Pub Date : 2026-01-17DOI: 10.1016/j.endmts.2026.100289
Fatima Lami Ciroma , Sarah Nuhu Kase , Amaechi Dennis , Christy Chinyere Fredrick , Maryam Baraka Akor-Dewu , Joseph O. Ayo , Umar A. Muhammad , Ogenetega ThankGod Oweh , Garba Ninani , Ini Patrick Ekpe
Background
Metabolic syndrome (MS) is a cluster of clinical abnormalities that increases the risk of cardiovascular diseases as well as type 2 diabetes mellitus. Adiponectin, an energy-regulating hormone secreted by adipocytes, has been implicated in metabolic health and may be inversely related to MS. This cross-sectional study assessed serum adiponectin levels and the prevalence of MS among adults in a Nigerian university community.
Methodology
A total of 273 participants (181 males, 92 females) were evaluated. Serum adiponectin was measured using ELISA, anthropometric indices were recorded using standard protocols, and BMI was used to categorize participants into normal, overweight, and obese groups.
Results
Descriptive statistics were presented as means ± standard deviation. Chi-square analysis assessed the association between sex and MS. Independent t-tests compared adiponectin levels across BMI categories and between participants with and without MS. A p-value < 0.05 (p < 0.05) was considered statistically significant. Similar (p > 0.05) Adiponectin levels were seen between normal and obese males (p = 0.890) or females (p = 0.448), nor between individuals with and without MS (p = 0.949). The overall prevalence of MS was 11.7%, with a significantly higher prevalence in females (20.7%) than males (7.2%) (p = 0.001). Females had higher odds of developing MS (OR = 2.875; 95% CI: 1.487–5.560).
Conclusion
While MS was more prevalent among females, serum adiponectin levels were not significantly influenced by BMI or MS status. Further research is recommended to better understand adiponectin's role in MS within this population.
{"title":"Adiponectin levels and metabolic syndrome: Sex-based insights from a Nigerian university community","authors":"Fatima Lami Ciroma , Sarah Nuhu Kase , Amaechi Dennis , Christy Chinyere Fredrick , Maryam Baraka Akor-Dewu , Joseph O. Ayo , Umar A. Muhammad , Ogenetega ThankGod Oweh , Garba Ninani , Ini Patrick Ekpe","doi":"10.1016/j.endmts.2026.100289","DOIUrl":"10.1016/j.endmts.2026.100289","url":null,"abstract":"<div><h3>Background</h3><div>Metabolic syndrome (MS) is a cluster of clinical abnormalities that increases the risk of cardiovascular diseases as well as type 2 diabetes mellitus. Adiponectin, an energy-regulating hormone secreted by adipocytes, has been implicated in metabolic health and may be inversely related to MS. This cross-sectional study assessed serum adiponectin levels and the prevalence of MS among adults in a Nigerian university community.</div></div><div><h3>Methodology</h3><div>A total of 273 participants (181 males, 92 females) were evaluated. Serum adiponectin was measured using ELISA, anthropometric indices were recorded using standard protocols, and BMI was used to categorize participants into normal, overweight, and obese groups.</div></div><div><h3>Results</h3><div>Descriptive statistics were presented as means ± standard deviation. Chi-square analysis assessed the association between sex and MS. Independent <em>t</em>-tests compared adiponectin levels across BMI categories and between participants with and without MS. A p-value < 0.05 (p < 0.05) was considered statistically significant. Similar (p > 0.05) Adiponectin levels were seen between normal and obese males (p = 0.890) or females (p = 0.448), nor between individuals with and without MS (p = 0.949). The overall prevalence of MS was 11.7%, with a significantly higher prevalence in females (20.7%) than males (7.2%) (p = 0.001). Females had higher odds of developing MS (OR = 2.875; 95% CI: 1.487–5.560).</div></div><div><h3>Conclusion</h3><div>While MS was more prevalent among females, serum adiponectin levels were not significantly influenced by BMI or MS status. Further research is recommended to better understand adiponectin's role in MS within this population.</div></div>","PeriodicalId":34427,"journal":{"name":"Endocrine and Metabolic Science","volume":"20 ","pages":"Article 100289"},"PeriodicalIF":0.0,"publicationDate":"2026-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146037670","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 : 2026-01-03DOI: 10.1016/j.endmts.2025.100288
Mohammad Shamsher Ali , Md. Jubaidul Islam , Akio Ebihara , A.H.M. Nurun Nabi
Type 2 diabetes mellitus (T2DM) exhibits noticeable ethnic disparities in prevalence, pathophysiology, and treatment response. Nuclear genome-wide association studies explain only a fraction of T2DM heritability. Mitochondrial DNA (mtDNA) variants, copy number alterations, and haplogroups have been implicated in disease susceptibility, but prior evidence has been inconsistent and population-specific. We systematically searched seven databases (PubMed, Embase, Web of Science, Google Scholar, ScienceDirect, Scopus, CNKI) from 1998 to 2025, following PRISMA 2020 guidelines. Qualified studies included investigations of mtDNA variants, copy number, and haplogroups in relation to T2DM. Two authors independently screened, extracted data, and assessed quality using the Newcastle-Ottawa Scale and the Q-Genie tool specific to genetic association studies. Sensitivity analyses were conducted restricting to studies meeting key genetic quality criteria: Hardy-Weinberg equilibrium testing, population stratification control, and multiple testing corrections. Random-effects meta-analyses and subgroup analyses were conducted. From a systematic review of 48 studies (comprising of 28,178 participants), we identified 30 studies (24,467 participants) suitable for quantitative meta-analysis. Higher mtDNA copy number has been found to play protective role against developing T2D i.e., risk of T2DM increases by 32 % with each unit decrease in mtDNA-copy number [OR = 0.68 (95 % CI: 0.52–0.89, p = 0.005] with moderate heterogeneity (I2 = 64 %). This association was consistent across European, Asian, and American populations. Variant A3243G represented the most pathogenic variant across all populations (OR = 3.45). We also identified associations of novel D-loop variant T16189C that were stronger in Asian populations (OR = 1.31, p = 0.001). Haplogroup N9a was protective in East Asians (OR = 0.71) conferring 29 % protection. Mechanistic observation highlighted impaired oxidative phosphorylation, elevated reactive oxygen species, and inflammatory activation. This seven-database meta-analysis provides the most definitive evidence to date for mtDNA contributions to T2DM, demonstrating universal copy number effects and ancestry-dependent variant associations. Findings support the integration of mtDNA biomarkers into risk prediction, ancestry-informed clinical algorithms, and pharmacogenomic strategies, offering a pathway toward precision medicine in diabetes prevention and management.
2型糖尿病（T2DM）在患病率、病理生理和治疗反应方面表现出明显的种族差异。核全基因组关联研究只能解释T2DM遗传的一小部分。线粒体DNA （mtDNA）变异、拷贝数改变和单倍群与疾病易感性有关，但先前的证据不一致，且具有人群特异性。我们按照PRISMA 2020指南，从1998年到2025年系统检索了7个数据库（PubMed、Embase、Web of Science、b谷歌Scholar、ScienceDirect、Scopus、CNKI）。合格的研究包括mtDNA变异、拷贝数和与T2DM相关的单倍群的调查。两位作者独立筛选、提取数据，并使用纽卡斯尔-渥太华量表和Q-Genie工具评估遗传关联研究的质量。敏感性分析仅限于满足关键遗传质量标准的研究：Hardy-Weinberg平衡检验、群体分层控制和多重检验校正。进行随机效应荟萃分析和亚组分析。从48项研究（包括28,178名受试者）的系统综述中，我们确定了30项研究（24,467名受试者）适合进行定量荟萃分析。较高的mtDNA拷贝数已被发现对发生T2D起保护作用，即mtDNA拷贝数每减少一个单位，T2DM的风险增加32% [OR = 0.68 (95% CI: 0.52-0.89, p = 0.005]，具有中等异质性（I2 = 64%）。这种关联在欧洲、亚洲和美洲人群中都是一致的。变异A3243G是所有人群中致病性最高的变异（OR = 3.45）。我们还发现，新型D-loop变体T16189C在亚洲人群中的相关性更强（OR = 1.31, p = 0.001）。单倍群N9a对东亚人具有保护作用（OR = 0.71），保护率为29%。机制观察强调氧化磷酸化受损，活性氧升高和炎症活化。这项包含7个数据库的荟萃分析为mtDNA对T2DM的影响提供了迄今为止最明确的证据，证明了普遍的拷贝数效应和依赖于祖先的变异关联。研究结果支持将mtDNA生物标志物整合到风险预测、基于祖先的临床算法和药物基因组学策略中，为糖尿病预防和管理的精准医学提供了一条途径。
{"title":"Mitochondrial DNA variants, copy number and haplogroups in type 2 diabetes: A systematic review and meta-analysis in different ethnic population","authors":"Mohammad Shamsher Ali , Md. Jubaidul Islam , Akio Ebihara , A.H.M. Nurun Nabi","doi":"10.1016/j.endmts.2025.100288","DOIUrl":"10.1016/j.endmts.2025.100288","url":null,"abstract":"<div><div>Type 2 diabetes mellitus (T2DM) exhibits noticeable ethnic disparities in prevalence, pathophysiology, and treatment response. Nuclear genome-wide association studies explain only a fraction of T2DM heritability. Mitochondrial DNA (mtDNA) variants, copy number alterations, and haplogroups have been implicated in disease susceptibility, but prior evidence has been inconsistent and population-specific. We systematically searched seven databases (PubMed, Embase, Web of Science, Google Scholar, ScienceDirect, Scopus, CNKI) from 1998 to 2025, following PRISMA 2020 guidelines. Qualified studies included investigations of mtDNA variants, copy number, and haplogroups in relation to T2DM. Two authors independently screened, extracted data, and assessed quality using the Newcastle-Ottawa Scale and the Q-Genie tool specific to genetic association studies. Sensitivity analyses were conducted restricting to studies meeting key genetic quality criteria: Hardy-Weinberg equilibrium testing, population stratification control, and multiple testing corrections. Random-effects meta-analyses and subgroup analyses were conducted. From a systematic review of 48 studies (comprising of 28,178 participants), we identified 30 studies (24,467 participants) suitable for quantitative meta-analysis. Higher mtDNA copy number has been found to play protective role against developing T2D i.e., risk of T2DM increases by 32 % with each unit decrease in mtDNA-copy number [OR = 0.68 (95 % CI: 0.52–0.89, <em>p</em> = 0.005] with moderate heterogeneity (I<sup>2</sup> = 64 %). This association was consistent across European, Asian, and American populations. Variant A3243G represented the most pathogenic variant across all populations (OR = 3.45). We also identified associations of novel D-loop variant T16189C that were stronger in Asian populations (OR = 1.31, <em>p</em> = 0.001). Haplogroup N9a was protective in East Asians (OR = 0.71) conferring 29 % protection. Mechanistic observation highlighted impaired oxidative phosphorylation, elevated reactive oxygen species, and inflammatory activation. This seven-database meta-analysis provides the most definitive evidence to date for mtDNA contributions to T2DM, demonstrating universal copy number effects and ancestry-dependent variant associations. Findings support the integration of mtDNA biomarkers into risk prediction, ancestry-informed clinical algorithms, and pharmacogenomic strategies, offering a pathway toward precision medicine in diabetes prevention and management.</div></div>","PeriodicalId":34427,"journal":{"name":"Endocrine and Metabolic Science","volume":"20 ","pages":"Article 100288"},"PeriodicalIF":0.0,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939383","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}
Monosodium glutamate (MSG) is a widely used food additive consumed daily through dietary sources. Regulatory agencies such as JECFA, FDA, and EFSA have established an acceptable daily intake (ADI) of 30 mg/kg body weight/day (expressed as glutamic acid), and its use is restricted in infant foods in many countries. Strong evidence from animal studies indicates that MSG exerts toxic effects, particularly targeting hepatic function, whereas human data remain limited and largely derived from epidemiological observations, anecdotal reports, or high-dose acute exposures.
Objective
This study evaluated the protective effects of Coenzyme Q10 (CoQ10) on liver enzyme activity alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and histopathological alterations in adult male Sprague-Dawley rats exposed to MSG.
Methods
Twenty-five rats were randomly assigned to five groups: control, sham (vehicle), MSG-treated (3 g/kg), and two groups co-treated with MSG and CoQ10 (10 or 20 mg/kg). Treatments were administered orally for four weeks. Blood samples were collected under anesthesia for enzymatic analysis, and liver tissues were fixed in 10 % formalin for histopathology. Data were analyzed using SPSS v23 with Tukey and Kruskal–Wallis tests.
Results
MSG significantly elevated ALT and AST, increased Kupffer cell counts, and reduced hepatocyte numbers (P < 0.05). Histology revealed hepatic congestion, inflammatory infiltration, vacuolization, and sinusoidal dilation. CoQ10, particularly at 20 mg/kg, mitigated these abnormalities (P < 0.05).
Conclusion
CoQ10 exhibits greater hepatoprotective efficacy at 20 mg/kg compared to 10 mg/kg against MSG-induced liver injury, supporting its potential as a therapeutic agent.
{"title":"Coenzyme Q10 mitigates monosodium glutamate-induced hepatic damage: Enzymatic and histological insights from a rat model","authors":"Elahe Ershadifar , Morteza Golbashirzadeh , Atousa Moradzadegan","doi":"10.1016/j.endmts.2025.100287","DOIUrl":"10.1016/j.endmts.2025.100287","url":null,"abstract":"<div><h3>Background</h3><div>Monosodium glutamate (MSG) is a widely used food additive consumed daily through dietary sources. Regulatory agencies such as JECFA, FDA, and EFSA have established an acceptable daily intake (ADI) of 30 mg/kg body weight/day (expressed as glutamic acid), and its use is restricted in infant foods in many countries. Strong evidence from animal studies indicates that MSG exerts toxic effects, particularly targeting hepatic function, whereas human data remain limited and largely derived from epidemiological observations, anecdotal reports, or high-dose acute exposures.</div></div><div><h3>Objective</h3><div>This study evaluated the protective effects of Coenzyme Q10 (CoQ10) on liver enzyme activity alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and histopathological alterations in adult male Sprague-Dawley rats exposed to MSG.</div></div><div><h3>Methods</h3><div>Twenty-five rats were randomly assigned to five groups: control, sham (vehicle), MSG-treated (3 g/kg), and two groups co-treated with MSG and CoQ10 (10 or 20 mg/kg). Treatments were administered orally for four weeks. Blood samples were collected under anesthesia for enzymatic analysis, and liver tissues were fixed in 10 % formalin for histopathology. Data were analyzed using SPSS v23 with Tukey and Kruskal–Wallis tests.</div></div><div><h3>Results</h3><div>MSG significantly elevated ALT and AST, increased Kupffer cell counts, and reduced hepatocyte numbers (<em>P</em> < 0.05). Histology revealed hepatic congestion, inflammatory infiltration, vacuolization, and sinusoidal dilation. CoQ10, particularly at 20 mg/kg, mitigated these abnormalities (<em>P</em> < 0.05).</div></div><div><h3>Conclusion</h3><div>CoQ10 exhibits greater hepatoprotective efficacy at 20 mg/kg compared to 10 mg/kg against MSG-induced liver injury, supporting its potential as a therapeutic agent.</div></div>","PeriodicalId":34427,"journal":{"name":"Endocrine and Metabolic Science","volume":"20 ","pages":"Article 100287"},"PeriodicalIF":0.0,"publicationDate":"2025-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939384","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 : 2025-12-24DOI: 10.1016/j.endmts.2025.100286
Ruiqing Liu , Xudong Cao , Zhijuan Fan , Yaqiong Tian , Guangru Li , Yanna Shen , LiHong Guo , Jiandong Zhang , Zhi Qi
Background
Diabetes mellitus (DM) leads to severe complications, including diabetic cardiomyopathy (DCM). Oxidative stress (OS) is a pivotal pathogenic mechanism contributes to cardiovascular disease in patients with DM. However, the relationship between DCM and OS remain unclear. This study aims to investigate the role and underlying mechanisms of caveolin-1 (Cav-1) in OS under hyperglycemia.
Methods
We used neonatal rat ventricular myocytes (NRVMs) as an in vitro model to investigate the effects of proteins on high-glucose (HG) -induced OS. We used western blotting, RT-PCR, Co-IP, ROS assay, mitochondrial membrane potential detection, and Enzyme-Linked Immunosorbent Assay, with or without siRNA pretreatment, to conduct our experiments.
Results
HG stimulation increased ROS production and decreased the mitochondrial membrane potential. Additionally, we found that Cav-1 inhibited the expression of haemoxygenase-1 (Ho-1) by directly interacting with Nrf2 under HG stimulation. Treatment with Cav-1-siRNA significantly enhanced the expression level of Nrf2 and the transcription levels of antioxidant enzymes, which in turn reduced ROS production and restored mitochondrial membrane potential. Notably, Cav-1 also played a role in regulating apoptosis and CK-MB secretion induced by HG stimulation.
Conclusion
In summary, our findings, for the first time, suggest that the Cav-1/Nrf2/Keap1 signaling pathway may be pivotal in the antioxidant system and apoptosis in response to HG stimulation.
{"title":"Hyperglycemia aggravates cardiomyocyte oxidative stress via Caveolin-1/Nrf2/Keap1 signaling axis activation","authors":"Ruiqing Liu , Xudong Cao , Zhijuan Fan , Yaqiong Tian , Guangru Li , Yanna Shen , LiHong Guo , Jiandong Zhang , Zhi Qi","doi":"10.1016/j.endmts.2025.100286","DOIUrl":"10.1016/j.endmts.2025.100286","url":null,"abstract":"<div><h3>Background</h3><div>Diabetes mellitus (DM) leads to severe complications, including diabetic cardiomyopathy (DCM). Oxidative stress (OS) is a pivotal pathogenic mechanism contributes to cardiovascular disease in patients with DM. However, the relationship between DCM and OS remain unclear. This study aims to investigate the role and underlying mechanisms of caveolin-1 (Cav-1) in OS under hyperglycemia.</div></div><div><h3>Methods</h3><div>We used neonatal rat ventricular myocytes (NRVMs) as an <em>in vitro</em> model to investigate the effects of proteins on high-glucose (HG) -induced OS. We used western blotting, RT-PCR, Co-IP, ROS assay, mitochondrial membrane potential detection, and Enzyme-Linked Immunosorbent Assay, with or without siRNA pretreatment, to conduct our experiments.</div></div><div><h3>Results</h3><div>HG stimulation increased ROS production and decreased the mitochondrial membrane potential. Additionally, we found that Cav-1 inhibited the expression of haemoxygenase-1 (Ho-1) by directly interacting with Nrf2 under HG stimulation. Treatment with Cav-1-siRNA significantly enhanced the expression level of Nrf2 and the transcription levels of antioxidant enzymes, which in turn reduced ROS production and restored mitochondrial membrane potential. Notably, Cav-1 also played a role in regulating apoptosis and CK-MB secretion induced by HG stimulation.</div></div><div><h3>Conclusion</h3><div>In summary, our findings, for the first time, suggest that the Cav-1/Nrf2/Keap1 signaling pathway may be pivotal in the antioxidant system and apoptosis in response to HG stimulation.</div></div>","PeriodicalId":34427,"journal":{"name":"Endocrine and Metabolic Science","volume":"20 ","pages":"Article 100286"},"PeriodicalIF":0.0,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939294","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 : 2025-12-08DOI: 10.1016/j.endmts.2025.100285
Jhosmer Ballena-Caicedo , Lupita Ana Maria Valladolid-Sandoval , Fiorella E. Zuzunaga-Montoya , Víctor Juan Vera-Ponce
Background
Gestational diabetes mellitus (GDM) confers a markedly elevated risk of progression to type 2 diabetes mellitus (T2DM), although the precise magnitude of this risk and its temporal evolution remain inadequately characterized for clinical decision-making.
Objective
To systematically synthesize reviews on glycemic alterations following GDM, quantifying prevalence, incidence, and risk estimates, and to critically assess the use of causal frameworks for inference regarding risk factors.
Methods
We conducted an umbrella review with searches in PubMed/MEDLINE, Embase, Web of Science, and Scopus through September 2025. For reviews that synthesized risk factors, we assessed whether they employed directed acyclic graphs to guide adjustment for confounders.
Results
Fifteen reviews with data from more than 3 million women were included. Prior GDM conferred a 6- to 13-fold increased risk of T2DM compared with normoglycemic pregnancies, with cumulative incidence of 9–32 % depending on ethnicity, follow-up duration, and diagnostic criteria. The incidence rate was 26.20 per 1000 person-years, projecting to 20 % at 10 years. Twenty-seven percent presented glycemic alterations at 6–12 weeks postpartum. The most consistent predictors included glycemic markers during pregnancy, insulin requirement, elevated body mass index, family history, and non-White ethnicity. Critically, no review employed directed acyclic graphs to support confounder adjustment, introducing substantial risk of residual bias in the reported point estimates, although the direction of associations showed robust consistency across temporal windows and independent reviews.
Conclusions
GDM substantially increases T2DM risk, with glycemic burden evident from early postpartum. The universal absence of DAGs limits causal inference regarding point estimates, although the direction of associations is robust.
背景：妊娠期糖尿病（GDM）可显著增加进展为2型糖尿病（T2DM）的风险，尽管这种风险的确切程度及其时间演变仍未充分表征临床决策。目的系统地综合关于GDM后血糖改变的综述，量化患病率、发病率和风险估计，并批判性地评估因果框架对危险因素推断的使用。方法我们对截至2025年9月的PubMed/MEDLINE、Embase、Web of Science和Scopus进行了总结性综述。对于综合危险因素的综述，我们评估了它们是否使用有向无环图来指导混杂因素的调整。结果纳入了15篇综述，数据来自300多万女性。与血糖正常妊娠相比，先前的GDM使T2DM的风险增加6- 13倍，根据种族、随访时间和诊断标准，累积发病率为9 - 32%。发病率为每1000人年26.20例，预计10年后为20%。27%的人在产后6-12周出现血糖改变。最一致的预测因素包括怀孕期间的血糖指标、胰岛素需求、体重指数升高、家族史和非白人种族。关键的是，没有一篇综述采用有向无环图来支持混杂因素调整，这在报告的点估计中引入了大量残留偏倚的风险，尽管关联的方向在时间窗口和独立综述中显示出强大的一致性。结论妊娠期糖尿病显著增加2型糖尿病风险，产后早期血糖负荷明显增加。尽管关联的方向是稳健的，但普遍缺乏dag限制了关于点估计的因果推断。
{"title":"Progression to type 2 diabetes mellitus after gestational diabetes: An umbrella review of 15 systematic reviews and assessment of causal frameworks","authors":"Jhosmer Ballena-Caicedo , Lupita Ana Maria Valladolid-Sandoval , Fiorella E. Zuzunaga-Montoya , Víctor Juan Vera-Ponce","doi":"10.1016/j.endmts.2025.100285","DOIUrl":"10.1016/j.endmts.2025.100285","url":null,"abstract":"<div><h3>Background</h3><div>Gestational diabetes mellitus (GDM) confers a markedly elevated risk of progression to type 2 diabetes mellitus (T2DM), although the precise magnitude of this risk and its temporal evolution remain inadequately characterized for clinical decision-making.</div></div><div><h3>Objective</h3><div>To systematically synthesize reviews on glycemic alterations following GDM, quantifying prevalence, incidence, and risk estimates, and to critically assess the use of causal frameworks for inference regarding risk factors.</div></div><div><h3>Methods</h3><div>We conducted an umbrella review with searches in PubMed/MEDLINE, Embase, Web of Science, and Scopus through September 2025. For reviews that synthesized risk factors, we assessed whether they employed directed acyclic graphs to guide adjustment for confounders.</div></div><div><h3>Results</h3><div>Fifteen reviews with data from more than 3 million women were included. Prior GDM conferred a 6- to 13-fold increased risk of T2DM compared with normoglycemic pregnancies, with cumulative incidence of 9–32 % depending on ethnicity, follow-up duration, and diagnostic criteria. The incidence rate was 26.20 per 1000 person-years, projecting to 20 % at 10 years. Twenty-seven percent presented glycemic alterations at 6–12 weeks postpartum. The most consistent predictors included glycemic markers during pregnancy, insulin requirement, elevated body mass index, family history, and non-White ethnicity. Critically, no review employed directed acyclic graphs to support confounder adjustment, introducing substantial risk of residual bias in the reported point estimates, although the direction of associations showed robust consistency across temporal windows and independent reviews.</div></div><div><h3>Conclusions</h3><div>GDM substantially increases T2DM risk, with glycemic burden evident from early postpartum. The universal absence of DAGs limits causal inference regarding point estimates, although the direction of associations is robust.</div></div>","PeriodicalId":34427,"journal":{"name":"Endocrine and Metabolic Science","volume":"20 ","pages":"Article 100285"},"PeriodicalIF":0.0,"publicationDate":"2025-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145711809","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}
Diabetic ketoacidosis (DKA) is an acute complication of diabetes mellitus with significant mortality. Emerging evidence suggests a potential role for thiamine, as an adjuvant therapy in DKA management. This study explored the effect of thiamine supplementation on the resolution of DKA.
Methods
An open-label, randomized controlled trial was conducted at a tertiary care facility. Sixty adult DKA patients were randomized into two groups, using online randomization generator. Thirty patients (intervention group) received thiamine supplementation with standard DKA therapy, and thirty patients (active control group) received only standard DKA therapy. Baseline investigations were performed and statistical analyses were conducted to compare time to resolution of ketoacidosis, morbidity, mortality, and adverse events between the two groups.
Results
The study showed no significant difference between the demographic, clinical and laboratory parameters within the two groups. In the intervention vs the active control group, time to resolution of DKA (9.6 vs. 9.9 h, p = 0.342), duration of hospital stays (4.2 vs. 3.7 days, p = 0.157), and complications (20 % vs. 10 %, p = 0.472) showed no significant statistical differences. Infections (41.7 %) and non-compliance (38.3 %) were leading causes for precipitation of DKA. No adverse events were observed.
Conclusion
There was no statistically significant difference between the two study groups. Given the safety profile, easy availability and cost effectiveness of thiamine, further research is warranted in larger cohorts to validate the potential therapeutic role of thiamine as adjuvant in DKA management.
背景：糖尿病酮症酸中毒（DKA）是糖尿病的急性并发症，死亡率很高。新出现的证据表明，硫胺素作为辅助治疗在DKA管理中的潜在作用。本研究探讨了补充硫胺素对DKA分解的影响。方法在一家三级医疗机构进行一项开放标签、随机对照试验。采用在线随机发生器将60例成人DKA患者随机分为两组。30例患者（干预组）在补充硫胺素的同时接受标准DKA治疗，30例患者（积极对照组）仅接受标准DKA治疗。进行基线调查并进行统计分析，比较两组之间酮症酸中毒的消退时间、发病率、死亡率和不良事件。结果两组患者的人口学、临床及实验室指标均无统计学差异。干预组与积极对照组DKA缓解时间（9.6 h vs. 9.9 h, p = 0.342）、住院时间（4.2 d vs. 3.7 d, p = 0.157）、并发症（20% vs. 10%, p = 0.472）差异无统计学意义。感染（41.7%）和不遵医嘱（38.3%）是导致DKA沉淀的主要原因。未观察到不良事件。结论两组间无统计学差异。鉴于硫胺素的安全性、易得性和成本效益，进一步的研究需要在更大的队列中验证硫胺素作为DKA治疗辅助剂的潜在治疗作用。
{"title":"Thiamine supplementation in the management of diabetic ketoacidosis: An open-label, randomized controlled trial","authors":"Alisha Khan , Shiva Narang , Amitesh Aggarwal , Nishant Raizada","doi":"10.1016/j.endmts.2025.100284","DOIUrl":"10.1016/j.endmts.2025.100284","url":null,"abstract":"<div><h3>Background</h3><div>Diabetic ketoacidosis (DKA) is an acute complication of diabetes mellitus with significant mortality. Emerging evidence suggests a potential role for thiamine, as an adjuvant therapy in DKA management. This study explored the effect of thiamine supplementation on the resolution of DKA.</div></div><div><h3>Methods</h3><div>An open-label, randomized controlled trial was conducted at a tertiary care facility. Sixty adult DKA patients were randomized into two groups, using online randomization generator. Thirty patients (intervention group) received thiamine supplementation with standard DKA therapy, and thirty patients (active control group) received only standard DKA therapy. Baseline investigations were performed and statistical analyses were conducted to compare time to resolution of ketoacidosis, morbidity, mortality, and adverse events between the two groups.</div></div><div><h3>Results</h3><div>The study showed no significant difference between the demographic, clinical and laboratory parameters within the two groups. In the intervention vs the active control group, time to resolution of DKA (9.6 vs. 9.9 h, <em>p</em> = 0.342), duration of hospital stays (4.2 vs. 3.7 days, <em>p</em> = 0.157), and complications (20 % vs. 10 %, <em>p</em> = 0.472) showed no significant statistical differences. Infections (41.7 %) and non-compliance (38.3 %) were leading causes for precipitation of DKA. No adverse events were observed.</div></div><div><h3>Conclusion</h3><div>There was no statistically significant difference between the two study groups. Given the safety profile, easy availability and cost effectiveness of thiamine, further research is warranted in larger cohorts to validate the potential therapeutic role of thiamine as adjuvant in DKA management.</div></div>","PeriodicalId":34427,"journal":{"name":"Endocrine and Metabolic Science","volume":"20 ","pages":"Article 100284"},"PeriodicalIF":0.0,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145711808","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 : 2025-11-15DOI: 10.1016/j.endmts.2025.100281
Samer Younes
Developing healthier food products and dietary habits to combat non-communicable diseases (NCDs) globally requires a deeper understanding of how nutrients interact with the gut microbiota. Emerging studies in humans and model organisms suggest that gut microbes play a crucial role in shaping an individual's micronutrient status by influencing their synthesis, bioavailability, and metabolic effects.
Micronutrients can modulate the symbiotic relationship between gut bacteria and the host, impacting endocrine pathways that regulate glucose metabolism. Minerals and trace elements, for example, can alter gut microbiota composition, strengthen intestinal barrier function, mitigate metabolic inflammation, and influence cellular glucose uptake, as well as insulin and thyroid hormone activity. Similarly, dietary vitamins affect microbial populations, while gut bacteria themselves can modify and produce vitamins. These interactions have downstream effects on immunity, lipid and glucose metabolism, and pancreatic beta-cell function.
Despite these insights, the precise mechanisms linking micronutrient deficiencies or excesses to gut microbiota shifts and their subsequent impact on metabolic disease risk remain unclear. Additionally, the causal relationships between vitamins and microbial function require further investigation. This review explores the interplay between micronutrients and gut microbiota, shedding light on their collective role in metabolic health.
{"title":"The role of micronutrients in gut microbiota and metabolic health","authors":"Samer Younes","doi":"10.1016/j.endmts.2025.100281","DOIUrl":"10.1016/j.endmts.2025.100281","url":null,"abstract":"<div><div>Developing healthier food products and dietary habits to combat non-communicable diseases (NCDs) globally requires a deeper understanding of how nutrients interact with the gut microbiota. Emerging studies in humans and model organisms suggest that gut microbes play a crucial role in shaping an individual's micronutrient status by influencing their synthesis, bioavailability, and metabolic effects.</div><div>Micronutrients can modulate the symbiotic relationship between gut bacteria and the host, impacting endocrine pathways that regulate glucose metabolism. Minerals and trace elements, for example, can alter gut microbiota composition, strengthen intestinal barrier function, mitigate metabolic inflammation, and influence cellular glucose uptake, as well as insulin and thyroid hormone activity. Similarly, dietary vitamins affect microbial populations, while gut bacteria themselves can modify and produce vitamins. These interactions have downstream effects on immunity, lipid and glucose metabolism, and pancreatic beta-cell function.</div><div>Despite these insights, the precise mechanisms linking micronutrient deficiencies or excesses to gut microbiota shifts and their subsequent impact on metabolic disease risk remain unclear. Additionally, the causal relationships between vitamins and microbial function require further investigation. This review explores the interplay between micronutrients and gut microbiota, shedding light on their collective role in metabolic health.</div></div>","PeriodicalId":34427,"journal":{"name":"Endocrine and Metabolic Science","volume":"19 ","pages":"Article 100281"},"PeriodicalIF":0.0,"publicationDate":"2025-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145568482","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}
Hyperthyroidism is an endocrine disorder in which excessive levels of thyroid hormones are circulating, either because of an exogenous source such as a prescription error or excessive hormone production by the thyroid gland. The present brief review aims to summarize the current treatment options and provide a medical guide for professionals. There are many treatment options for hyperthyroidism. The choice of treatment depends on the cause and severity of the disease, the presence of contraindications to a particular treatment modality, and the patient's preference. Treating the disease will prevent long-term health problems and relieve uncomfortable symptoms. Antithyroid drugs, radioactive iodine, beta-blockers and surgery are the primary treatment options for persistent hyperthyroidism. Each therapeutic method can produce beneficial effects if used appropriately.
{"title":"Hyperthyroidism treatment: A brief review with recommendations","authors":"Wissal Abassi , Nejmeddine Ouerghi , Nidhal Jebabli , Moncef Feki , Anissa Bouassida , Katja Weiss , Beat Knechtle","doi":"10.1016/j.endmts.2025.100282","DOIUrl":"10.1016/j.endmts.2025.100282","url":null,"abstract":"<div><div>Hyperthyroidism is an endocrine disorder in which excessive levels of thyroid hormones are circulating, either because of an exogenous source such as a prescription error or excessive hormone production by the thyroid gland. The present brief review aims to summarize the current treatment options and provide a medical guide for professionals. There are many treatment options for hyperthyroidism. The choice of treatment depends on the cause and severity of the disease, the presence of contraindications to a particular treatment modality, and the patient's preference. Treating the disease will prevent long-term health problems and relieve uncomfortable symptoms. Antithyroid drugs, radioactive iodine, beta-blockers and surgery are the primary treatment options for persistent hyperthyroidism. Each therapeutic method can produce beneficial effects if used appropriately.</div></div>","PeriodicalId":34427,"journal":{"name":"Endocrine and Metabolic Science","volume":"19 ","pages":"Article 100282"},"PeriodicalIF":0.0,"publicationDate":"2025-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145568483","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 : 2025-11-14DOI: 10.1016/j.endmts.2025.100283
Murat Ay , Alper Sari
Objective
In this study, it was shown that cardiovascular risk can be reduced by controlling risk factors, and this can be achieved by measuring the carotid intima-media thickness (CIMT) and performing follow-up. An increase in atherosclerosis and cardiovascular risk factors is seen in the prediabetic stage, and CIMT measurement may help in preventing complications before developing diabetes and inflammatory processes.
Method
Total 89 patients and 40 healthy controls were analyzed to determine the relationship between their mean HbA1c levels, laboratory data, and CIMT in patients with identified chronic diseases.
Results
No significant correlation was noted between the mean HbA1c and right and left CIMT in patients with diabetes mellitus. In the prediabetic patient group, the a weak positive and significant correlation was found between mean HbA1c and bilateral CIMT analysis.
Conclusion
In conclusion, the risk of atherosclerosis and cardiovascular complications is increased in the prediabetic stage and non-invasive evaluation with treatment and follow-up may prevent complications, especially cardiovascular ones, in the diabetic stage.
{"title":"Relationship between HbA1c levels and thickness of carotid intima media in prediabetic and diabetic patients","authors":"Murat Ay , Alper Sari","doi":"10.1016/j.endmts.2025.100283","DOIUrl":"10.1016/j.endmts.2025.100283","url":null,"abstract":"<div><h3>Objective</h3><div>In this study, it was shown that cardiovascular risk can be reduced by controlling risk factors, and this can be achieved by measuring the carotid intima-media thickness (CIMT) and performing follow-up. An increase in atherosclerosis and cardiovascular risk factors is seen in the prediabetic stage, and CIMT measurement may help in preventing complications before developing diabetes and inflammatory processes.</div></div><div><h3>Method</h3><div>Total 89 patients and 40 healthy controls were analyzed to determine the relationship between their mean HbA1c levels, laboratory data, and CIMT in patients with identified chronic diseases.</div></div><div><h3>Results</h3><div>No significant correlation was noted between the mean HbA1c and right and left CIMT in patients with diabetes mellitus. In the prediabetic patient group, the a weak positive and significant correlation was found between mean HbA1c and bilateral CIMT analysis.</div></div><div><h3>Conclusion</h3><div>In conclusion, the risk of atherosclerosis and cardiovascular complications is increased in the prediabetic stage and non-invasive evaluation with treatment and follow-up may prevent complications, especially cardiovascular ones, in the diabetic stage.</div></div>","PeriodicalId":34427,"journal":{"name":"Endocrine and Metabolic Science","volume":"19 ","pages":"Article 100283"},"PeriodicalIF":0.0,"publicationDate":"2025-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145519721","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 : 2025-10-26DOI: 10.1016/j.endmts.2025.100280
Mohamad Fleifel , Amal Al Zoghbi , Jana Tabaja , Andrew El Alam , Khaled Abi Farraj , Randa Al Zaatari , Yara Skaff , Rami Tabbikha , Kamar Eid , Rana Attieh , Soha Bayda , Wassim Assaad , Dana El Masri , Ali Al Dailaty , Naya Fadel , Nesrine Abi Saad , Omar El Tarras , Georges Namnoum , Pascale Salameh , Rola Husni-Samaha , Jocelyn Eid Fares
Background
The residual effects of coronavirus (CoV) disease 2019 (COVID-19) remains to this day as modern research continues to further investigate the disease. COVID-19 patients with diabetes mellitus (DM) seem to have a poorer prognosis overall. Lebanon's DM prevalence has been previously well described in the literature, and some studies have documented some of COVID-19's drastic morbidity and mortality in type 2 DM (T2DM) patients. As per our literature review, there has not been any study in Lebanon, which exclusively describes the state of T2DM and hyperglycemia among COVID-19 adult inpatients.
Aim
To describe T2DM and hyperglycemia in relation to selected patients' clinical characteristics, paraclinical data, and mortality outcomes of COVID-19 pneumonia among patients admitted to the Lebanese American University Medical Center-Rizk Hospital (LAUMC-RH), a large tertiary care medical center in Beirut, Lebanon.
Methodology
This was an observational retrospective study of COVID-19 patients admitted to LAUMC-RH over a near course of 8 months. The eligible subjects were hospitalized adult (≥18 years old) male and nonpregnant female patients with COVID-19 pneumonia. The total eligible sample was 484 patients. All analyses were evaluated at 0.05 significance level. Cross tabulation of the results was done along with odds ratio when applicable. Cross tabulation of the results was done along with odds ratio when applicable. Multivariate analysis, survival analysis, and cox regression were also performed.
Results
Among the admitted COVID-19 patients, 33.7 % had T2DM and 9.2 % of the DM patients had previously undiagnosed T2DM. Approximately 4.5 % of the COVID-19 patients had documented hypoglycemia, and 55 % had hyperglycemia. Comparing T2DM to non-T2DM patients, approximately 48.2 % of hypertension (HTN), 52.6 % of dyslipidemia (DL), and 58.9 % of coronary artery disease (CAD) COVID-19 patients had T2DM (p-values <0.05). Around 69.6 % of patients who remained between 5 and 10 days in the intensive care unit (ICU) had T2DM (p-value <0.05). 36.8 % of the deceased inpatients had T2DM; however, the result was statistically insignificant. 55.3 % and 68.2 % of the patients with hyperglycemia and hypoglycemia, respectively, had T2DM (p-values <0.05). Hyperglycemic emergencies occurred mostly in patients with T2DM (p-value <0.05), with intravenous (IV) insulin drip being used in 77.1 % among T2DM patients (p-value <0.05). The mean glycated haemoglobin (HbA1c) for T2DM patients alone was 8.12 ± 1.68 %. Approximately 94.7 % of patients who had in-hospital hyperglycemia where on steroids (p-value <0.05). Patients with HTN, DL, CAD, overweight, and obesity all had T2DM and in-hospital hyperglycemia (p-values <0.05). Patients on home sulfonylureas (SU) or metformin were more likely to survive post hosp
{"title":"Type 2 diabetes mellitus and hyperglycemia among hospitalized COVID-19 patients: A single center study from Lebanon","authors":"Mohamad Fleifel , Amal Al Zoghbi , Jana Tabaja , Andrew El Alam , Khaled Abi Farraj , Randa Al Zaatari , Yara Skaff , Rami Tabbikha , Kamar Eid , Rana Attieh , Soha Bayda , Wassim Assaad , Dana El Masri , Ali Al Dailaty , Naya Fadel , Nesrine Abi Saad , Omar El Tarras , Georges Namnoum , Pascale Salameh , Rola Husni-Samaha , Jocelyn Eid Fares","doi":"10.1016/j.endmts.2025.100280","DOIUrl":"10.1016/j.endmts.2025.100280","url":null,"abstract":"<div><h3>Background</h3><div>The residual effects of coronavirus (CoV) disease 2019 (COVID-19) remains to this day as modern research continues to further investigate the disease. COVID-19 patients with diabetes mellitus (DM) seem to have a poorer prognosis overall. Lebanon's DM prevalence has been previously well described in the literature, and some studies have documented some of COVID-19's drastic morbidity and mortality in type 2 DM (T2DM) patients. As per our literature review, there has not been any study in Lebanon, which exclusively describes the state of T2DM and hyperglycemia among COVID-19 adult inpatients.</div></div><div><h3>Aim</h3><div>To describe T2DM and hyperglycemia in relation to selected patients' clinical characteristics, paraclinical data, and mortality outcomes of COVID-19 pneumonia among patients admitted to the Lebanese American University Medical Center-Rizk Hospital (LAUMC-RH), a large tertiary care medical center in Beirut, Lebanon.</div></div><div><h3>Methodology</h3><div>This was an observational retrospective study of COVID-19 patients admitted to LAUMC-RH over a near course of 8 months. The eligible subjects were hospitalized adult (≥18 years old) male and nonpregnant female patients with COVID-19 pneumonia. The total eligible sample was 484 patients. All analyses were evaluated at 0.05 significance level. Cross tabulation of the results was done along with odds ratio when applicable. Cross tabulation of the results was done along with odds ratio when applicable. Multivariate analysis, survival analysis, and cox regression were also performed.</div></div><div><h3>Results</h3><div>Among the admitted COVID-19 patients, 33.7 % had T2DM and 9.2 % of the DM patients had previously undiagnosed T2DM. Approximately 4.5 % of the COVID-19 patients had documented hypoglycemia, and 55 % had hyperglycemia. Comparing T2DM to non-T2DM patients, approximately 48.2 % of hypertension (HTN), 52.6 % of dyslipidemia (DL), and 58.9 % of coronary artery disease (CAD) COVID-19 patients had T2DM (<em>p</em>-values <0.05). Around 69.6 % of patients who remained between 5 and 10 days in the intensive care unit (ICU) had T2DM (p-value <0.05). 36.8 % of the deceased inpatients had T2DM; however, the result was statistically insignificant. 55.3 % and 68.2 % of the patients with hyperglycemia and hypoglycemia, respectively, had T2DM (<em>p</em>-values <0.05). Hyperglycemic emergencies occurred mostly in patients with T2DM (p-value <0.05), with intravenous (IV) insulin drip being used in 77.1 % among T2DM patients (<em>p</em>-value <0.05). The mean glycated haemoglobin (HbA1c) for T2DM patients alone was 8.12 ± 1.68 %. Approximately 94.7 % of patients who had in-hospital hyperglycemia where on steroids (p-value <0.05). Patients with HTN, DL, CAD, overweight, and obesity all had T2DM and in-hospital hyperglycemia (<em>p</em>-values <0.05). Patients on home sulfonylureas (SU) or metformin were more likely to survive post hosp","PeriodicalId":34427,"journal":{"name":"Endocrine and Metabolic Science","volume":"19 ","pages":"Article 100280"},"PeriodicalIF":0.0,"publicationDate":"2025-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145415597","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}
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