Background Heart failure (HF) is closely associated with abnormalities in glucose metabolism, which substantially influence clinical outcomes. The hemoglobin glycation index (HGI), reflecting the discrepancy between observed and predicted glycated hemoglobin, has emerged as a marker of interindividual variation in glycation beyond conventional HbA1c. However, the prognostic significance of HGI in hospitalized patients with HF remains unclear. Methods In this retrospective cohort study, we analyzed data from the MIMIC-IV database and included 3,470 adult patients hospitalized with HF. HGI was calculated as the difference between measured HbA1c and predicted HbA1c derived from fasting plasma glucose, and participants were categorized into quartiles. The primary outcome was 365-day all-cause mortality, and the secondary outcome was 30-day all-cause mortality. Kaplan–Meier survival analysis, restricted cubic spline modeling, multivariable Cox regression, and subgroup analyses were performed to evaluate the association between HGI and mortality. Results Among the 3,470 included patients, 837 (24.1%) died within 365 days after discharge. Restricted cubic spline analysis demonstrated a predominantly L-shaped association between HGI and both 30-day and 365-day all-cause mortality, with excess mortality risk mainly concentrated at low HGI values. In multivariable Cox models, compared with the lowest quartile, higher HGI quartiles were associated with significantly lower risks of both short-term and long-term mortality, supporting the particular vulnerability of patients with extremely low HGI. Subgroup analyses generally supported the robustness of these findings, although a significant interaction with diabetes status was observed for 365-day mortality. Conclusions HGI was independently associated with short-term and long-term all-cause mortality in hospitalized patients with HF, with a predominantly L-shaped pattern observed. Excess mortality risk was mainly concentrated at low HGI values. HGI may serve as a simple and accessible marker for risk stratification in this population.
Background Type 2 diabetes mellitus (T2DM) involves alterations in lipid metabolism beyond conventional cholesterol profiles. We examined whether specific plasma lipidomic signatures are related to pericoronary adipose tissue (PCAT) inflammation and coronary artery disease (CAD) burden. Methods This cross-sectional analysis included 176 T2DM participants from the GADA study. PCAT inflammation was measured by the fat attenuation index (FAI), CAD burden by Gensini/SYNTAX scores and plasma lipid species by targeted LC-MS. Multivariable regression were used to identify lipid species associated with FAI and CAD burden. For lipid species linked to both, mediation analyses were performed. Results We quantified 660 lipid molecular species across 20 classes. Five species were associated with FAI: sphingomyelin (SM) (34:4), phosphatidylcholines (PC) (16:0/20:4), Lysophosphatidylethanolamine (LPE) (18:1), LPE (20:4), and LPE (18:2). The three LPE species remained independently associated with both Gensini and SYNTAX scores after adjustment for clinical risk factors, conventional lipid measures, triglycerides, and hsCRP. Mediation analyses indicated that FAI accounted for part of the associations between these LPE species and CAD burden. Conclusions In T2DM patients, circulating LPE (18:1), LPE (20:4), and LPE (18:2) were associated with both PCAT inflammation and CAD burden. These findings point to altered LPE metabolism as a lipid-inflammatory signature linked to residual atherosclerotic burden beyond conventional lipid and glycemic measures.
Depression is a clinically important comorbidity in people living with diabetes, yet biological pathways linking these conditions remain unclear. Chronic inflammation has been proposed as one mechanism connecting metabolic dysfunction with depressive symptoms. This scoping review examined knowledge on inflammation and depression/depressive symptoms in adults with diabetes, with attention to differences by diabetes type and sex. Thirty-seven studies met inclusion criteria, predominantly observational and focused on type 2 diabetes. Inflammatory markers were more frequently associated with depressive symptoms in type 2 diabetes than in type 1. CRP/hs-CRP was the most commonly studied biomarker and was often positively associated with depressive symptoms, while composite immune-metabolic indices reflected depressive symptom burden across studies. In contrast, findings for individual cytokines, including IL-6 and TNF-α, were heterogenous and appeared dependent on adiposity, metabolic health, or vascular comorbidity. Evidence in type 1 diabetes was less uniform, with studies suggesting involvement of vascular, lipid-associated, or non-classical inflammatory pathways. Sex appeared to modify inflammation and depression associations, although patterns varied across biomarkers and study populations. Overall, the literature suggests that inflammation is relevant to depression in diabetes, particularly in type 2, but that this relationship is heterogeneous and shaped by diabetes type, sex, adiposity, and vascular burden.
Background Atherosclerotic cardiovascular disease (ASCVD) is one of the common complications in patients with type 2 diabetes mellitus (T2DM). Thyroid hormones affect cardiovascular function through multiple pathways. Purpose To explore the relationships between impaired thyroid hormone sensitivity and the 10-year risk of ASCVD in euthyroid patients with T2DM. Methods 899 patients with T2DM were divided into three groups according to the different ASCVD risk levels, the difference of thyroid hormone sensitivity indices [Parametric Thyroid Feedback Quantile-based Index (PTFQI), Thyroid Feedback Quantile-based Index (TFQI), Thyroid Stimulating Hormone Index (TSHI), Serum-Free triiodothyronine to Free thyroxine (FT3/FT4) ratio, and Thyrotropin Thyroxine Resistance Index (TT4RI)] between three groups were compared. Results As the 10-year ASCVD risk grade increased, TT4RI level showed a gradually rising trend, while FT3/FT4 ratio exhibited a decreasing trend ( P < 0.05). PTFQI, TFQI, TSHI, and TT4RI were positively, and FT3/FT4 was negatively correlated with ASCVD risk (all P < 0.05). Thyroid hormone sensitivity indicators had a linear dose-response relationships with ASCVD risk. As the levels of PTFQI, TFQI, TSHI, and TT4RI increase and the level of FT3/FT4 decreases, the ASCVD risk showed an upward trend. Conclusion To patients with T2DM, impaired thyroid hormone sensitivity is associated with ASCVD risk.
Peptides have emerged as key regulators of cardiovascular physiology and increasingly important tools in the diagnosis and management of cardiovascular disease (CVD). Endogenous peptide systems, including natriuretic peptides (NPs), the renin angiotensin system (RAS), and vasopressin, play central roles in maintaining vascular tone, fluid balance, and cardiac remodeling, while their dysregulation contributes to disease progression. Clinically, peptide-based biomarkers such as NPs and copeptin are widely used for diagnosis, risk stratification, and prognostic assessment. Beyond their diagnostic utility, peptides have gained significant attention as therapeutic targets. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have demonstrated cardiometabolic benefits, including reductions in cardiovascular events and improvements in metabolic profiles. In parallel, advances in peptide engineering have enabled the development of innovative therapeutic strategies, including targeted drug delivery systems, regenerative therapies, and enzyme-responsive biomaterials designed to enhance myocardial repair. This review provides a comprehensive overview of the biological, diagnostic, and therapeutic roles of peptides in cardiovascular medicine. Collectively, these findings highlight the expanding clinical relevance of peptides and their potential to support precision-based approaches in cardiovascular care.
Diabetic retinopathy (DR) is a leading cause of vision impairment among individuals with diabetes, driven by microvascular damage and retinal degeneration. Recent evidence implicates ceramides—bioactive sphingolipids—as critical mediators in DR pathogenesis. These lipids influence critical cellular processes, including apoptosis, inflammation, and oxidative stress. Emerging data suggests that ceramide accumulation exacerbates retinal neurodegeneration in DR by modulating key molecular pathways. This review synthesizes current knowledge on the role of ceramides in DR development and progression, examines the factors influencing their activity, and explores the therapeutic potential of targeting ceramide metabolism. By integrating recent findings, this article aims to provide insights for future research and clinical strategies in DR management.
Purpose To elucidate the dynamic molecular evolution and immune heterogeneity in diabetic retinopathy (DR) and identify diagnostic biomarkers. Methods Multi-omics integrative analysis was performed on peripheral blood transcriptomic data from diabetic patients with and without DR. Techniques included differential expression analysis, immune infiltration profiling, unsupervised clustering, and LASSO regression for biomarker selection. Findings were validated in an independent high-glucose-treated endothelial cell model. Results DR progression exhibits staged molecular evolution from diabetes (immune suppression) to early DR (cell cycle inhibition, immune burst) and advanced DR (metabolic stress, persistent immune dysregulation). Six co-downregulated immune modules indicated systemic immune suppression. Patients were classified into three immune subtypes: vascular-inflammatory, metabolic disorder, and oxidative stress-tissue remodeling. A diagnostic model based on IK, PLBD2, FLNA, H6PD, and ZMAT2 achieved an AUC of 0.876 for distinguishing DR from diabetes alone. Conclusion This study delineates the dynamic molecular landscape and immune heterogeneity of DR, providing a potential multi-gene diagnostic signature and a framework for patient stratification, which may facilitate early detection and personalized management.
Aims Sensory tests such as vibration perception threshold (VPT), monofilament, pinprick, and temperature sensation are used to detect diabetic peripheral neuropathy (DPN). This study examined associations between these tests and chronic diabetic complications in type 2 diabetes, focusing on the clinical relevance of VPT. Methods In this retrospective study, 652 patients with type 2 diabetes evaluated at a tertiary center (2014–2024) underwent standardized neurological assessments. Based on VPT, patients were categorized as normal (<16 V), borderline (16–24 V), or abnormal (≥25 V). Associations between sensory tests and retinopathy, nephropathy, ischemic heart disease (IHD), cerebrovascular disease (CeVD), and diabetic foot ulcer (DFU) were examined in cross-sectional and longitudinal analyses. Results Abnormal VPT was present in 31.3% of patients and was independently associated with all five complications after multivariable adjustment: IHD (OR: 2.15), CeVD (OR: 3.31), DFU (OR: 15.94), retinopathy (OR: 7.66), and nephropathy (OR: 2.56). Borderline VPT was also independently associated with several outcomes. In a longitudinal subset (n=221; median follow-up ∼5 years), abnormal VPT was associated with incident IHD, DFU, retinopathy, and nephropathy. Conclusion VPT showed strong associations with microvascular and macrovascular complications, supporting its role as a practical indicator of systemic disease burden in type 2 diabetes.
Objective This work aimed to verify the value of miR-143-3p in diabetic cardiomyopathy (DCM). Methods The ROC curve, correlation analysis, and multivariate Logistic regression analysis assessed the diagnostic value, association with DCM, and DCM risk factors. Bioinformatic analysis predicted the downstream targets of miR-143-3p. Dula-luciferase reporter assay validated the interaction between miR-143-3p and ERBB3. In vitro high glucose (HG)-stimulated cardiomyocyte (AC16) injury was employed to clarify the mechanism of the miR-143-3p/ERBB3 axis in DCM. Results Upregulation of miR-143-3p was observed in the DM group and further elevated in the DCM group compared with healthy individuals. The upregulated miR-143-3p expression distinguished subjects with DM from healthy individuals and diagnosed subjects with DCM from DM. MiR-143-3p expression was associated with blood glucose, myocardial injury, and cardiac function of DCM, and predicted the risk for DCM development. In vitro, the inhibition of miR-143-3p attenuated HG-induced AC16 cell injury through improving cell proliferation, suppressing apoptosis, inflammation, oxidative stress, and the release of myocardial enzymes by upregulating the ERBB3 expression. Conclusions Upregulation of miR-143-3p showed a diagnostic potential for DCM and predicted the progression of DCM. In vitro, miR-143-3p promoted HG-induced cardiomyocyte injury by targeting ERBB3, which might provide novel insights for DCM clinical management.
Introduction Metabolic dysfunction–associated steatotic liver disease (MASLD) is a recognized cardiometabolic risk factor in adults, but its relevance to early vascular remodeling in youth with type 1 diabetes (T1D) remains unclear. We evaluated the independent associations of hepatic fat and body composition with early structural vascular remodeling in youth with T1D. Methods This cross-sectional study included 49 late-pubertal youth with T1D (mean age 16.1±2.6 years; duration 7.5±4.3 years). Hepatic fat was quantified using MRI–proton density fat fraction (PDFF), while body composition and estimated insulin sensitivity (eIS) were assessed using dual-energy X-ray absorptiometry and a validated pediatric equation. Carotid intima–media thickness (cIMT), measured by ultrasound, served as the primary outcome. Hierarchical linear regression assessed independent associations after adjustment for age, sex, and diabetes duration. Results Mean hepatic fat was 1.87±1.22%, with no participants meeting criteria for steatosis. Hepatic fat, eIS, and diabetes duration were not associated with cIMT. Lean body mass was the primary independent associate of cIMT (β=0.44, p=0.02). Although eIS was strongly associated with waist circumference (r=−0.76, p<0.001), neither variable was associated with cIMT. Conclusions In this sub-steatotic cohort, cIMT was primarily associated with lean body mass, reflecting physiologic growth, while central adiposity was associated with metabolic dysfunction but not vascular structure.
Diabetes mellitus (DM) approximately doubles the risk of atherosclerotic cardiovascular disease (ASCVD) events, but the molecular basis is poorly understood. Using RNA-sequencing data from two arterial sites in >90 people with DM and >330 controls, we defined differentially expressed genes (DEGs) associated with DM. UK Biobank (UKB) was then used to corroborate that DEGs in their plasma protein form were differentially abundant in people with DM and associated with ASCVD events. 619 and 356 DEGs were associated with DM in the thoracic aorta and tibial artery, respectively. Of these, 22 were common to both arteries, all of which were directionally concordant. Of these, 5 were included in the UKB plasma proteomics dataset and we corroborated 4 (ACP5, LEFTY2, LILRA5 and PSME2) as showing concordant differential abundance in people with DM; all were associated with a range of incident ASCVD events. Addition of the 4 proteins to the SCORE2 and SCORE2-Diabetes risk models (for people without and with DM, respectively) improved the population-level discrimination, classification and calibration of these models. These data show that DM is associated with a distinct arterial gene expression profile, hits from which are associated with ASCVD events and add value to risk prediction.
Background With the increasing use of GLP-1 receptor agonists and dual GIP/GLP-1 agonists for managing obesity and type 2 diabetes, understanding their real-world effectiveness and safety is essential. This TriNetX analysis directly compares clinical outcomes among patients treated with tirzepatide vs semaglutide. Method We utilized data from the TriNetX Research Network, identifying patients aged > 40 years or with obesity (“BMI ≥ 30 kg/m2”) and type 2 diabetes (HbA1c ≥ 6.5% or fasting glucose.≥ 125 mg/dL). Qualifying events were restricted to May 1, 2022, through November 21, 2024. We established two cohorts: one initiating tirzepatide and another semaglutide, ensuring each patient had at least three prescriptions and no prior exposure to the comparator drug or other GLP-1 receptor agonists. The index date was defined as the first co-occurrence of the obesity/diabetes criteria and the respective drug prescription. To ensure comparability, we performed 1:1 propensity matching, resulting in 47,804 patients in each cohort. Outcomes, including all-cause mortality, MACE, heart failure exacerbation, ischemic stroke/TIA, hospitalization/ED use, dementia, UTI, adverse Gastrointestinal (GI) effects, and changes in HbA1c, were assessed within a 1-year window after the index date. Results Our matched cohort had a mean age of 75 years, with 45% male patients and 74% identified as white. Patients treated with tirzepatide experienced a significantly lower incidence of MACE at “(“3.7% vs 4.1% (RR 0.918, 95% CI 0.862-0.978). All-cause mortality was also lower with tirzepatide (0.2% vs. 0.4%; Risk Ratio 0.436, 95% CI 0.338-0.562). The tirzapetide group achieved better glycemic control with a lower mean HbA1c (6.565% vs. 6.848%; p < 0.001) during the follow-up. There was no significant difference in heart failure exacerbation or UTI incidence. GI side effects were slightly less frequent in the tirzepatide cohort (9.8% vs. 10.2%; Risk Ratio 0.959, 95% CI 0.924-0.997), while hospitalization or emergency visits were comparable between the two groups. Conclusion In this propensity matched cohort of patients with obesity and type 2 diabetes, tirzepatide demonstrated improved cardiometabolic outcomes compared to semaglutide, including lower all-cause mortality and lower HbA1c. These findings support the cardiovascular safety and efficacy of tirzapetide and highlight the need for further studies to evaluate its effectiveness in broader clinical populations.
Background Cardiovascular complications are the leading cause of mortality in patients with diabetes mellitus (DM) undergoing percutaneous coronary intervention (PCI). This systematic review aims to evaluate the association between HbA1c levels and major adverse cardiovascular events (MACE) in patients with DM post-PCI. Methods A comprehensive literature search was conducted following PRISMA guidelines. Eligible studies included randomized controlled trials, cohort studies, and observational analyses assessing the impact of strict, moderate, and poor glycaemic control on cardiovascular outcomes. Data extraction focused on HbA1c levels, MACE incidence, cardiovascular mortality, and cardiovascular complications. Results Nine studies with 24,978 participants were included. U-shaped and J-shaped relationships were found between HbA1c levels and cardiovascular outcomes. Moderate glycaemic control (HbA1c 6.5%–7.5%) was associated with the lowest risk of MACE and mortality. In contrast, strict glycaemic control (HbA1c <6.5%) and poor control (HbA1c >7.5%) were linked to increased cardiovascular risk. Patients with HbA1c below 5.5% exhibited a significantly higher risk of cardiovascular mortality, while HbA1c above 8% was also associated with poor outcomes. Conclusion Maintaining HbA1c levels in the moderate range (6.5%–7.5%) appears to provide optimal cardiovascular protection for patients with DM post-PCI. Strict or poor glycaemic control increases the risk of adverse outcomes.
BackgroundDiabetes mellitus (DM) has paradoxically been associated with slower abdominal aortic aneurysm (AAA) growth, despite its adverse vascular profile.MethodsWe present a focused synthesis of contemporary longitudinal cohort studies reporting AAA growth rates according to diabetes status and metformin exposure.ResultsAcross six independent cohorts, patients with diabetes consistently exhibited slower aneurysm expansion compared with patients without diabetes, with reported differences of approximately 0.5-1.5 mm/year. Three cohorts further demonstrated that metformin use was independently associated with additional attenuation of AAA growth, with an adjusted reduction of approximately 0.3-0.4 mm/year.ConclusionAvailable clinical evidence consistently supports an inverse association between diabetes and AAA growth, with metformin emerging as a potential disease-modifying factor. These findings highlight metabolic modulation as a promising avenue for individualized surveillance strategies and future therapeutic investigation in AAA.
Background Cardiovascular disease (CVD) is the leading cause of death in individuals with type 1 diabetes (T1D). Epidemiological studies indicate that women with T1D are at greater risk of CVD compared to men with T1D. The present study sought to investigate differences in vascular health between men and women with T1D. Methods 53 women with T1D and 25 men with T1D participated in this study. The flow-mediated dilation (FMD) test assessed endothelial-dependent conduit vessel function and nitroglycerin (NTG) was used to assess endothelial-independent vasodilation. In addition, cutaneous post-occlusive reactive hyperemia (PORH), local thermal heating (LTH), and iontophoresis of acetylcholine (ACH) were conducted to assess microvascular function, and pulse wave velocity (PWV) and pulse wave analysis (AIx75) were used as indices of arterial and aortic stiffness, respectively. Near-infrared spectroscopy was utilized to assess skeletal muscle oxidative capacity (SMOC). Results Hemoglobin A 1c ( p =0.904) was similar between men and women with T1D. Women with T1D exhibited higher FMD ( p =0.010) and AIx75 ( p <0.001) compared with men with T1D. There were no differences in PORH, LTH, ACH, PWV, or SMOC between groups (all p >0.05). Discussion Findings from the present investigation demonstrate that women with T1D exhibit greater conduit vessel endothelial function yet increased aortic stiffness compared to men with T1D. This paradox of enhanced endothelial function and arterial stiffness highlights the complex relationship between vascular structure and function in T1D and the need to assess multiple indices of vascular health when evaluating cardiovascular disease risk in men and women with T1D.
Micronutrients have become one of the potentially adjustable determinants of the pathophysiology and complications of T2DM. Of them, vitamin D and B12 have been particularly highlighted. Objectives: to estimate the prevalence of both vitamin D and B12 deficiencies in parallel association with T2DM patients and their relationships with major metabolic and hepatic parameters. This study adopted a cross-sectional analytical design performed in a healthcare center located in the district of Ramallah in Palestine. In total, 295 patients fulfilled these criteria and were included in this final analysis. The present study underlines the high prevalence of vitamin D deficiency and the relatively lower, but clinically relevant, incidence of vitamin B12 deficiency in patients affected by type 2 diabetes mellitus within the adult population of the Ramallah district in Palestine. It also demonstrated that low levels of vitamin D were strongly associated with important metabolic and cardiovascular risk factors.
Objective This study investigated the expression and diagnostic significance of LINC00861 in DN and explored its functional mechanisms in high glucose-induced cell damage. Methods We enrolled 285 participants: 92 healthy controls, 98 uncomplicated T2DM patients, and 95 DN patients. Serum LINC00861 and miR-378a-3p levels were measured via qRT-PCR. Correlations with clinical parameters were assessed using Pearson analysis. Logistic regression identified risk factors for DN progression, and ROC curves evaluated diagnostic accuracy. In vitro, LINC00861 was knocked down to assess its effects on proliferation, inflammation, and oxidative stress under high glucose. Targeting of miR-378a-3p was confirmed by dual-luciferase and RIP assays. Results The LINC00861 expression was significantly elevated in DN patients compared to T2DM and healthy controls, and correlated positively with FBG, HbA1c, and albuminuria, but negatively with eGFR. Multivariate analysis identified LINC00861 as an independent risk factor for DN. The AUC for distinguishing T2DM from DN was 0.918. miR-378a-3p expression was significantly lower in DN patients than in those with T2DM or healthy controls. LINC00861 silencing may alleviate HG induced aberrant proliferation, inflammatory responses, and oxidative stress, possibly via the regulation of miR-378a-3p. Conclusion The LINC00861 is upregulated in DN and may facilitate renal injury by sponging miR-378a-3p, indicating its potential as a diagnostic biomarker and therapeutic target.
ObjectiveTo descriptively compare the clinical outcomes of drug-coated balloons (DCB) and plain balloon angioplasty (POBA) in hemodialysis patients with Below-The-Knee (BTK) peripheral artery disease.MethodsThis retrospective study included 96 hemodialysis patients (DCB:55 POBA:41). Outcomes included changes in Rutherford grade, wound healing, freedom from target lesion revascularization (CD-TLR), survival, and amputation-free survival.ResultsBoth groups demonstrated improvement in Rutherford grade at 12 months. Wound healing occurred in 60.6% (95% CI 42.1-76.8) of the DCB group and 50.0% (95% CI 32.0-67.9) of the POBA group. Amputation-free survival was 72.7% (95% CI 59.0-83.0) with DCB and 67.7% (95% CI 52.5-80.0) with POBA. Freedom from CD-TLR was 78.9% (95% CI 65.0-88.5) for DCB and 91.6% (95% CI 79.0-97.0) for POBA. No clear between-group differences were observed.ConclusionNo significant differences were observed between DCB and POBA in this small retrospective cohort.
Aims Colchicine is effective for secondary prevention of major adverse cardiovascular events (MACE), yet its benefit in individuals with diabetes remains uncertain despite their elevated cardiovascular risk. This systematic review and meta-analysis assessed the impact of colchicine on cardiovascular outcomes in individuals with diabetes. Methods Databases were searched from inception to November 2024 for randomized controlled trials assessing colchicine for reducing MACE. A meta-analysis was performed using RevMan 5.4 with a fixed-effects inverse-variance model to generate pooled risk ratios (RR, HR). PROSPERO registration: CRD42024575366. Results Five RCTs were included, comprising 2977 participants with diabetes (1492 (50%) colchicine; 1485 (50%) placebo/usual care). Most were males over 60 years. Colchicine significantly reduced MACE, HR 0.79 (95% CI 0.67–0.94, p = 0.006). Subgroup analysis of diabetic versus non-diabetic participants yielded a similar effect, HR 0.75 (95% CI 0.67–0.83, p < 0.001). Colchicine did not increase adverse events: composite events RR 0.81 (95% CI 0.68–0.96; p = 0.02), gastrointestinal events RR 1.09 (95% CI 0.98–1.20, p = 0.12), or musculoskeletal events RR 0.77 (95% CI 0.43–1.38, p = 0.39). Benefits were observed with 0.5 mg daily over a median 28.6 months. Conclusion Colchicine is associated with a reduction in major cardiovascular events in individuals with diabetes, with consistent long-term benefit at low doses without an increase in adverse effects.
IntroductionPreviously, we observed that subgroups of type 2 diabetes (T2D) - mild obesity-related diabetes (MOD), mild age-related diabetes (MARD), severe insulin-resistant diabetes (SIRD) - had distinct characteristics and complications. This study aims to investigate if movement behaviour also differs by T2D subgroup. Given that physical activity (PA) reduces the risk of complications, identifying less active subgroups could inform more targeted interventions.MethodsUsing age at T2D onset, body mass index, hbA1c, homeostasis model assessment 2 estimates of beta-cell function and insulin resistance, 706 study participants were classified into T2D subgroups. Using time spent in light PA, moderate-vigorous PA, day inactivity and night sleep per 24-hour, the participants were classified into three profiles. Regression models were used to examine the association between T2D subgroup (exposure) and movement behaviour (outcome).ResultsCompared to MOD, the relative risk ratio (RRR) of having the least active profile was 0.69 (95%CI 0.43-1.10), while the RRR of having the most active profile was 1.53 (95%CI 0.82-2.83) for MARD. The RRRs of having the least and most active profile was 1.32 (95%CI 0.85-2.04) and 1.44 (95%CI 0.76-2.72) respectively for SIRD.ConclusionUnderstanding the relationship between T2D subgroups and movement behaviour is a step towards advocating for PA intervention tailored to each subgroup's unique characteristics.
