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Objective: To evaluate the effectiveness and safety of combining SGLT2 inhibitors with or without DPP4 inhibitors as an add-on therapy for type 2 diabetes patients. Study Design: Quasi-Experimental Study Place and Duration of Study: Dr. Ruth KM Pfau Civil Hospital and Dow University Hospital Ojha Campus, Dow University of Health Sciences, Karachi, Pakistan, from Mar 21 to Dec 23.  Methodology: The study assessed type 2 diabetes patients on Metformin alone with an HbA1c level exceeding 7% and evaluated various clinical and biochemical markers. Results: In a study of 239 obese and poorly controlled diabetic patients, 58.58% were female, and 41.42% were male, with an age range of 40-60 years. Diabetes duration was below 5 years in 17.57% of patients, between 5 and 10 years in 44.45%, and over 10 years in 38.07%. The treatment groups were as follows: Metformin + SGLT2 inhibitors (27.00%), Metformin + DPP4 inhibitors (32.00%), and all three combinations (41.00%). During a span of 36 weeks, a significant difference was seen in the levels of HbA1c (p < 0.001). Moreover, the BMI of male subjects. In addition, there were significant decreases in FBS, RBS, and triglyceride levels, whereas creatinine levels did not change. Conclusion: Metformin, when combined with SGLT2 and DPP4 inhibitors, improves glycaemic control and weight reduction in morbid obesity patients, especially in males, with significant changes in HbA1c, fasting, and postprandial glucose levels.

This 10-year study aimed to evaluate how glycaemic control, diabetes duration and coronary stenosis severity affect mortality in patients with stable coronary artery disease (CAD) and type 2 diabetes mellitus (T2DM) and to perform multifactorial risk analysis to find key modifiable factors for better risk stratification and secondary prevention. This retrospective cohort study involved 150 patients with T2DM with chronic coronary syndrome who had coronary angiography at a single centre between 2011 and 2012. Demographic and biochemical data were collected. Patients were divided into intensified and relaxed control groups based on glycated haemoglobin (HbA1c) levels (≤7.5% and >7.5%). The Gensini score was used to assess coronary angiography results. Multivariate Cox regression analysis was used to find risk factors. Kaplan-Meier analysis was used to compare glycaemic control incidence in subgroups. The median diabetes duration was 2.0 years. Adjusted hazard ratios (95% CI) for all-cause mortality were 1.10 (1.06-1.15) for age, 1.29 (1.12-1.48) for HbA1c, 1.06 (1.02-1.10) for diabetic duration and 1.02 (1.01-1.02) for Gensini score. For cardiovascular mortality, the ratios were 1.10 (1.05-1.15) for age, 1.36 (1.16-1.58) for HbA1c, 1.06 (1.00-1.10) for diabetic duration, 1.12 (1.04-1.23) for direct bilirubin, 0.89 (0.83-0.95) for serum total protein and 1.02 (1.01-1.03) for Gensini score. Kaplan-Meier analysis showed higher cardiovascular mortality in patients with HbA1c >7.5% and diabetic duration >10 years ( = 0.0004). When deciding on glycaemic control, individual frailty, life expectancy, diabetes duration and coronary stenosis should be considered. This study combines diabetes duration, Gensini-scored coronary stenosis severity and glycaemic control into a prognostic model, providing a new framework for personalised risk stratification in patients with T2DM with stable CAD.

Aims/hypothesis The aim of this study was to examine the relationship between glycaemic control and hospitalisation for heart failure in patients with type 2 diabetes. Methods Patients included in the Swedish National Diabetes Register (NDR) during 1998–2003 were followed until hospitalisation for heart failure, death or 31 December 2009. Unadjusted and adjusted incidence rates for heart failure were estimated by Poisson regression and relative risk was estimated by Cox regression. Results In 83,021 patients with type 2 diabetes, 10,969 (13.2%) were hospitalised with a primary or secondary diagnosis of heart failure during a mean follow-up of 7.2 years. The incidence increased by male sex ( p  < 0.001), older age ( p  < 0.001) and longer diabetes duration ( p  < 0.001). In Cox regression adjusting for risk factors of heart failure the HR per each percentage unit higher HbA 1c (10 mmol/mol) for heart-failure hospitalisation was 1.12 (95% CI 1.10, 1.14). By category of HbA 1c the HR for heart failure hospitalisation was: HbA 1c 6.0 to <7.0% (42 to <53 mmol/mol), 0.91 (95% CI 0.84, 0.98); HbA 1c 7.0 to <8.0% (53 to <64 mmol/mol), 0.99 (95% CI 0.91, 1.07); HbA 1c 8.0 to <9.0% (64 to <75 mmol/mol), 1.10 (95% CI 1.01, 1.20); HbA 1c 9.0 to <10.0% (75 to <86 mmol/mol), 1.27 (95% CI 1.15, 1.41); HbA 1c ≥10.0 % (≥86 mmol/mol), 1.71 (1.51, 1.93) (reference HbA 1c <6% [42 mmol/mol]). The HR for patients with HbA 1c 7.0 to <8.0% (53 to <64 mmol/mol) compared with patients with HbA 1c 6.0 to <7.0% (42 to <53 mmol/mol) was 1.09 (95% CI 1.03, 1.14). Conclusions/interpretation Poor glycaemic control (HbA 1c >7% [53 mmol/mol]) is associated with an increased risk of hospitalisation for heart failure in patients with type 2 diabetes.

Aims/hypothesis: Our study aims to uncover glycaemic phenotype heterogeneity in type 1 diabetes.Methods: In the Study of the French-speaking Society of Type 1 Diabetes (SFDT1), we characterised glycaemic heterogeneity thanks to a set of complementary metrics: HbA1c, time in range (TIR), time below range (TBR), CV, Gold score and glycaemia risk index (GRI). Applying the Discriminative Dimensionality Reduction with Trees (DDRTree) algorithm, we created a phenotypic tree, i.e. a 2D visual mapping. We also carried out a clustering analysis for comparison.Results: We included 618 participants with type 1 diabetes (52.9% men, mean age 40.6 years [SD 14.1]). Our phenotypic tree identified seven glycaemic phenotypes. The 2D phenotypic tree comprised a main branch in the proximal region and glycaemic phenotypes in the distal areas. Dimension 1, the horizontal dimension, was positively associated with GRI (coefficient [95% CI]) (0.54 [0.52, 0.57]), HbA1c (0.39 [0.35, 0.42]), CV (0.24 [0.19, 0.28]) and TBR (0.11 [0.06, 0.15]), and negatively with TIR (-0.52 [-0.54, -0.49]). The vertical dimension was positively associated with TBR (0.41 [0.38, 0.44]), CV (0.40 [0.37, 0.43]), TIR (0.16 [0.12, 0.20]), Gold score (0.10 [0.06, 0.15]) and GRI (0.06 [0.02, 0.11]), and negatively with HbA1c (-0.21 [-0.25, -0.17]). Notably, socioeconomic factors, cardiovascular risk indicators, retinopathy and treatment strategy were significant determinants of glycaemic phenotype diversity. The phenotypic tree enabled more granularity than traditional clustering in revealing clinically relevant subgroups of people with type 1 diabetes.Conclusions/interpretation: Our study advances the current understanding of the complex glycaemic profile in people with type 1 diabetes and suggests that strategies based on isolated glycaemic metrics might not capture the complexity of the glycaemic phenotypes in real life. Relying on these phenotypes could improve patient stratification in type 1 diabetes care and personalise disease management.

Individuals of South Asian (SA) descent display a higher risk for cardiovascular disease and type 2 diabetes mellitus than their White European (WE) counterparts. Heat therapy, such as hot water immersion (HWI), can improve microvascular function and glycaemic control, although effects across racial groups are unknown. This study compared how repeated HWI influenced microvascular function, glycaemic control and markers of inflammation in males of WE and SA descent. Ten WE and SA males completed ten 60 min HWI sessions over 14 days. Before and after HWI, forearm and great toe cutaneous vascular conductance (CVC) responses to postocclusive reactive hyperaemia and local heating (LH) were measured, resting blood samples were collected, and an oral glucose tolerance test (OGTT) was conducted. Baseline great toe CVC did not differ between racial groups ( P  = 0.670), but forearm CVC was lower in SA ( P  = 0.010). For postocclusive reactive hyperaemia, forearm and great toe peak CVC and area under the curve were unchanged by HWI ( P  ≥ 0.300), whereas CVC during 42°C LH increased at both sites after HWI ( P  ≤ 0.037), as did great toe CVC during 44°C LH ( P  = 0.021). Glucose and insulin concentrations were elevated in SA during the OGTT ( P  ≤ 0.035); glucose concentration and peak insulin reduced after HWI in SA ( P  ≤ 0.024), but not in WE. The interleukin‐6:interleukin‐10 ratio was unchanged by HWI ( P  = 0.159), but elevated in SA ( P  = 0.006). Repeated HWI increased microvascular responses to LH to a similar extent between racial groups and reduced early‐phase OGTT glucose concentrations in SA, although insulin sensitivity was unchanged. These findings support HWI as a health‐promoting intervention. What is the central question of this study? Are there racial differences in the effects of repeated hot water immersion on microvascular function, glycaemic control and inflammatory markers between White European and South Asian males? What is the main finding and its importance? Hot water immersion increased microvascular responses to cutaneous local heating to a similar extent between racial groups and reduced glucose concentrations during an oral glucose tolerance test in South Asians, although insulin sensitivity was unchanged. These findings support hot water immersion as a health‐promoting intervention, particularly for South Asian males, who typically present with elevated microvascular and metabolic dysfunction.

Aims/hypothesisThe aim of this work was to assess the effectiveness of continuous glucose monitoring (CGM) vs self-monitoring of blood glucose (SMBG) in maintaining glycaemic control among people with type 1 diabetes mellitus.MethodsCochrane Library, PubMed, Embase, CINAHL, Scopus, trial registries and grey literature were searched from 9 June 2011 until 22 December 2020 for RCTs comparing CGM intervention against SMBG control among the non-pregnant individuals with type 1 diabetes mellitus of all ages and both sexes on multiple daily injections or continuous subcutaneous insulin infusion with HbA1c levels, severe hypoglycaemia and diabetic ketoacidosis (DKA) as outcomes. Studies also included any individual or caregiver-led CGM systems. Studies involving GlucoWatch were excluded. Risk of bias was appraised with Cochrane risk of bias tool. Meta-analysis and meta-regression were performed using Review Manager software and R software, respectively. Heterogeneity was evaluated using χ2 and I2 statistics. Overall effects and certainty of evidence were evaluated using Z statistic and GRADE (Grading of Recommendations, Assessment, Development and Evaluation) software.ResultsTwenty-two studies, involving 2188 individuals with type 1 diabetes, were identified. Most studies had low risk of bias. Meta-analysis of 21 studies involving 2149 individuals revealed that CGM significantly decreased HbA1c levels compared with SMBG (mean difference −2.46 mmol/mol [−0.23%] [95% CI −3.83, −1.08], Z = 3.50, p=0.0005), with larger effects experienced among higher baseline HbA1c >64 mmol/mol (>8%) individuals (mean difference −4.67 mmol/mol [−0.43%] [95% CI −6.04, −3.30], Z = 6.69, p<0.00001). However, CGM had no influence on the number of severe hypoglycaemia (p=0.13) and DKA events (p=0.88). Certainty of evidence was moderate.Conclusions/interpretationCGM is superior to SMBG in improving glycaemic control among individuals with type 1 diabetes in the community, especially in those with uncontrolled glycaemia. Individuals with type 1 diabetes with HbA1c >64 mmol/mol (>8%) are most likely to benefit from CGM. Current findings could not confer a concrete conclusion on the effectiveness of CGM on DKA outcome as DKA incidences were rare. Current evidence is also limited to outpatient settings. Future research should evaluate the accuracy of CGM and the effectiveness of CGM across different age groups and insulin regimens as these remain unclear in this paper.PROSPERO registrationRegistration no. CRD42020207042.FundingThis research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.

Diabetes is one of the most prevalent cardiometabolic disorders on the planet. Type 1 diabetes accounts for only a minority of all cases (recently estimated to be ~2% globally); however, since this is a disorder with an early onset, many people live with type 1 diabetes for a long time. CVD and premature death are the main long-term outcomes for both types of diabetes; however, the type of diabetes that carries the highest risk of these outcomes is a controversial topic and has not been widely studied. Because of the association between diabetes and CVD, the rise in type 2 diabetes prevalence over the past decades has huge effects on global health. The excess risk in people with diabetes compared with those without depends, to a large extent, on the presence of other factors, such as general cardiovascular risk factors (e.g. elevated LDL-cholesterol, hypertension and smoking) and also factors that are more specific to diabetes (e.g. HbA1c, and micro- and macroalbuminuria). Some contributory factors are modifiable, while others are not, such as age, sex and type of diabetes. Older people with type 2 diabetes who have risk factors that are under control can achieve levels of CVD risk that are similar to that of the general population, while younger individuals with type 1 diabetes are mostly unable to achieve similar levels of risk, probably because of long and cumulative exposure to raised blood glucose levels. Despite reports of declining rates of CVD among people with type 1 and type 2 diabetes, rising rates of both types of diabetes lead to a continuing rise in the number of people with cardiometabolic disorders worldwide, offsetting the progress made in many countries. Comparison between individuals with type 1 and type 2 diabetes with respect to risk of CVD is fraught with difficulties and highly dependent on other, concomitant factors, some of which are modifiable and others not. Nonetheless, as a whole, what matters most in determining the management of diabetes is absolute risk and lifetime risk. Life-long efforts to achieve glycaemic control, control of lipids and hypertension, and not smoking are key to prevention, with a healthy lifestyle and pharmacological therapy to be implemented as needed. Graphical abstract

To assess the glycaemic response after ingestion of two specialised oral and enteral nutrition formulas for glycaemic control. The participants were sixteen healthy volunteers, aged 21–49 years, with normal glucose tolerance. The volunteers attended the tests fasting for 10 h, for 5 weeks, and consumed the reference food – glucose solution – for 3 weeks, and the two formulas DiamaxO and DiamaxIG in the following weeks, in amounts equivalent to 25 g of available carbohydrates. During the period of 120 min, seven blood samples were taken through capillary blood sampling to determine the glycaemic response. The glycaemic index (GI) was calculated according to the trapezoidal rule, ignoring areas below the fasting line. The glycaemic load (GL) was determined by the formula GL = ((GI(glucose = reference) × ‘g’ of available carbohydrate per serving]/100. The formulas showed low GI and GL. GI = 37·8 and GL = 6·6 for DiamaxO and GI = 21·5 and GL = 3·5 for DiamaxIG. The peak of the glycaemic response occurred 30 min after ingestion, with a marked difference in blood glucose between the Diamax products in relation to glucose. Differences were also significant at times 15, 45, 60 and 90 min in relation to glucose (ANOVA with post hoc Bonferroni, P < 0·005), but not between the two products. However, the AUC and the GI of DiamaxIG are significantly smaller than that of the DiamaxO second t test (P = 0·0059). The glycaemic response to the products is quite reduced, presenting a curve with a little accentuated shape, without high peak, especially in the modified product.

CONTEXT: Neurodevelopmental disorders are more prevalent in childhood-onset type 1 diabetes than in the general population, and the symptoms may limit the individual's ability of diabetes management. It remains unknown whether comorbid neurodevelopmental disorders are associated with long-term glycaemic control and risk of diabetic complications. METHODS: This population-based cohort study used longitudinally collected data from Swedish registers. We identified 11,326 individuals born 1973-2013, diagnosed with type 1 diabetes 1990-2013 (median onset age: 9.6 years). Out of them, 764 had a comorbid neurodevelopmental disorder, including attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder, and intellectual disability. We used multinomial logistic regression to calculate odds ratios (ORs) of having poor glycaemic control (assessed by mean of glycated haemoglobin [HbA1c]) and Cox regression to estimate hazard ratios (HRs) of nephropathy and retinopathy. RESULTS: The median of follow-up was 7.5 (IQR 3.9, 11.2) years. Having any neurodevelopmental disorder (ORadjusted 1.51 [95%CI 1.13, 2.03]), or ADHD (ORadjusted 2.31 [95%CI 1.54, 3.45]) was associated with poor glycaemic control (mean HbA1c >8.5%). Increased risk of diabetic complications was observed in patients with comorbid neurodevelopmental disorders (HRadjusted 1.72 [95%CI 1.21, 2.44] for nephropathy, HRadjusted 1.18 [95%CI 1.00, 1.40] for retinopathy) and patients with ADHD (HRadjusted 1.90 [95%CI 1.20, 3.00] for nephropathy, HRadjusted 1.33 [95%CI 1.07, 1.66] for retinopathy). Patients with intellectual disability have a particularly higher risk of nephropathy (HRadjusted 2.64 [95%CI 1.30, 5.37]). CONCLUSIONS: Comorbid neurodevelopmental disorders, primarily ADHD and intellectual disability, were associated with poor glycaemic control and a higher risk of diabetic complications in childhood-onset type 1 diabetes.

A panel of primary care and diabetes specialists conducted focused literature searches on the current role of glycaemic control in the management of type 2 diabetes and revisited the evolution of evidence supporting the importance of early and intensive blood glucose control as a central strategy to reduce the risk of adverse long-term outcomes. The optimal approach to type 2 diabetes management has evolved over time as the evidence base has expanded from data from trials that established the role of optimising glycaemic control to recent data from cardiovascular outcomes trials (CVOTs) demonstrating organ-protective effects of newer glucose-lowering drugs (GLDs). The results from these CVOTs were derived mainly from people with type 2 diabetes and prior cardiovascular and kidney disease or multiple risk factors. In more recent years, earlier diagnosis in high-risk individuals has contributed to the large proportion of people with type 2 diabetes who do not have complications. In these individuals, a legacy effect of early and optimal control of blood glucose and cardiometabolic risk factors has been proven to reduce cardiovascular and kidney disease events and all-cause mortality. As there is a lack of RCTs investigating the potential synergistic effects of intensive glucose control and organ-protective effects of newer GLDs, this article re-evaluates the evolution of the scientific evidence and highlights the importance of integrating glycaemic control as a pivotal early therapeutic goal in most people with type 2 diabetes, while targeting existing cardiovascular and kidney disease. We also emphasise the importance of implementing multifactorial management using a multidisciplinary approach to facilitate regular review, patient empowerment and the possibility of tailoring interventions to account for the heterogeneity of type 2 diabetes. Graphical Abstract