Type 2 diabetes mellitus (T2DM) represents one of the most significant global public health challenges of the twenty-first century. The International Diabetes Federation (IDF) estimated that approximately 537 million adults worldwide were living with diabetes in 2021, with projections indicating an increase to 783 million by 2045 [1]. India bears a disproportionately high burden, harboring over 77 million individuals with diabetes, thus earning the sobriquet of the “diabetes capital of the world” [2]. The escalating prevalence is attributable to a confluence of factors, including rapid urbanization, sedentary lifestyles, dietary transitions, genetic predisposition, and an expanding aging population [3].

The pathophysiology of T2DM is characterized by progressive beta-cell dysfunction and insulin resistance, which necessitates a stepwise approach to pharmacotherapy [4]. Metformin remains the cornerstone of initial pharmacological management, endorsed as the first-line agent by virtually all major clinical practice guidelines, including those of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) [5,6]. Metformin exerts its glucose-lowering effect primarily through suppression of hepatic glucose production, enhancement of peripheral insulin sensitivity, and modulation of gut-mediated glucose metabolism [7]. However, the progressive nature of T2DM implies that a substantial proportion of patients will require combination therapy to maintain glycemic targets over time [8].

Sodium-glucose co-transporter 2 (SGLT2) inhibitors represent a relatively novel class of antihyperglycemic agents that act through an insulin-independent mechanism by inhibiting glucose reabsorption in the proximal renal tubule, thereby promoting glucosuria [9]. Dapagliflozin, a selective SGLT2 inhibitor, has demonstrated consistent efficacy in reducing glycated hemoglobin (HbA1c), fasting plasma glucose, body weight, and blood pressure in multiple randomized controlled trials [10,11]. Importantly, the landmark DECLARE-TIMI 58 trial established the cardiovascular safety of dapagliflozin and demonstrated its superiority in reducing the composite endpoint of hospitalization for heart failure or cardiovascular death [12]. Furthermore, the DAPA-CKD trial underscored the renoprotective properties of dapagliflozin in patients with chronic kidney disease, irrespective of diabetes status [13].

The complementary mechanisms of metformin and dapagliflozin—targeting hepatic glucose output and renal glucose reabsorption, respectively—provide a robust pharmacological rationale for their use in combination [14]. Several randomized controlled trials have demonstrated the additive glucose-lowering efficacy of this combination with additional benefits in terms of weight reduction and blood pressure lowering [15,16]. However, the majority of these studies have been conducted in Western populations, and real-world evidence from the Indian subcontinent remains sparse. Given the distinct metabolic phenotype of South Asian populations, characterized by higher visceral adiposity, earlier onset of insulin resistance, and a greater propensity for beta-cell failure at lower BMI thresholds, population-specific data are imperative to inform clinical decision-making [17,18].

The present study was designed to evaluate the efficacy and safety of dapagliflozin (10 mg/day) added to metformin compared with metformin monotherapy in patients with inadequately controlled T2DM in a real-world Indian clinical setting. The study aimed to bridge the evidence gap by generating observational data from a multicenter cohort in Bangalore, Karnataka.

Study Design and Setting This was a prospective, multicenter, observational cohort study conducted at the Department of General Medicine, Shri Atal Bihari Vajpayee Medical College and Research Institute, and its affiliated teaching hospitals in Bangalore, Karnataka, India. The study was carried out over a period of 12 months, from February 2025 to January 2026. The study was conducted in accordance with the ethical principles outlined in the Declaration of Helsinki (2013 revision) and adhered to the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines [19]. Study Population A total of 200 patients diagnosed with T2DM attending the outpatient departments of the participating centers were enrolled using a consecutive sampling method. Patients were allocated into two groups based on their existing treatment regimen at the discretion of the treating physician: the combination group (n=104), receiving dapagliflozin 10 mg once daily in addition to metformin (1000–2000 mg/day in divided doses), and the control group (n=96), receiving metformin monotherapy (1000–2000 mg/day in divided doses). Inclusion Criteria The inclusion criteria were as follows: adults aged 30–65 years with a confirmed diagnosis of T2DM (as per ADA 2022 criteria [5]); HbA1c between 7.5% and 10.0% at enrollment; stable metformin dose for at least 8 weeks prior to enrollment; estimated glomerular filtration rate (eGFR) ≥45 mL/min/1.73 m²; and willingness to provide written informed consent and attend scheduled follow-up visits. Exclusion Criteria Patients were excluded if they had type 1 diabetes mellitus; a history of diabetic ketoacidosis; severe hepatic impairment (Child-Pugh class C); recurrent urinary tract or genital infections (>3 episodes in the preceding year); current pregnancy or lactation; concomitant use of insulin or other antihyperglycemic agents (sulfonylureas, DPP-4 inhibitors, GLP-1 receptor agonists, or thiazolidinediones); a history of hypersensitivity to SGLT2 inhibitors; or significant comorbidities including unstable cardiovascular disease, active malignancy, or any condition that, in the investigator’s judgment, would preclude safe participation. Data Collection and Outcome Measures Baseline demographic data, clinical characteristics, and laboratory parameters were recorded at enrollment. Follow-up assessments were conducted at 3-month intervals (months 3, 6, 9, and 12). At each visit, the following parameters were measured: HbA1c (by high-performance liquid chromatography), fasting blood glucose (enzymatic hexokinase method), body weight, body mass index, systolic and diastolic blood pressure, fasting lipid profile (total cholesterol, low-density lipoprotein cholesterol [LDL-C], high-density lipoprotein cholesterol [HDL-C], and triglycerides), serum creatinine, eGFR (calculated using the Chronic Kidney Disease Epidemiology Collaboration [CKD-EPI] equation), and urine albumin-to-creatinine ratio. Adverse events were documented at each follow-up visit through patient interview and clinical examination. The primary endpoints were the change from baseline in HbA1c and fasting blood glucose at 12 months. Secondary endpoints included changes in body weight, BMI, systolic and diastolic blood pressure, lipid profile, eGFR, UACR, the proportion of patients achieving HbA1c <7.0% and <7.5%, and the incidence and nature of adverse events. Statistical Analysis Continuous variables were expressed as mean ± standard deviation (SD) and categorical variables as frequencies and percentages. The normality of data distribution was assessed using the Shapiro-Wilk test. Between-group comparisons for continuous variables were performed using the independent samples t-test for normally distributed data and the Mann-Whitney U test for non-normally distributed data. Within-group comparisons over time were analyzed using the paired t-test or the Wilcoxon signed-rank test, as appropriate. Categorical variables were compared using the chi-square test or Fisher’s exact test. Analysis of covariance (ANCOVA) was used to compare treatment effects while adjusting for baseline values and potential confounders (age, sex, duration of diabetes, and baseline BMI). A two-sided p-value of <0.05 was considered statistically significant. All statistical analyses were performed using IBM SPSS Statistics version 26.0 (IBM Corp., Armonk, NY, USA) and GraphPad Prism version 9.0 (GraphPad Software, San Diego, CA, USA).

Baseline Characteristics

A total of 200 patients were enrolled, of whom 104 were allocated to the dapagliflozin-metformin combination group and 96 to the metformin monotherapy group. The baseline demographic and clinical characteristics of the two groups are presented in Table 1. The groups were well balanced with respect to age, sex distribution, duration of diabetes, BMI, and all laboratory parameters at baseline. The mean age of participants was 51.8 ± 8.6 years in the combination group and 52.4 ± 9.1 years in the control group (p=0.62). The mean baseline HbA1c was 8.42 ± 1.08% and 8.38 ± 1.04% in the combination and control groups, respectively (p=0.78). No statistically significant differences were observed between the groups at baseline for any of the measured parameters.

Table 1: Baseline Demographic and Clinical Characteristics of the Study Population

Data expressed as mean ± SD or n (%). BMI: Body Mass Index; BP: Blood Pressure; FBG: Fasting Blood Glucose; LDL-C: Low-Density Lipoprotein Cholesterol; HDL-C: High-Density Lipoprotein Cholesterol; eGFR: estimated Glomerular Filtration Rate; UACR: Urine Albumin-to-Creatinine Ratio; T2DM: Type 2 Diabetes Mellitus.

Primary Outcomes

At 12 months, the combination group demonstrated a significantly greater reduction in HbA1c compared with the metformin monotherapy group (mean change: −1.34 ± 0.48% vs. −0.77 ± 0.42%; p<0.001). The mean HbA1c declined from 8.42 ± 1.08% at baseline to 7.08 ± 0.86% at 12 months in the combination group, whereas it decreased from 8.38 ± 1.04% to 7.61 ± 0.92% in the control group. The between-group difference in HbA1c change, adjusted for baseline values and covariates using ANCOVA, was −0.57% (95% CI: −0.74 to −0.40; p<0.001), favoring the combination group. Notably, HbA1c reductions were progressive and sustained throughout the study period, with the most rapid decline observed during the first 6 months (Figure 1).

Similarly, fasting blood glucose decreased significantly more in the combination group (−46.6 ± 18.2 mg/dL) than in the metformin monotherapy group (−26.5 ± 15.8 mg/dL; p<0.001). The mean FBG at 12 months was 125.8 ± 22.4 mg/dL and 142.3 ± 26.8 mg/dL in the combination and control groups, respectively (Figure 2).

Figure 1: Trends in HbA1c (%) over the 12-month study period. Values are expressed as mean ± SE. *p<0.05 between groups at each time point.

Figure 2: Trends in fasting blood glucose (mg/dL) over the 12-month study period. Values are expressed as mean ± SE.

Secondary Outcomes

The detailed changes in primary and secondary outcome measures from baseline to 12 months are summarized in Table 2. The combination group exhibited a significantly greater reduction in body weight (−3.8 ± 1.6 kg vs. −1.3 ± 1.2 kg; p<0.001) and BMI (−1.4 ± 0.6 vs. −0.5 ± 0.4 kg/m²; p<0.001) compared with the control group (Figure 3). Systolic blood pressure decreased by 7.8 ± 4.2 mmHg in the combination group versus 3.4 ± 3.8 mmHg in the control group (p<0.001). Diastolic blood pressure reductions were 4.2 ± 2.8 mmHg and 2.0 ± 2.4 mmHg, respectively (p<0.001).

With respect to the lipid profile, the combination group showed significantly greater improvements in total cholesterol, LDL-C, and triglycerides compared with metformin monotherapy. The mean reduction in LDL-C was 14.2 ± 8.6 mg/dL in the combination group versus 8.4 ± 6.2 mg/dL in the control group (p<0.001). HDL-C increased by 3.6 ± 2.8 mg/dL and 1.8 ± 2.2 mg/dL in the respective groups (p<0.001). There was no clinically significant difference in eGFR between the groups at 12 months; however, the combination group showed a trend toward improvement in UACR (−12.4 ± 8.6 vs. −5.8 ± 6.4 mg/g; p<0.001), suggesting a potential renoprotective effect.

Table 2: Changes in Clinical and Metabolic Parameters from Baseline to 12 Months

Data expressed as mean ± SD. †p-value for between-group difference in change from baseline (ANCOVA adjusted for baseline value, age, sex, diabetes duration, and baseline BMI). SBP: Systolic Blood Pressure; DBP: Diastolic Blood Pressure; TC: Total Cholesterol; TG: Triglycerides.

Figure 3: Changes in body weight (kg) over the 12-month study period. Values are expressed as mean ± SE.

Glycemic Target Achievement

The proportion of patients achieving the glycemic target of HbA1c <7.0% at 12 months was significantly higher in the combination group compared with the metformin monotherapy group (42.3% vs. 22.9%; p=0.004). Similarly, a greater proportion of patients in the combination group achieved an HbA1c <7.5% (68.3% vs. 45.8%; p=0.001) and a fasting blood glucose <130 mg/dL (64.4% vs. 38.5%; p<0.001). These findings are illustrated in Figure 5 and detailed in Table 3.

Table 3: Proportion of Patients Achieving Glycemic Targets at 12 Months

Chi-square test used for comparison between groups.

Figure 5: Proportion of patients achieving glycemic targets at 12 months. *p<0.05, **p<0.01 between groups.

Safety and Adverse Events

The safety profile of both treatment groups over the 12-month study period is summarized in Table 4 and Figure 4. Overall, adverse events were reported in 34 patients (32.7%) in the combination group and 22 patients (22.9%) in the control group (p=0.13). No serious adverse events, including diabetic ketoacidosis, major hypoglycemic episodes, or lower-limb amputations, were recorded in either group. No patient discontinued the study due to adverse events.

Urinary tract infections (UTIs) were more frequent in the combination group (7.7% vs. 3.1%; p=0.16), as were genital mycotic infections (5.8% vs. 1.0%; p=0.06). All infections were mild to moderate in severity (grade 1–2) and resolved with standard antimicrobial or antifungal therapy without necessitating treatment discontinuation. Gastrointestinal discomfort, comprising nausea, abdominal bloating, and diarrhea, was the most common adverse event in both groups but was slightly more prevalent in the metformin monotherapy group (14.6% vs. 11.5%). Hypoglycemia was uncommon in both groups (2.9% vs. 2.1%), and all episodes were mild (blood glucose >54 mg/dL) and self-resolving. Volume depletion-related symptoms (dizziness, postural hypotension) occurred in 3.8% of patients in the combination group versus 1.0% in the control group; all cases responded to fluid replacement and dose adjustment.

Table 4: Adverse Events During the 12-Month Study Period

Data expressed as n (%). Chi-square test or Fisher’s exact test used for comparison. GI: Gastrointestinal; AE: Adverse Event.

Figure 4: Comparison of adverse events between treatment groups during the 12-month study period.

The present multicenter observational study provides real-world evidence supporting the efficacy and safety of dapagliflozin combined with metformin in Indian patients with inadequately controlled T2DM. The combination therapy demonstrated clinically meaningful and statistically significant reductions in HbA1c, fasting blood glucose, body weight, blood pressure, and adverse lipid parameters over a 12-month observation period, while maintaining an acceptable safety profile. The HbA1c reduction of 1.34% observed in the combination group in our study is consistent with the findings of pivotal randomized controlled trials evaluating dapagliflozin as add-on therapy to metformin. In a landmark study by Bailey et al. (2010), dapagliflozin 10 mg added to metformin produced an HbA1c reduction of 0.84% over 24 weeks [15]. The greater magnitude of reduction in our study may be attributable to the longer follow-up period (12 months), higher baseline HbA1c, and the observational design that reflects real-world prescribing to patients with greater glycemic burden. Similarly, a 52-week extension study by Bailey et al. (2013) reported sustained HbA1c reductions of 0.78% with dapagliflozin 10 mg, closely paralleling the trajectory observed in our cohort [20]. The finding that 42.3% of patients in the combination group achieved an HbA1c <7.0% is noteworthy and aligns with the proportions reported in earlier studies. Henry et al. (2012) reported that approximately 46% of patients receiving dapagliflozin plus metformin achieved an HbA1c <7.0% at 24 weeks [21]. The slightly lower rate in our study may reflect the higher baseline HbA1c and the longer follow-up, during which some glycemic attrition is anticipated. Nonetheless, the significantly higher target achievement rate compared with metformin monotherapy (22.9%) reinforces the clinical benefit of adding dapagliflozin in patients failing to achieve adequate control with metformin alone. The weight loss of 3.8 kg observed in the combination group represents a clinically significant finding, given the well-established association between weight gain and cardiovascular risk in T2DM [22]. This degree of weight reduction is consistent with the mechanism of action of SGLT2 inhibitors, which promote caloric loss through urinary glucose excretion, estimated at approximately 60–80 g/day (240–320 kcal/day) [23]. The weight-lowering effect of dapagliflozin complements the weight-neutral to mildly weight-reducing effect of metformin, providing a synergistic benefit that is particularly relevant in the South Asian population, where central adiposity is a prominent contributor to metabolic risk [17]. Our findings are concordant with a systematic review and meta-analysis by Cai et al. (2018), which reported a mean weight reduction of 2.0–3.3 kg with SGLT2 inhibitors in combination with metformin [24]. The reductions in systolic (−7.8 mmHg) and diastolic (−4.2 mmHg) blood pressure in the combination group are clinically meaningful and exceed the reductions typically reported in clinical trials (3–5 mmHg for systolic BP) [25]. This may be related to the osmotic diuretic effect of SGLT2 inhibitors and concurrent weight loss. Given that hypertension is a common comorbidity in T2DM, affecting approximately 50% of our study population, the blood pressure-lowering effect of dapagliflozin offers an additional cardiometabolic advantage that may translate into reduced cardiovascular event rates, as suggested by the DECLARE-TIMI 58 trial [12]. The favorable effects on the lipid profile observed in the combination group are consistent with previous reports. A meta-analysis by Storgaard et al. (2016) demonstrated modest reductions in triglycerides and LDL-C, with a small increase in HDL-C, with SGLT2 inhibitor therapy [26]. These lipid-modulating effects, though modest, may contribute to the overall cardiovascular risk reduction associated with SGLT2 inhibitor therapy. The improvement in UACR observed in the combination group (−12.4 mg/g) is of particular clinical relevance, as albuminuria is an established independent risk factor for both renal progression and cardiovascular events in T2DM [27]. The renoprotective effects of SGLT2 inhibitors are mediated through tubuloglomerular feedback restoration, reduction in glomerular hyperfiltration, and anti-inflammatory and antifibrotic mechanisms [28]. The DAPA-CKD trial demonstrated a 39% reduction in the composite renal endpoint with dapagliflozin [13], and our real-world data extend these findings to the Indian population. The safety profile of the combination therapy was consistent with the known adverse effect spectrum of SGLT2 inhibitors. The slightly higher incidence of urinary tract infections and genital mycotic infections in the combination group is attributable to the glucosuric mechanism of dapagliflozin, which creates a favorable environment for microbial proliferation in the urogenital tract [29]. Importantly, all infectious episodes were mild and did not necessitate treatment discontinuation, consistent with the safety data from the DECLARE-TIMI 58 and DAPA-HF trials [12,30]. The absence of severe hypoglycemia in either group is reassuring and reflects the intrinsic glucose-dependent mechanism of SGLT2 inhibition, which minimizes the risk of hypoglycemia [9]. This study has several strengths, including its prospective design, 12-month follow-up with serial assessments, and real-world clinical setting that enhances external validity. The multicenter design and the inclusion of a well-matched control group strengthen the internal validity of the findings. Furthermore, the study provides much-needed data from the Indian population, which has a unique metabolic phenotype and a high burden of T2DM. However, certain limitations must be acknowledged. First, the observational design precludes definitive causal inference, and residual confounding cannot be entirely excluded despite statistical adjustment. Second, the relatively small sample size limits the power to detect differences in less common adverse events. Third, treatment allocation was non-randomized and based on physician preference, introducing the possibility of selection bias. Fourth, the 12-month follow-up, while adequate for assessing glycemic and metabolic outcomes, is insufficient to evaluate long-term cardiovascular and renal endpoints. Fifth, the study did not assess patient-reported outcomes, treatment satisfaction, or adherence measures. Future large-scale, randomized controlled trials with longer follow-up and hard clinical endpoints are warranted to confirm these findings.

The present study demonstrates that the addition of dapagliflozin to metformin provides superior glycemic control, significant weight loss, and favorable effects on blood pressure, lipid profile, and albuminuria compared with metformin monotherapy in Indian patients with T2DM. The combination therapy exhibited an acceptable safety profile, with no serious adverse events reported. These findings support the use of the dapagliflozin-metformin combination as an effective and well-tolerated second-line therapeutic strategy in clinical practice. Population-specific data such as those generated in this study are essential to inform evidence-based prescribing in the Indian context and to optimize outcomes for the millions of individuals living with T2DM in the subcontinent.

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