{"title":"Enhancing postpartum cardiometabolic health for women with previous gestational diabetes: Next steps and unanswered questions for pharmacological and lifestyle strategies.","authors":"Rajna Golubic, Josip Car, Kypros Nicolaides","doi":"10.1111/dom.16070","DOIUrl":"https://doi.org/10.1111/dom.16070","url":null,"abstract":"","PeriodicalId":158,"journal":{"name":"Diabetes, Obesity & Metabolism","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Correction to \"Real-world evaluation of the effects of tirzepatide in patients with type 2 diabetes mellitus\".","authors":"","doi":"10.1111/dom.16083","DOIUrl":"https://doi.org/10.1111/dom.16083","url":null,"abstract":"","PeriodicalId":158,"journal":{"name":"Diabetes, Obesity & Metabolism","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ida M Gether, Emilie S Andersen, Signe Foghsgaard, Anne-Marie Ellegaard, Louise Kelstrup, David P Sonne, Andreas Brønden, Matthew P Gillum, Jens J Holst, Bolette Hartmann, Jens F Rehfeld, Tina Vilsbøll, Filip K Knop
{"title":"Increased gallbladder emptying and reduced GLP-1 response in pregnancy with and without gestational diabetes mellitus.","authors":"Ida M Gether, Emilie S Andersen, Signe Foghsgaard, Anne-Marie Ellegaard, Louise Kelstrup, David P Sonne, Andreas Brønden, Matthew P Gillum, Jens J Holst, Bolette Hartmann, Jens F Rehfeld, Tina Vilsbøll, Filip K Knop","doi":"10.1111/dom.16064","DOIUrl":"10.1111/dom.16064","url":null,"abstract":"<p><strong>Aim: </strong>Gestational diabetes mellitus (GDM) has been associated with reduced postprandial glucagon-like peptide 1 (GLP-1) responses. As pregnancy induces changes in gallbladder motility and bile acids stimulate GLP-1 secretion, we investigated postprandial gallbladder emptying and GLP-1 responses in women with GDM.</p><p><strong>Methods: </strong>Women with and without GDM underwent two 240-min mixed meal tests; one during third trimester of pregnancy and one 3-6 months postpartum. We evaluated ultrasonography-assessed gallbladder emptying, plasma concentrations of glucometabolic hormones including GLP-1, paracetamol absorption (proxy for gastric emptying) and circulating factors known to affect gallbladder dynamics.</p><p><strong>Results: </strong>Fifteen women with GDM and 15 pregnant women with normal glucose tolerance (NGT) (baseline median age 31 (interquartile range 29;33) versus 32 (28;33) years, body mass index (BMI) 27.2 (24.7;30.7) versus 28.4 (26.2;31.0) kg/m<sup>2</sup>, HbA<sub>1c</sub> 30 (29;32) versus 30 (28;31) mmol/mol) were included. No differences in postprandial gallbladder emptying or GLP-1 responses were observed between women with and without GDM, neither during pregnancy nor postpartum. Pregnancy increased fasting gallbladder volumes by 69 (30;122)% and 103 (59;156)% and postprandial gallbladder emptying by 77 (28;236)% and 99 (37;190)% compared with postpartum in women with and without GDM, respectively. Postprandial GLP-1 responses were reduced by 60 (3;82)% and 81 (11;90)% during pregnancy compared with postpartum in women with and without GDM, respectively.</p><p><strong>Conclusion: </strong>Pregnancy-induced changes in gallbladder motility seem to play no or a limited role in previously reported GDM-associated reduced postprandial GLP-1 responses as gallbladder emptying was greater and postprandial GLP-1 response was lower in pregnancy than postpartum regardless of GDM status.</p>","PeriodicalId":158,"journal":{"name":"Diabetes, Obesity & Metabolism","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Paloma Rodriguez, Nikki Breslaw, Huijun Xiao, Jim Bena, Kimberly Jenkins, Diana Isaacs, Keren Zhou, Marcio L Griebeler, Bartolome Burguera, Kevin M Pantalone
{"title":"De-intensification of basal-bolus therapy by replacing prandial insulin with once-weekly subcutaneous semaglutide in individuals with well-controlled type 2 diabetes: A single-centre, open-label randomised trial (TRANSITION-T2D).","authors":"Paloma Rodriguez, Nikki Breslaw, Huijun Xiao, Jim Bena, Kimberly Jenkins, Diana Isaacs, Keren Zhou, Marcio L Griebeler, Bartolome Burguera, Kevin M Pantalone","doi":"10.1111/dom.16057","DOIUrl":"https://doi.org/10.1111/dom.16057","url":null,"abstract":"<p><strong>Aims: </strong>The study aims to examine the outcome of replacement of prandial insulin with once-weekly subcutaneous semaglutide in people with type 2 diabetes reasonably controlled on multiple daily insulin injections (MDI).</p><p><strong>Materials and methods: </strong>This single-centre, randomised, open-label trial enrolled a statistically predetermined sample of 60 adults with HbA1c ≤7.5% (58 mmol/mol) receiving MDI, with a total daily dose (TDD) ≤120 units/day. Participants were assigned 2:1 to subcutaneous semaglutide 1.0 mg plus insulin degludec, or to continue MDI. The primary outcome was percentage of subjects maintaining HbA1c ≤7.5% (58 mmol/mol) at Week 26.</p><p><strong>Results: </strong>At Week 26, 90% of semaglutide and 75% of MDI subjects maintained HbA<sub>1c</sub> ≤7.5% (≤58 mmol/mol) (p = 0.18). Mean changes (95% CI) in HbA<sub>1c</sub>, weight and percentage body weight for semaglutide versus MDI, respectively, were -0.5% (-0.7, -0.3) versus 0.0% (-0.3, 0.3; p = 0.009); -8.9 kg (-9.9, -7.8) versus 1.5 kg (-0.1, 3.1; p < 0.001); and -8.6% (-9.6, -7.6) versus 1.4% (0.0, 2.8; p < 0.001). Insulin TDD decreased 56.0% (-62.3, -49.7) with semaglutide and increased 6.7% (-2.5, 16.0) with MDI (p < 0.001). Among semaglutide subjects, 58% reduced insulin TDD > 50%, 97.5% stopped prandial insulin and 45% lost >10% body weight. Participant treatment satisfaction scores trended higher with semaglutide. Hypoglycaemia frequency was similar between groups.</p><p><strong>Conclusions: </strong>In people with type 2 diabetes well controlled (HbA<sub>1c</sub> ≤7.5% [≤58 mmol/mol]) on MDI ≤120 units/day, replacing multiple daily injections of prandial insulin with once-weekly subcutaneous semaglutide can maintain and even improve HbA<sub>1c</sub>, lower body weight and lessen the burden of management.</p>","PeriodicalId":158,"journal":{"name":"Diabetes, Obesity & Metabolism","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rosa C Golomb, Sascha R Tittel, Alena Welters, Wolfram Karges, Svenja Meyhöfer, Michael Hummel, Julia K Mader, Jörg-C Kämmer, Nanette C Schloot, Reinhard W Holl
{"title":"Increased cardiovascular risk in people with LADA in comparison to type 1 diabetes and type 2 diabetes: Findings from the DPV registry in Germany and Austria.","authors":"Rosa C Golomb, Sascha R Tittel, Alena Welters, Wolfram Karges, Svenja Meyhöfer, Michael Hummel, Julia K Mader, Jörg-C Kämmer, Nanette C Schloot, Reinhard W Holl","doi":"10.1111/dom.16048","DOIUrl":"https://doi.org/10.1111/dom.16048","url":null,"abstract":"<p><strong>Introduction: </strong>We aimed to characterise and compare individuals diagnosed with type 1 diabetes (T1D), latent autoimmune diabetes in adults (LADA) and type 2 diabetes (T2D), in a real-world setting.</p><p><strong>Methods: </strong>Anthropometric and clinical data from 36 959 people with diabetes diagnosed at age 30-70 years enrolled in the prospective diabetes patients follow-up (DPV) registry from 1995 to 2022 were analysed cross-sectionally at diagnosis and follow-up (≥6 months after diagnosis). LADA was defined as clinical diagnosis of T2D, positivity of ≥1 islet autoantibody and an insulin-free interval of ≥6 months upon diabetes diagnosis.</p><p><strong>Results: </strong>At diagnosis, age, body mass index, waist circumference, C-peptide and HbA1c in people with LADA (n = 747) fell in between individuals with T1D (n = 940) and T2D (n = 35 272) (all p-values < 0.01). At follow-up, after adjusting for age, sex and diabetes duration, the prevalence of dyslipidemia and hypertension was the highest in people with LADA (90.6%, 77.7%) compared to people with T2D (81.8%, 60.4%) and T1D (75.7%, 39.7%) (p < 0.01). The prevalence of diabetic kidney disease (DKD) was higher in LADA (44.2%), than in T1D (19.9%) (p < 0.01). The prevalence of peripheral neuropathy was higher in individuals with LADA (55.1%) than in T2D (43.9%) and T1D (42.1%) (p < 0.05). Coverage of treatment for hypertension and dyslipidemia were 22.4% and 15.0% in T1D, 63.0% and 36.6% in LADA and 29.4% and 18.2% in T2D.</p><p><strong>Conclusion: </strong>People with LADA had a higher prevalence of cardiovascular risk factors (dyslipidemia, hypertension) and cardiovascular complications (DKD and peripheral neuropathy), suggesting that people with LADA are at need for improved recognition and care.</p>","PeriodicalId":158,"journal":{"name":"Diabetes, Obesity & Metabolism","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Time in tight range: A key metric for optimal glucose control in the era of advanced diabetes technologies and therapeutics.","authors":"Ziyi Zhang, Yaxin Wang, Jingyi Lu, Jian Zhou","doi":"10.1111/dom.16033","DOIUrl":"https://doi.org/10.1111/dom.16033","url":null,"abstract":"<p><p>Compared to glycated haemoglobin A1c (HbA1c), the rapidly developing continuous glucose monitoring (CGM) technology provides more detailed information about glycemic control. Amongst the new glucose metrics derived from CGM, time in target range of 3.9-10.0 mmol/L (time in range, TIR) has been widely used for the assessment of glucose control. In recent years, the rise of new technologies and therapies including advanced hybrid closed-loop automated insulin delivery systems and new hypoglycemic drugs has made it possible to achieve better glycemic control. In this context, the concept of time in tight range (TITR), defined as the percentage of time spent in target glucose range of 3.9-7.8 mmol/L, has gained increasing attention. Whilst TITR is highly correlated with TIR, there are still differences between the two metrics. These differences make TITR a more appropriate indicator in certain situations, such as when glucose levels are close to normal or when tighter glycemic control is required. This review summarizes recent studies related to TITR.</p>","PeriodicalId":158,"journal":{"name":"Diabetes, Obesity & Metabolism","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jaycie Koh, Ayman Mohamed, Gwyneth Kong, Esther Wong, Yiming Chen, Vickram Vijay Anand, Bryan Chong, Yip Han Chin, Jiong-Wei Wang, Chin Meng Khoo, Siew Pang Chan, Mark Muthiah, Georgios K Dimitriadis, Mark Yan-Yee Chan, Poay-Huan Loh, Nicholas W S Chew
{"title":"Long-term all-cause mortality of metabolic-dysfunction associated steatotic liver disease based on body weight phenotypes following acute myocardial infarction: A retrospective cohort study.","authors":"Jaycie Koh, Ayman Mohamed, Gwyneth Kong, Esther Wong, Yiming Chen, Vickram Vijay Anand, Bryan Chong, Yip Han Chin, Jiong-Wei Wang, Chin Meng Khoo, Siew Pang Chan, Mark Muthiah, Georgios K Dimitriadis, Mark Yan-Yee Chan, Poay-Huan Loh, Nicholas W S Chew","doi":"10.1111/dom.16062","DOIUrl":"https://doi.org/10.1111/dom.16062","url":null,"abstract":"<p><strong>Objective: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD) and obesity increases risk of cardiovascular disease. This cohort study examines the prognostic value of MASLD, across body weight categories, in a secondary preventative acute myocardial infarction (AMI) cohort.</p><p><strong>Methods: </strong>Patients with AMI were stratified into four phenotypes-obesity MASLD, non-obesity MASLD, obesity non-MASLD, non-obesity non-MASLD. The primary outcome was all-cause mortality. Cox regression analysis was performed to investigate determinants of long-term all-cause mortality.</p><p><strong>Results: </strong>Of 5702 patients, majority were in the non-obesity non-MASLD group (66.7%), followed by obesity MASLD (16.1%), non-obesity MASLD (11.2%) and non-obesity MASLD (6.0%). Across the four phenotypes, obesity MASLD had the highest cardiometabolic burden, followed by non-obesity MASLD. Non-obesity MASLD had the highest risk of heart failure (p = 0.034), cardiogenic shock (p < 0.001), and all-cause long-term mortality (p = 0.019). The non-obesity MASLD (HR 1.400, 95%CI 1.077-1.820, p = 0.012) and obesity MASLD phenotypes (HR 1.222, 95%CI 1.005-1.485, p = 0.044) were independently associated with long-term all-cause mortality.</p><p><strong>Conclusions: </strong>Obesity and non-obesity MASLD phenotypes were predictors of all-cause mortality following AMI, with an even larger magnitude of mortality risk in the non-obesity MASLD group. The recognition of MASLD and its body weight phenotypes will be beneficial in the prognostication following AMI.</p>","PeriodicalId":158,"journal":{"name":"Diabetes, Obesity & Metabolism","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Joseph Magagnoli, Tammy H Cummings, James W Hardin, Jayakrishna Ambati, S Scott Sutton
{"title":"Targeting the cholinergic anti-inflammatory pathway for type 2 diabetes prevention: A retrospective cohort study.","authors":"Joseph Magagnoli, Tammy H Cummings, James W Hardin, Jayakrishna Ambati, S Scott Sutton","doi":"10.1111/dom.16060","DOIUrl":"https://doi.org/10.1111/dom.16060","url":null,"abstract":"<p><strong>Background: </strong>Chronic inflammation is a key factor in type 2 diabetes mellitus (T2DM) development. The cholinergic anti-inflammatory pathway (CAP) reduces inflammation by activating α7 nicotinic acetylcholine receptors (α7nAChRs) on macrophages, suppressing proinflammatory cytokines. Acetylcholinesterase inhibitors (AChEis), primarily used for Alzheimer's disease (AD), may exert anti-inflammatory effects through the CAP. One AChEi, galantamine, also directly agonizes α7nAChRs, potentially enhancing its anti-inflammatory properties.</p><p><strong>Objective: </strong>This study aimed to investigate the association between AChEi use, particularly galantamine, and T2DM risk in AD patients.</p><p><strong>Methods: </strong>We conducted a retrospective analysis of Veterans Health Administration (VA) data, examining early- and late-onset AD patients receiving galantamine or other AD medications. Propensity score matching was used to balance groups and minimize confounding. Cox proportional hazard models assessed T2DM risk for galantamine, other AChEis and memantine.</p><p><strong>Results: </strong>A total of 40 065 AD patients were included in the study. Among early-onset AD patients, galantamine use significantly reduced T2DM risk (hazard ratio [HR] = 0.80, 95% confidence interval [CI]: 0.66-0.98). Memantine also showed a protective effect (HR = 0.82, 95% CI: 0.69-1) in this group. Neither galantamine nor memantine influenced T2DM risk in late-onset AD. Other AD medications showed no association with T2DM risk.</p><p><strong>Conclusion: </strong>Galantamine use was associated with a lower risk of T2DM in early-onset AD patients, potentially due to enhanced anti-inflammatory effects through both AChE inhibition and direct α7nAChR agonism. Memantine also demonstrated a protective effect. These findings suggest potential new applications for existing AD medications in T2DM prevention, particularly in early-onset AD patients. Further research, including randomized controlled trials with diverse populations, is needed to confirm these results and the underlying mechanisms.</p>","PeriodicalId":158,"journal":{"name":"Diabetes, Obesity & Metabolism","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"L-aspartate ameliorates diet-induced obesity by increasing adipocyte energy expenditure.","authors":"Shi-Yao Guo, Yu-Tao Hu, Yong Rao, Zhi Jiang, Chan Li, Yu-Wei Lin, Shu-Min Xu, Dan-Dan Zhao, Li-Yuan Wei, Shi-Liang Huang, Qing-Jiang Li, Jia-Heng Tan, Shuo-Bin Chen, Zhi-Shu Huang","doi":"10.1111/dom.16053","DOIUrl":"https://doi.org/10.1111/dom.16053","url":null,"abstract":"<p><strong>Aims: </strong>Obesity always leads to profound perturbation of metabolome. Metabolome studies enrich the knowledge on associations between endogenous metabolites and obesity, potentially providing innovative strategies for the development of novel anti-obesity pharmacotherapy. This study aims to identify an endogenous metabolite that regulates energy expenditure and to explore its application for obesity treatment.</p><p><strong>Materials and methods: </strong>C57BL/6 mice were fed with a high-fat and high-cholesterol (HFC) diet, comprising 60% fat and 1.2% cholesterol, for 12 weeks to induce obesity. Significant metabolites were identified in the livers of both health and obese mice through comparative hepatic metabolomics analysis. Correlation between serum or adipose L-aspartate level and body weight in obese mice, as well as human body mass index (BMI), was evaluated. In addition, saline or 200 mg/kg L-aspartate was orally administrated to HFC diet mice and HFC diet-induced obese mice for 6-7 weeks. Body weight, adipose tissue weight, glucose tolerance and liver damage were assessed to evaluate the effect on obesity prevention and treatment. Comprehensive lab animal monitoring system (CLAMS) and seahorse assay were employed to investigate the regulatory effect of L-aspartate on energy metabolism in vivo and in vitro, respectively. 3T3-L1 preadipocytes and murine white adipose tissue (WAT) were utilized to examine the impact of L-aspartate on adipocyte adipogenesis and lipogenesis and cellular signalling pathway in vitro and in vivo.</p><p><strong>Results: </strong>L-aspartate, an approved drug for liver injury and chronic fatigue, was identified as an endogenous inducer of energy expenditure. Serum or adipose L-aspartate levels were found to be negatively correlated with the severity of obesity in both humans and mice. Administration of L-aspartate to HFC diet mice led to a significant reduction in body weight, with decreases of 14.5% in HFC diet mice and 8.5% in HFC diet-induced obese mice, respectively. In addition, the treatment improved related metabolic syndrome (Figure 2 and Figure S3). These therapeutics were associated with enhancements in whole-body energy expenditure and suppression of adipocyte adipogenesis along with activation of Adenosine 5'-monophosphate-activated protein kinase (AMPK) signalling pathway.</p><p><strong>Conclusion: </strong>L-aspartate may serve as a novel endogenous inducer of energy expenditure and suppressor of adipogenesis and lipogenesis along with activation of AMPK, thereby offering a promising therapeutic strategy for obesity prevention and treatment.</p>","PeriodicalId":158,"journal":{"name":"Diabetes, Obesity & Metabolism","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
David R Riley, Alex Henney, Matthew Anson, Gema Hernadez, Sizheng S Zhao, Uazman Alam, John P H Wilding, Sonya Craig, Daniel J Cuthbertson
{"title":"The cumulative impact of type 2 diabetes and obstructive sleep apnoea on cardiovascular, liver, diabetes-related and cancer outcomes.","authors":"David R Riley, Alex Henney, Matthew Anson, Gema Hernadez, Sizheng S Zhao, Uazman Alam, John P H Wilding, Sonya Craig, Daniel J Cuthbertson","doi":"10.1111/dom.16059","DOIUrl":"https://doi.org/10.1111/dom.16059","url":null,"abstract":"<p><strong>Aim: </strong>A bidirectional relationship exists between obstructive sleep apnoea (OSA) and type 2 diabetes (T2D). We aimed to examine the cumulative impact of having both OSA and T2D on patient outcomes, relative to having either condition alone.</p><p><strong>Materials and methods: </strong>Using TriNetX, a global federated research network (n = 128 million), we undertook two retrospective cohort studies, using time-to-event analysis. Analysis 1 compared OSA with T2D versus OSA alone; analysis 2 compared T2D with OSA versus T2D alone. Propensity score matching using greedy nearest neighbour (calliper 0.1) balanced the cohorts (1:1) for significant covariates. Primary outcomes were cardiovascular, liver, diabetes-related (microvascular) and cancer events over 1-5 years.</p><p><strong>Results: </strong>Analysis 1 (n = 179 688): A codiagnosis of T2D/OSA significantly increased risk of all-cause mortality (hazard ratio [HR] 1.52; confidence interval [CI]: 1.48, 1.57), dementia (HR 1.19; CI: 1.12, 1.26), liver (HR 2.20; CI: 1.77, 2.73), pancreatic (HR 1.62; CI: 1.35, 1.93), colon, renal and endometrial cancers; all cardiovascular, microvascular and liver related outcomes versus OSA alone over 1-5 5 years following OSA diagnosis. Analysis 2 (n = 240 094): A codiagnosis of OSA/T2D significantly increased the risk of peripheral (HR 1.39; CI: 1.36, 1.43) and autonomic (HR 1.63; CI: 1.51, 1.75) neuropathy; retinopathy (HR 1.13; CI: 1.09, 1.18), CKD (HR 1.21; CI: 1.18, 1.23); all cardiovascular and liver outcomes; all-cause mortality and several obesity related cancers versus T2D alone.</p><p><strong>Conclusions: </strong>T2D significantly potentiates risk of cardiovascular, malignancy and liver-related outcomes in individuals with OSA. OSA, in individuals with T2D, significantly potentiates risk of cardiovascular disease, malignancy, death and several microvascular complications (retinopathy, CKD, peripheral/autonomic neuropathy).</p>","PeriodicalId":158,"journal":{"name":"Diabetes, Obesity & Metabolism","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}