.1016/j.obmed.2025.100628
Nadia J. Sweis , Manal Said Qarain , Sanjay Marasini
Background
Child obesity is a serious public health concern and is known to cause a significant burden on health care costs across the world. This systematic review aimed to determine the cost of care for child obesity during 2015–2024.
Method
MEDLINE, Embase, Scopus and Cochrane CENTRAL were searched on November 15, 2024 to identify original articles conducted in children and adolescents (aged 0–20 years) which reported the costs of care of children with obesity and without obesity. The outcome measures included relative and direct costs of care attributed to child obesity.
Results
In total, 745 studies that reported obesity were identified, of which eight studies were included in the qualitative synthesis. The included studies had either used the real-world data collected from different data sources (database studies, n = 5) or epidemiological and economic sources (modeling studies, n = 3) to estimate medical care expenditure. The relative costs of care were 35 % higher and direct of care were between 0.4 % and 88 % higher in children with obesity than normal weight children. In absolute terms, the excess costs (USD, 2024) for treating overweight and children with obesity ranged from $32.44 to $1225.35. The annual per capita health care costs (USD) differed across countries, which was attributed to methodological differences in cost estimation and durations of the studies.
Conclusion
Childhood obesity incurs country specific higher direct costs of care.
{"title":"Direct medical costs of childhood obesity during 2015–2024: A systematic review","authors":"Nadia J. Sweis , Manal Said Qarain , Sanjay Marasini","doi":"10.1016/j.obmed.2025.100628","DOIUrl":"10.1016/j.obmed.2025.100628","url":null,"abstract":"<div><h3>Background</h3><div>Child obesity is a serious public health concern and is known to cause a significant burden on health care costs across the world. This systematic review aimed to determine the cost of care for child obesity during 2015–2024.</div></div><div><h3>Method</h3><div>MEDLINE, Embase, Scopus and Cochrane CENTRAL were searched on November 15, 2024 to identify original articles conducted in children and adolescents (aged 0–20 years) which reported the costs of care of children with obesity and without obesity. The outcome measures included relative and direct costs of care attributed to child obesity.</div></div><div><h3>Results</h3><div>In total, 745 studies that reported obesity were identified, of which eight studies were included in the qualitative synthesis. The included studies had either used the real-world data collected from different data sources (database studies, n = 5) or epidemiological and economic sources (modeling studies, n = 3) to estimate medical care expenditure. The relative costs of care were 35 % higher and direct of care were between 0.4 % and 88 % higher in children with obesity than normal weight children. In absolute terms, the excess costs (USD, 2024) for treating overweight and children with obesity ranged from $32.44 to $1225.35. The annual per capita health care costs (USD) differed across countries, which was attributed to methodological differences in cost estimation and durations of the studies.</div></div><div><h3>Conclusion</h3><div>Childhood obesity incurs country specific higher direct costs of care.</div></div>","PeriodicalId":37876,"journal":{"name":"Obesity Medicine","volume":"56 ","pages":"Article 100628"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144631365","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}