Diabetology & Metabolic Syndrome最新文献

{"title":"Assessing the impact of magnesium-based nutritional education on lipid profiles in individuals with type 2 diabetes mellitus: a quasi-experimental study.","authors":"Eram Albajri, Arwa S Almasaudi, Hala H Mosli, Noor A Hakim, Reem O Basaqr, Manal Naseeb","doi":"10.1186/s13098-024-01566-8","DOIUrl":"10.1186/s13098-024-01566-8","url":null,"abstract":"<p><strong>Background: </strong>The potential therapeutic role of magnesium (Mg) in type 2 diabetes mellitus (T2DM) remains insufficiently studied despite its known involvement in critical processes like lipid metabolism and insulin sensitivity. This study examines the impact of Mg-focused nutritional education on lipid profile parameters, total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) in T2DM patients.</p><p><strong>Methods: </strong>Thirty participants with T2DM were recruited for this within-subject experimental study. Participants underwent a three-month dietary intervention focused on increasing the intake of Mg-rich foods through nutritional education. Anthropometric measurements and lipids were assessed at baseline and after the intervention period, with the primary outcome variables including changes in lipid parameters.</p><p><strong>Results: </strong>The findings showed a significant inverse association between dietary Mg intake and total cholesterol levels (r = - 0.36, p = 0.05). However, other parameters, TG, LDL-C, and HDL-C, were not found to be associated with Mg intake.</p><p><strong>Conclusion: </strong>The study demonstrated an inverse association between Mg intake and cholesterol level. Providing nutritional education and guidance on incorporating Mg-rich foods into the diet may be a crucial strategy for improving the health and well-being of T2DM patients in Saudi Arabia. The feasibility and practicality of focused nutritional education as an intervention make it a low-cost, scalable, and sustainable approach that can be readily implemented in clinical and community settings. Further studies are needed to explore the long-term impact of dietary Mg interventions on a larger sample with longer education periods.</p>","PeriodicalId":11106,"journal":{"name":"Diabetology & Metabolic Syndrome","volume":"17 1","pages":"3"},"PeriodicalIF":3.4,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Semaglutide restores astrocyte-vascular interactions and blood-brain barrier integrity in a model of diet-induced metabolic syndrome.","authors":"Vanessa Estato, Nathalie Obadia, Paulo Henrique Chateaubriand, Vivian Figueiredo, Marcela Curty, Mariana Costa Silva, Renata Gabriela Lustosa Ferreira, Juliane Santa-Ritta, Marcela Campos Baroni, Alessandra Aragão, João Oliveira Góes Neno, Clara Avelar Mendes Vasconcellos, Joana Costa D'Avila, Marcelo Gomes Granja, Hugo Caire de Castro Faria-Neto","doi":"10.1186/s13098-024-01528-0","DOIUrl":"10.1186/s13098-024-01528-0","url":null,"abstract":"<p><strong>Introduction: </strong>Metabolic syndrome (MetS) is a metabolic disorder related to obesity and insulin resistance and is the primary determinant of the development of low-intensity chronic inflammation. This continuous inflammatory response culminates in neuroimmune-endocrine dysregulation responsible for the metabolic abnormalities and morbidities observed in individuals with MetS. Events such as the accumulation of visceral adipose tissue, increased plasma concentrations of free fatty acids, tissue hypoxia, and sympathetic hyperactivity in individuals with MetS may contribute to the activation of the innate immune response, which compromises cerebral microcirculation and the neurovascular unit, leading to the onset or progression of neurodegenerative diseases.</p><p><strong>Objective: </strong>This study aimed to evaluate the effects of chronic treatment with a GLP-1 receptor agonist (semaglutide) on cerebral microcirculation and neurovascular unit (NVU) integrity.</p><p><strong>Methods: </strong>C57BL/6 mice were fed a standard normolipidic diet or a high-fat diet (HFD) for 24 weeks and then treated for 4 weeks with semaglutide (HFD SEMA) or saline solution (HFD SAL). At the end of pharmacological treatment, biochemical analyses, immunohistochemistry analysis, and intravital microscopy of the brain microcirculation were carried out to quantify leukocyte-endothelium interactions and to assess structural capillary density, astrocyte coverage on cerebral vessels and microglial activation.</p><p><strong>Results: </strong>We observed that SEMA attenuates high-fat diet-induced metabolic alterations in mice fed with HFD for 24 weeks. SEMA also reversed cerebral microcirculation effects of HFD by reducing capillary rarefaction and the interaction of leukocytes in postcapillary brain venules. The HFD-SEMA group exhibited improved astrocyte coverage on vessels. However, SEMA did not reverse microglial activation.</p><p><strong>Conclusions: </strong>Semaglutide can reverse microvascular rarefaction in metabolic syndrome by restoring the integrity of the neurovascular unit. Adverse dietary stimuli can compromise microglial homeostasis that is not reversed by semaglutide.</p>","PeriodicalId":11106,"journal":{"name":"Diabetology & Metabolic Syndrome","volume":"17 1","pages":"2"},"PeriodicalIF":3.4,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship between BMI, indicators of lipid metabolism and diabetic neuropathy: a Mendelian randomization study.","authors":"Yuanyuan Jia, Guanying Liu, Xuesong Li, Lijun Duan, Lifeng Zhao","doi":"10.1186/s13098-024-01543-1","DOIUrl":"https://doi.org/10.1186/s13098-024-01543-1","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;To identify the relationship between BMI or lipid metabolism and diabetic neuropathy using a Mendelian randomization (MR) study.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Body constitution-related phenotypes, namely BMI (kg/m&lt;sup&gt;2&lt;/sup&gt;), total cholesterol (TC), and triglyceride (TG), were investigated in this study. Despite the disparate origins of these data, all were accessible through the IEU OPEN GWAS database ( https://gwas.mrcieu.ac.uk/ ). Instrumental variables and F-statistics for each exposure-outcome pair were determined in weighted mode, weighted median, MR-Egger and Inverse-Variance Weighted (IVW) MR analyses. The p-value threshold was consistently set at 5.00E-08, following established methodology. The preliminary analysis utilized the IVW method to explore potential causal relationships between body constitution-related phenotypes and diabetic neuropathy. Inverse variance weighting, a technique amalgamating random variables, assigns weights inversely proportional to each variable's variance, commonly used for merging findings from independent studies. The weighted median method provides a causal estimate even when up to 50% of the instruments are invalid, enhancing robustness. The weighted mode method identifies the most common causal effect, reducing bias when some instruments exhibit horizontal pleiotropy. The Wald ratio method was utilized to calculate exposure-outcome effects, employing a range of methodologies to ensure result accuracy across different scenarios. This study addresses the critical gap in understanding the causal relationship between BMI, lipid metabolism, and diabetic neuropathy (DN). Employing a MR approach, it highlights BMI as a predictive factor for DN progression, providing insights into potential risk management strategies.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;IVW analysis showed that BMI (P = 0.033, OR = 2.53, 95% CI 1.08-5.96) and triglycerides level (P = 0.593, OR = 1.11, 95% CI 0.77-1.60) were positively associated with the initiation of DN, indicating that the values of BMI and triglycerides are potentially the risk factors in DN development. Additionally, TC was negatively associated with the DN (P = 0.069, OR = 0.72, 95% CI = 0.50-1.03).The forest plot of advanced analysis between BMI and DN relationship indicated a positive correlation between increasing BMI and the risk of DN. In addition, it is evident that with the increase in BMI, the risk of diabetic polyneuropathy also rises. This research demonstrates a positive association between BMI and DN risk (P = 0.033, OR = 2.53, 95% CI = 1.08-5.96). However, no significant correlation was observed between triglycerides (P = 0.593) or total cholesterol (P = 0.069) and DN development, underscoring the complex interplay between lipid metabolism and DN.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;This research demonstrates a positive association between the risk of DN and BMI, while no significant correlation exists between TG or TC and the dev","PeriodicalId":11106,"journal":{"name":"Diabetology & Metabolic Syndrome","volume":"17 1","pages":"1"},"PeriodicalIF":3.4,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11697912/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of stress hyperglycemia ratio upon long-lasting prognosis in coronary artery disease patients with or lacking chronic renal impairment: findings from a Chinese multi-center observational study.","authors":"Jielan Wu, Jin Liu, Ziyao Yuan, Shangyi Tang, Weipeng Zhang, Yulong Xiang, Jinming Chen, Qiqiang Lin, Wei Guo, Yibo He, Haozhang Huang, Xiaozhao Lu, Jingru Deng, Huangtao Ruan, Rengui Jiang, Shiqun Chen, Yong Liu","doi":"10.1186/s13098-024-01521-7","DOIUrl":"10.1186/s13098-024-01521-7","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Lately, numerous researches have portrayed stress hyperglycemia ratio (SHR) is predominantly connected with short-term adverse prognosis among individuals who have acute coronary syndrome. Nevertheless, the relation of SHR with prolonged effects and the value of SHR in predicting in coronary artery disease (CAD) patients with or lacking chronic kidney disease (CKD) remain unclear. The present study was designed to elucidate the relation of SHR with prolonged prognosis and the value of SHR in predicting the long-term all-cause and cardiovascular death of CAD patients with CKD or non-CKD.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We assessed 45,780 adults with CAD from a Chinese multi-center registry. SHR was computed via a formula [SHR = (admission glucose) (mmol/L) / (1.59 * HbA1c [%] - 2.59)]. Based on the presence or absence of CKD and SHR levels, patients were categorized into four groups. Long-term all-cause and cardiovascular mortality were the primary endpoints. The Kaplan-Meier method, restricted cubic spline (RCS), cox regression analysis, subgroups analysis, and sensitivity analysis were employed to estimate the connection between SHR and all-cause as well as cardiovascular mortality.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;During a median follow-up of 5.2 years ( IQR 3.0-8.0), among 45,780 CAD patients (mean age [SD]: 62.8 ± 10.6 years; 23.9% female), the number of all-cause deaths was 7144(15.6%), and cardiovascular-related deaths was 3255 (7.1%). In cohorts with CKD, patients with high SHR had higher all-cause mortality (30.2% vs. 27.6%; adjusted hazard ratio HR 1.13, 95% CI 1.04-1.22; P = 0.003) and cardiovascular mortality (18.2% vs. 15.6%; HR adjusted 1.17, 95% CI 1.06-1.30; P = 0.002) compared to the individuals in low SHR. However, this was not the case in CAD cohorts without CKD [all-cause mortality (12.9% vs. 11.9%; HR adjusted 1.04, 95%CI 0.98-1.10, P = 0.206); cardiovascular mortality (5.1% vs. 4.4%; HR adjusted 1.09, 95%CI 0.99-1.20, P = 0.084)]. KM analysis revealed that high SHR is linked with all-cause mortality [CKD (log-rank P &lt; 0.001); no-CKD (log-rank P = 0.024)] and cardiovascular mortality [CKD (log-rank P &lt; 0.001); no-CKD (log-rank P = 0.01)] in CAD patients with or without CKD. RCS demonstrated that the relation between SHR and all-cause mortality was U-shaped after full modification, which was shown for CKD patients (P for non-linearity = 0.003) and also for patients without CKD (P for non-linearity = 0.001). Analogous effects were discovered for cardiovascular mortality, which was the case for CKD patients (P for non-linearity &lt; 0.001) and also for patients without CKD (P for non-linearity = 0.001).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Among patients with CAD, an elevated stress hyperglycemia ratio (SHR) is implicated in a heightened risk of long-term outcomes, particularly in those with CKD. This signifies that SHR might have a latent function in the cardiovascular risk categorization of the CAD po","PeriodicalId":11106,"journal":{"name":"Diabetology & Metabolic Syndrome","volume":"16 1","pages":"316"},"PeriodicalIF":3.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11689691/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disentangling the genetic overlap between ischemic stroke and obesity.","authors":"Ren Yang, Tangfeng Zhang, Feng Han","doi":"10.1186/s13098-024-01555-x","DOIUrl":"10.1186/s13098-024-01555-x","url":null,"abstract":"<p><strong>Objective: </strong>Obesity has been recognized as a risk factor for cerebrovascular diseases, with observational studies suggesting a heightened incidence of stroke. However, the genetic epidemiology field has yet to reach a consensus on the causal relationship and genetic overlap between ischemic stroke (IS) and obesity.</p><p><strong>Methods: </strong>We utilized linkage disequilibrium score regression, high-definition likelihood, and local analysis of variant associations to assess the genetic correlation between body mass index (BMI) and IS. Bidirectional Mendelian randomization was employed to infer causality. We identified shared risk single nucleotide polymorphisms (SNPs) through cross-trait meta-analyses and estimated heritability using summary statistics. Summary-data-based Mendelian randomization (SMR) was applied to explore potential functional genes.</p><p><strong>Results: </strong>Our analysis revealed a significant positive genetic correlation between BMI and IS, supporting a causal link from BMI to IS. Cross-trait analysis yielded 9 and 16 shared risk SNPs for IS and small vessel stroke (SVS), respectively. We observed a notable enrichment of SNP heritability for IS and BMI in brain tissues, suggesting tissue-specific influences. The genes shared between the traits were predominantly involved in brain development, synaptic electrical activity, and immunoregulation. Notably, our SMR analysis identified the risk genes CHAF1A, CEP192, ULK4, CYP2D6, AS3MT, and WARS2 across the majority of the 14 enriched tissues shared by both traits.</p><p><strong>Conclusion: </strong>Our study uncovered a significant genetic correlation and identified shared risk SNPs between BMI and IS. The identification of CHAF1A, CEP192, ULK4, CYP2D6, AS3MT, and WARS2 as potential functional genes common to both obesity and IS enriched our understanding of their genetic interplay, potentially advanced our grasp of their pathogenesis and therapeutic targets.</p>","PeriodicalId":11106,"journal":{"name":"Diabetology & Metabolic Syndrome","volume":"16 1","pages":"314"},"PeriodicalIF":3.4,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142902700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Implications of prognostic nutritional index in predicting adverse outcomes of uncontrolled diabetic patients: a cohort study of the national health and nutrition examination survey from 2005 - 2018.","authors":"Fei Liu, Zhili Jiang, Wei Luo, Yunxiao Yang, Shuai Guo, Jiayi Yi, Geng Shen, Wei Li, Lin Wang, Xiuhuan Chen, Zhaogong Zhi, Tian Liu, Xuedong Zhao, Chen Li, Hai Gao","doi":"10.1186/s13098-024-01563-x","DOIUrl":"10.1186/s13098-024-01563-x","url":null,"abstract":"<p><strong>Background: </strong>Diabetes mellitus (DM) is a metabolic disorder with increasing prevalence and poor control rates, leading to adverse events. Prognostic nutritional value (PNI) has been identified as a protective factor in DM, but its role in uncontrolled DM remains unclear.</p><p><strong>Methods: </strong>This study based on the representative cohort of National Health and Nutrition Examination Survey from 2005 to 2018. A total of 3,313 participants with uncontrolled DM were included in our analyses. PNI was calculated as 5×lymphocyte count (10⁹/L)+ 10×serum albumin (g/L). The endpoints were DM-related and cardiovascular mortality, which were obtained from National Death Index. Univariable and multivariable cox proportional hazard regression were performed to investigate prognostic value of PNI.</p><p><strong>Results: </strong>Among 3,313 patients with uncontrolled DM (mean age of 61.75 ± 12.78 years, 53.4% male), PNI level was negatively associated with inflammatory markers and positively associated with metabolic markers of lipid and protein. During a median follow-up of 77 months, 247 DM-related deaths and 205 cardiovascular deaths occurred. Higher PNI levels independently predicted low DM-related (adjusted Hazard ratio [HR] = 0.872, 95% confidence interval [CI] 0.840-0.906, P < 0.001) and cardiovascular mortality (adjusted HR = 0.872, 95% CI 0.834-0.912, P < 0.001). The prognostic value of PNI significantly varied across different DM treatment conditions, which was more pronounced in patients receiving antidiabetic treatments (adjusted HR: insulin + oral antidiabetic drugs [OADs]: 0.832; insulin: 0.863; OADs: 0.894, all adjusted P < 0.001), but was absent in those without antidiabetic treatment.</p><p><strong>Conclusions: </strong>A higher PNI level is an independent protective predictor for DM-related and cardiovascular mortality in uncontrolled DM patients. Evaluation of PNI level in uncontrolled DM patients could conduce to stringent intervention. Improvement of PNI could enhance the effective of antidiabetic therapy, especially the insulin therapy, and reduce DM-related mortality.</p>","PeriodicalId":11106,"journal":{"name":"Diabetology & Metabolic Syndrome","volume":"16 1","pages":"315"},"PeriodicalIF":3.4,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142902703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The modified role including mediating and synergistic interactive effects of glucose tolerance status in the associations between relative fat mass and the risks of cardiovascular disease and all-cause mortality from the 4C cohort study.","authors":"Peiqiong Luo, Danpei Li, Yaming Guo, Xiaoyu Meng, Ranran Kan, Xuefeng Yu","doi":"10.1186/s13098-024-01558-8","DOIUrl":"10.1186/s13098-024-01558-8","url":null,"abstract":"<p><strong>Background: </strong>To investigate the associations between relative fat mass (RFM) and clinical outcomes in different glucose tolerance statuses and the modified effect of glucose tolerance status.</p><p><strong>Methods: </strong>We analyzed 8,224 participants from a Chinese cohort study, who were classified into normal glucose status (NGT), prediabetes, and diabetes. Outcomes included fatal, nonfatal cardiovascular disease (CVD) events and all-cause mortality. Associations between RFM and outcomes were assessed using Cox regression. The modified effect of glucose tolerance status was investigated using mediation, interaction, and joint analyses.</p><p><strong>Results: </strong>During up to 5 years of follow-up, 154 (1.9%) participants experienced fatal CVD, 153 (1.9%) experienced nonfatal CVD events, and 294 (3.6%) experienced all-cause death. 2,679 participants (32.6%) had NGT, 4,528 (54.8%) had prediabetes, and 1,037 (12.6%) had diabetes. RFM was associated with increased risk of fatal (HR [95% CI], 1.09 [1.06-1.12], p < 0.001), nonfatal CVD events (HR [95% CI], 1.12 [1.09-1.15], p < 0.001), and all-cause mortality (HR [95% CI], 1.10 [1.08-1.12), p < 0.001) in all and those with NGT, prediabetes, and diabetes, and these associations were modified by glucose tolerance status, which included mediating (mediation proportion ranges from 4.74% to 8.69%) and synergistic interactive effects (multiplicative effect ranges from 1.03 to 1.06). The joint analysis identified the subclassification that exhibited the highest HR among 12 subclassifications.</p><p><strong>Conclusions: </strong>RFM was associated with increased risk of fatal, nonfatal CVD events, and all-cause mortality in NGT, prediabetes, and diabetes, and these associations were modified by glucose tolerance status, which could significantly influence how clinicians assess high risk and could lead to more personalized, effective prevention strategies.</p>","PeriodicalId":11106,"journal":{"name":"Diabetology & Metabolic Syndrome","volume":"16 1","pages":"313"},"PeriodicalIF":3.4,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11670452/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The prognostic impact of stress hyperglycemia ratio on mortality in cardiogenic shock: a MIMIC-IV database analysis.","authors":"Linfeng Xie, Jing Chen, Yuanzhu Li, Bi Huang, Suxin Luo","doi":"10.1186/s13098-024-01562-y","DOIUrl":"10.1186/s13098-024-01562-y","url":null,"abstract":"<p><strong>Background: </strong>The stress hyperglycemia ratio (SHR) has been established as a predictor of unfavorable outcomes across various diseases. However, its relationship with prognosis in patients with cardiogenic shock (CS) remains unclear. This study aims to investigate the association between SHR and outcomes in CS patients.</p><p><strong>Methods: </strong>A total of 904 CS patients with their first ICU admission were included in this study, utilizing data from the American Medical Information Mart for Intensive Care (MIMIC-IV) database. The primary endpoints were all-cause mortality at 30 days and 360 days. Patients were stratified into three groups based on the tertiles of the SHR.</p><p><strong>Results: </strong>The mean age of the cohort was 67.62 years, with 67.3% of participants being men. During the follow-up period, 221 patients (24.4%) died within 30 days, and 360 patients (39.8%) died within 360 days. The 30-day all-cause mortality rates were 16.9%, 22.3%, and 34.2% in the T1, T2, and T3 groups, respectively (p < 0.001), while the 360-day all-cause mortality rates were 34.9%, 39.0%, and 45.6%, respectively (p = 0.015). Compared with patients in T1, those in T3 exhibited a significantly higher risk of 30-day all-cause mortality (HR = 2.140, 95% CI: 1.522-3.008, p < 0.001) and 360-day all-cause mortality (HR = 1.495, 95% CI: 1.157-1.931, p = 0.002). Restricted cubic spline (RCS) analyses demonstrated an approximately linear relationship between SHR and 360-day all-cause mortality (p for overall = 0.011; p for nonlinearity = 0.099). However, a nonlinear association was observed between SHR and 30-day all-cause mortality (p for overall < 0.001; p for nonlinearity = 0.030), with the risk increasing significantly when SHR exceeded 1.176. Subgroup analyses revealed that the effect of SHR was consistent across most subgroups except in patients with and without acute myocardial infarction (AMI). In patients with AMI, SHR was associated with a significantly elevated risk of mortality, whereas no significant association was observed in patients without AMI. For 30-day all-cause mortality, the HR was 1.059 (95% CI: 1.040-1.078) in patients with AMI and 1.002 (95% CI: 0.966-1.040) in those without AMI (p for interaction = 0.007). For 360-day all-cause mortality, the HR was 1.043 (95% CI: 1.026-1.061) in patients with AMI and 0.984 (95% CI: 0.955-1.014) in those without AMI (p for interaction < 0.001).</p><p><strong>Conclusion: </strong>Elevated SHR was significantly associated with increased 30-day and 360-day all-cause mortality in patients with CS, particularly in those with CS complicated by AMI. SHR may serve as a valuable marker for risk stratification and guiding subsequent interventions in CS patients. However, further prospective studies are needed to confirm these findings.</p>","PeriodicalId":11106,"journal":{"name":"Diabetology & Metabolic Syndrome","volume":"16 1","pages":"312"},"PeriodicalIF":3.4,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11667900/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142885246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling the role of lipopolysaccharide-related genes in diabetic retinopathy: identification of key biomarkers and immune infiltration analysis.","authors":"Hongyi Sun, Shaohua Liu, Chao Wei","doi":"10.1186/s13098-024-01557-9","DOIUrl":"10.1186/s13098-024-01557-9","url":null,"abstract":"<p><strong>Background: </strong>Growing evidence suggests a link between systemic lipopolysaccharide (LPS) exposure and worsening diabetic retinopathy (DR). This study aims to investigate DR's pathogenesis by analyzing LPS-related genes (LRGs) through bioinformatics.</p><p><strong>Methods: </strong>The CTD database was utilized to identify LRGs. The datasets associated with DR were acquired from the GEO database. The Venn diagram was used to identify the differentially expressed LRGs (DLRGs), and the putative molecular mechanism of these DLRGs was investigated through functional enrichment analysis. We used WGCNA, Lasso regression, and RF to identify hub DLRGs. The expression levels of these hub DLRGs were validated in an independent dataset (GSE102485) and cell experiments. Employing the CIBERSORT algorithm, we examined the infiltration of 22 distinct immune cell types in DR and assessed the association between key DLRGs and immune infiltrates through correlation analysis.</p><p><strong>Results: </strong>A total of 71 DLRGs were detected. These genes exhibited significant enrichment in pathways associated with inflammation. In addition, the in-depth analysis uncovered that five hub DLRGs (STK33 and EPHX2) linked to bacterial LPS displayed noteworthy diagnostic potential for individuals diagnosed with DR. The hub DLRGs expression in the high glucose-induced DR model was confirmed by qRT-PCR analysis. Furthermore, examination of immune infiltration indicated a significant association between these five genes and the extent of immune cell infiltration.</p><p><strong>Conclusion: </strong>STK33 and EPHX2 serve as biomarkers related to bacterial LPS. Exploring these genes in-depth could provide innovative ideas and a foundation for comprehending the progression of the disease and developing targeted treatments for DR.</p>","PeriodicalId":11106,"journal":{"name":"Diabetology & Metabolic Syndrome","volume":"16 1","pages":"309"},"PeriodicalIF":3.4,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11665249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the complex function of gut microbiota: its impact on the pathogenesis of obesity and beyond: a comprehensive review.","authors":"Aref Yarahmadi, Hamed Afkhami, Ali Javadi, Mojtaba Kashfi","doi":"10.1186/s13098-024-01561-z","DOIUrl":"10.1186/s13098-024-01561-z","url":null,"abstract":"<p><p>Obesity is a multifactorial condition influenced by genetic, environmental, and microbiome-related factors. The gut microbiome plays a vital role in maintaining intestinal health, increasing mucus creation, helping the intestinal epithelium mend, and regulating short-chain fatty acid (SCFA) production. These tasks are vital for managing metabolism and maintaining energy balance. Dysbiosis-an imbalance in the microbiome-leads to increased appetite and the rise of metabolic disorders, both fuel obesity and its issues. Furthermore, childhood obesity connects with unique shifts in gut microbiota makeup. For instance, there is a surge in pro-inflammatory bacteria compared to children who are not obese. Considering the intricate nature and variety of the gut microbiota, additional investigations are necessary to clarify its exact involvement in the beginnings and advancement of obesity and related metabolic dilemmas. Currently, therapeutic methods like probiotics, prebiotics, synbiotics, fecal microbiota transplantation (FMT), dietary interventions like Mediterranean and ketogenic diets, and physical activity show potential in adjusting the gut microbiome to fight obesity and aid weight loss. Furthermore, the review underscores the integration of microbial metabolites with pharmacological agents such as orlistat and semaglutide in restoring microbial homeostasis. However, more clinical tests are essential to refine the doses, frequency, and lasting effectiveness of these treatments. This narrative overview compiles the existing knowledge on the multifaceted role of gut microbiota in obesity and much more, showcasing possible treatment strategies for addressing these health challenges.</p>","PeriodicalId":11106,"journal":{"name":"Diabetology & Metabolic Syndrome","volume":"16 1","pages":"308"},"PeriodicalIF":3.4,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11664868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}