Sunder Mudaliar
· Clinical ProfessorVerifiedUniversity of California, San Diego · Endocrinology and Metabolism
Active 1995–2025
About
Sunder Mudaliar is a Clinical Professor of Medicine at UC San Diego, with a background in medicine, surgery, and obstetrics and gynecology from the University of Madras. He completed his MD in Internal Medicine in 1985 and earned his FRCP from the Royal College of Physicians in the UK in 1989. He further obtained ABIM certification in Internal Medicine and ABEM certification in Endocrinology/Metabolism from the University of Rochester and UC San Diego, respectively. His research activities focus on diabetes, endocrinology, and metabolism, with significant contributions to understanding the pathophysiology and treatment of diabetes and its complications. He has been involved in numerous NIH-funded projects, including studies on Alzheimer's disease related dementias in prediabetes and type 2 diabetes, intracranial arterial compliance, and cardiovascular outcomes in diabetes. His work emphasizes the integration of cardioprotective glucose-lowering medications into clinical practice and exploring mechanisms underlying the benefits of SGLT2 inhibitors, among other topics.
Research topics
- Internal medicine
- Medicine
- Endocrinology
- Chemistry
- Intensive care medicine
- Neuroscience
- Organic chemistry
- Pharmacology
- Ophthalmology
- Biology
- Family medicine
Selected publications
Diabetes Care · 2025-08-26 · 5 citations
articleOpen accessOBJECTIVE: Type 2 diabetes (T2D) and its associated complications develop heterogeneously over decades, but few studies span the progression from prediabetes to clinical events. We investigated whether long-term metabolic trajectories beginning in prediabetes delineate subgroups with differential complication risk. RESEARCH DESIGN AND METHODS: Clinical data from 1,732 Diabetes Prevention Program/Outcomes Study participants (follow-up 19 years) were analyzed across 12 phenotypes. Tensor decomposition was used to capture longitudinal patterns, and Gaussian mixture modeling was used to define longitudinal clusters. Cluster-specific complications were quantified with Cox and logistic regression. RESULTS: Four clusters emerged. Clusters 1 and 2 (73% of participants) maintained stable glycemia, blood pressure, and lipids. Although 49% and 71%, respectively, developed T2D, cumulative micro- and macrovascular events remained low. Cluster 3 (12%) showed the steepest rise in insulin resistance and hyperglycemia, with 92% of the subgroup progressing to T2D and a markedly higher rate of retinopathy (odds ratio [OR] 8.8, 95% CI 3.9-20.1) and neuropathy (OR 3.4, 95% CI 2.1-5.5). Cluster 4 (15%) presented with baseline microalbuminuria often prior to the development of T2D (73%). It was distinguished by progressive estimated glomerular filtration rate decline and a doubling of cardiovascular events (hazard ratio 2.0, 95% CI 1.4-3.0), despite serum lipids comparable with other groups. CONCLUSIONS: Two-thirds of individuals with prediabetes follow metabolically resilient trajectories, whereas distinct insulin-resistant or renal-dysfunction trajectories precede micro- or macrovascular complications, respectively. The optimal window for macrovascular complication prevention in individuals with prediabetes microalbuminuria may precede progression to T2D.
2025-08-29
articleOpen access<p dir="ltr">OBJECTIVE</p><p dir="ltr">To determine the effects of first-degree family history of diabetes on diabetes incidence in Diabetes Prevention Program (DPP)/DPP Outcomes Study (DPPOS) participants.</p><p dir="ltr">RESEARCH DESIGN AND METHODS</p><p dir="ltr">The DPP randomized adults with prediabetes to an intensive lifestyle intervention or metformin or placebo and followed them for incident diabetes. Upon study completion, 88% of eligible DPP participants re-enrolled in DPPOS for long-term follow-up. The present analysis includes all 3072 participants with family history information through DPPOS, with a median follow-up of 21 years (1975 had parental history {PH} [312 biparental, 947 maternal, 716 paternal]), 226 had only sibling history {SH}, and 871 denied any family history of diabetes {No-FH}). The primary outcome is incident diabetes based on American Diabetes Association criteria, adjusted for demographic and clinical variables, DPP randomization arm, and polygenic risk score (PRS). </p><p dir="ltr">RESULTS</p><p dir="ltr">The adjusted hazard ratio (HR) and 95% confidence interval [95% CI] were 1.21 [1.06, 1.38] for any family history, 1.19 [1.04, 1.35] for PH, and 1.15 [0.91, 1.44] for SH. Biparental history conferred greater hazard (1.44 [1.22, 1.69]) than maternal (1.22 [1.08, 1.38]) or paternal (1.22 [1.08, 1.39]) diabetes history alone. PRS explained 32% of the association of any family history with diabetes risk.</p><p dir="ltr">CONCLUSIONS</p><p dir="ltr">Parental history increased type 2 diabetes risk after controlling for DPP treatment groups. That effect was only partially explained by PRS, suggesting that rare gene variants, familial, and environmental factors may contribute to type 2 diabetes risk in people with prediabetes.</p>
Diabetes · 2025-06-13
articleIntroduction and Objective: To describe the prevalence and incidence of electrocardiogram (ECG) abnormalities and ECG evidence of cardiovascular (CV) autonomic neuropathy (CAN) by treatment group in the GRADE cohort of adults with type 2 diabetes (T2D) for &lt;10 years. Methods: The GRADE trial enrolled individuals with T2D &lt;10 years on metformin alone, randomized to insulin glargine, glimepiride, liraglutide, or sitagliptin, and followed for an average of five years. Resting ECGs were completed at baseline, 2-, and 4-years in 5029 participants (baseline mean ± SD age 57.2 ± 10.0 years; diabetes duration 4.2 ± 2.7 years; HbA1c 7.5 ± 0.5%; 36.4% women) and analyzed for overall, major, and minor abnormalities and heart rate variability (HRV), a measure of CAN. Incidence of new ECG abnormalities and CAN by treatment group were analyzed at years 2 and 4 using logistic repeated measures models, adjusted for baseline risk factors. As liraglutide is associated with CV outcomes benefit, ECG changes in the liraglutide vs. all other groups were also compared. Results: Participants with ECG abnormalities (57.1%) and ECG-defined CAN (52.8%) at baseline had longer diabetes duration, higher systolic blood pressure, more hyperlipidemia and lipid-lowering treatment, and beta blocker use. Across years 2 and 4, there were no between-group differences in overall or minor ECG abnormalities, but major ECG abnormalities occurred less often in the liraglutide vs. all other treatment groups (p=0.03; 9% [95% CI: 7%, 12%] vs 13% [11%, 14%] at year 4). ECG-defined CAN did not differ between liraglutide vs. non-liraglutide groups across years 2 and 4 (p=0.42). Conclusion: ECG abnormalities, including those of CAN, are common in T2D &lt;10 years and are associated with certain CV risk factors. The development of major ECG abnormalities may differ by glucose lowering treatment, as fewer occurred with liraglutide vs. the other treatments. Disclosure R. Pop-Busui: Board Member; American Diabetes Association. Consultant; Averitas Pharma, Inc. Research Support; Bayer Pharmaceuticals, Inc. Other Relationship; Biogen. Research Support; Juvenile Diabetes Research Foundation (JDRF). Advisory Panel; Lexicon Pharmaceuticals, Inc, Novo Nordisk. Research Support; Novo Nordisk, National Institute of Diabetes and Digestive and Kidney Diseases. Consultant; Roche Diagnostics. S. Rosin: None. N.M. Butera: None. H. Krause-Steinrauf: None. H. Abou Assi: Research Support; Novo Nordisk. Stock/Shareholder; Gilead Sciences, Inc, Regeneron Pharmaceuticals, Medtronic, Moderna, Inc, MannKind Corporation, Merck & Co., Inc, Pfizer Inc. R.K. Garg: None. S.E. Inzucchi: Consultant; Novo Nordisk, AstraZeneca, Boehringer-Ingelheim, Merck & Co., Inc, Pfizer Inc, Bayer Pharmaceuticals, Inc. A. Katona: None. J.B. McGill: Advisory Panel; Bayer Pharmaceuticals, Inc. Consultant; Jaeb Center for Health Research. Advisory Panel; Boehringer-Ingelheim, Lilly Diabetes, Novo Nordisk, MannKind Corporation. Research Support; Diagnode, Lexicon Pharmaceuticals, Inc, Biomea Fusion. S. Mudaliar: Consultant; Sun Pharmaceutical Industries Ltd. D.S. Schade: None. E.R. Seaquist: None. M. Tiktin: None. E.Z. Soliman: None. J.B. Green: Consultant; BI Lilly NovoNordisk Bayer Anji Vertex Valo Mineralys AstraZeneca. Research Support; BI Lilly Merck Bluedrop Roche. Funding NIDDK (U01DK098246, U34-DK-088043); American Diabetes Association; National Heart, Lung, and Blood Institute; The Centers for Disease Control and Prevention
2025-04-23
preprintOpen access<p dir="ltr">Objective: Weight gain with glucose-lowering medications may interfere with effective type 2 diabetes (T2D) management. We evaluated weight change and the effect of weight gain on outcomes over 5 years on four diabetes medications.</p><p dir="ltr">Research Design and Methods: The GRADE randomized trial compared the addition of insulin glargine, glimepiride, liraglutide, or sitagliptin to metformin in participants with T2D. We report weight change and hazard ratio (HR) per kg of weight change for HbA1c>7.5%; cardiovascular (CVD), kidney, and neuropathy outcomes; and diabetes treatment satisfaction. </p><p dir="ltr">Results: Participants (n=4,980) were 57+10 years, 44% non-White, with HbA1c 7.5%+0.5% and BMI 34.3+6.8kg/m2. Mean (95% CI) weight change (kg) during the first year was -3.5 (-3.8, -3.2) with liraglutide, -1.07 (-1.4, -0.78) with sitagliptin, 0.45 (0.16, 0.74) with glargine, and 0.89 (0.60, 1.2) with glimepiride (P<0.0001). Thereafter, weight decreased in all groups. Weight gain within the first six months was associated with increased risk of HbA1c>7.5%, with modest differences by treatment, and with subsequent CVD (HR 1.03 [1.005, 1.06]). Weight gain at 1 year was associated with increased risk of HbA1c>7.5% (HR 1.05 [1.04, 1.07]) and kidney disease (HR 1.03 [1.01, 1.06]). Baseline weight, but not weight gain, was associated with new-onset neuropathy. Weight gain was associated with lower diabetes treatment satisfaction.</p><p dir="ltr">Conclusions: Liraglutide and sitagliptin were associated with initial weight loss and glargine and glimepiride with slight weight gain followed by weight loss in metformin-treated T2D. Weight gain was associated with worsening glycemia and increased risk of cardiovascular and kidney outcomes largely independent of treatment. </p>
Diabetes Care · 2025-04-23 · 3 citations
articleOBJECTIVE: Weight gain with glucose-lowering medications may interfere with effective type 2 diabetes (T2D) management. We evaluated weight change and the effect of weight gain on outcomes over 5 years on four diabetes medications. RESEARCH DESIGN AND METHODS: The Glycemia Reduction Approaches in Diabetes: A Comparative Effectiveness Study (GRADE) randomized trial compared the addition of insulin glargine, glimepiride, liraglutide, or sitagliptin to metformin in participants with T2D. We report weight change and hazard ratio (HR) per kilogram of weight change for HbA1c >7.5%; cardiovascular disease (CVD), kidney disease, and neuropathy outcomes; and diabetes treatment satisfaction. RESULTS: Participants (n = 4,980) were 57 ± 10 years, 44% non-White, with HbA1c 7.5% ± 0.5%, and BMI 34.3 ± 6.8 kg/m2. Mean (95% CI) weight change (kg) during the first year was -3.5 (-3.8,-3.2) with liraglutide,-1.07 (-1.4,-0.78) with sitagliptin, 0.45 (0.16, 0.74) with glargine, and 0.89 (0.60, 1.2) with glimepiride (P < 0.0001). Thereafter, weight decreased in all groups. Weight gain within the first 6 months was associated with increased risk of HbA1c >7.5%, with modest differences by treatment, and with subsequent CVD (HR 1.03 [95% CI 1.005, 1.06]). Weight gain at 1 year was associated with increased risk of HbA1c >7.5% (HR 1.05 [1.04, 1.07]) and kidney disease (HR 1.03 [1.01, 1.06]). Baseline weight, but not weight gain, was associated with new-onset neuropathy. Weight gain was associated with lower diabetes treatment satisfaction. CONCLUSIONS: Liraglutide and sitagliptin were associated with initial weight loss and glargine and glimepiride with slight weight gain, followed by weight loss in metformin-treated T2D. Weight gain was associated with worsening glycemia and increased risk of cardiovascular and kidney outcomes largely independent of treatment.
Diabetes Care · 2025-09-23 · 1 citations
articleOpen accessOBJECTIVE: To describe the prevalence and incidence of electrocardiogram (ECG) abnormalities and ECG-derived cardiovascular autonomic neuropathy (CAN) in the GRADE cohort of adults with type 2 diabetes (T2D) <10 years. RESEARCH DESIGN AND METHODS: Individuals with T2D taking metformin alone were randomly assigned to add insulin glargine, glimepiride, liraglutide, or sitagliptin. Resting ECGs were completed at the baseline, 2-year, and 4-year study visits and analyzed for minor and major abnormalities and CAN assessed with heart rate variability (HRV) in 4,769 participants. Incidence of new major, minor, and any ECG abnormalities and CAN by treatment group was analyzed using logistic repeated-measures models at years 2 and 4 adjusted for baseline risk factors. RESULTS: At baseline, participants were a mean age of 57.2 ± 10.0 years, 36.3% were women, mean diabetes duration was 4.3 ± 2.8 years, and mean HbA1c was 7.5 ± 0.5%. Participants with ECG abnormalities at baseline (57.1%) and ECG-derived CAN (52.8%) were older and had more severe cardiovascular risk factors. The incidence of minor and major ECG abnormalities was similar among all treatment groups. However, at year 4, major ECG abnormalities were fewer in the liraglutide versus nonliraglutide groups (9% vs. 13%; P = 0.03). The incidence of CAN did not differ between the liraglutide and nonliraglutide groups across visits (P = 0.42); however, one measure of HRV (SD of normal-to-normal R-R intervals) was higher at year 2 in the liraglutide versus nonliraglutide groups (P = 0.02). CONCLUSIONS: ECG abnormalities, including those reflecting CAN, are common in individuals with T2D <10 years and more so in those with certain cardiovascular risk factors. The development of major ECG abnormalities may be lower with liraglutide.
Diabetes Care · 2025-08-29
articleOpen accessOBJECTIVE: To determine the effects of first-degree family history of diabetes on diabetes incidence in Diabetes Prevention Program (DPP) and Diabetes Prevention Program Outcomes Study (DPPOS) participants. RESEARCH DESIGN AND METHODS: In the DPP, adults with prediabetes were randomized to an intensive lifestyle intervention, metformin, or placebo and followed for incident diabetes. On study completion 88% of eligible DPP participants reenrolled in DPPOS for long-term follow-up. The present analysis includes all 3,072 participants with family history information through DPPOS, with a median follow-up of 21 years (1,975 had parental history of diabetes [PH] [312 biparental, 947 maternal, 716 paternal], 226 had only sibling history [SH], and 871 denied any family history). The primary outcome is incident diabetes based on American Diabetes Association criteria, with adjustment for demographic and clinical variables, DPP randomization arm, and polygenic risk score (PRS). RESULTS: Adjusted hazard ratio (HR) was 1.21 (95% CI 1.06, 1.38) for any family history, 1.19 (1.04, 1.35) for PH, and 1.15 (0.91, 1.44) for SH. Biparental history conferred greater hazard (HR 1.44 [95% CI 1.22, 1.69]) than maternal (1.22 [1.08, 1.38]) or paternal (1.22 [1.08, 1.39]) diabetes history alone. PRS explained 32% of the association of any family history with diabetes risk. CONCLUSIONS: PH increased type 2 diabetes risk after DPP treatment group was controlled for. That effect was only partially explained by PRS, suggesting that rare gene variants, familial, and environmental factors may contribute to type 2 diabetes risk in people with prediabetes.
2025-04-23
preprintOpen access<p dir="ltr">Objective: Weight gain with glucose-lowering medications may interfere with effective type 2 diabetes (T2D) management. We evaluated weight change and the effect of weight gain on outcomes over 5 years on four diabetes medications.</p><p dir="ltr">Research Design and Methods: The GRADE randomized trial compared the addition of insulin glargine, glimepiride, liraglutide, or sitagliptin to metformin in participants with T2D. We report weight change and hazard ratio (HR) per kg of weight change for HbA1c>7.5%; cardiovascular (CVD), kidney, and neuropathy outcomes; and diabetes treatment satisfaction. </p><p dir="ltr">Results: Participants (n=4,980) were 57+10 years, 44% non-White, with HbA1c 7.5%+0.5% and BMI 34.3+6.8kg/m2. Mean (95% CI) weight change (kg) during the first year was -3.5 (-3.8, -3.2) with liraglutide, -1.07 (-1.4, -0.78) with sitagliptin, 0.45 (0.16, 0.74) with glargine, and 0.89 (0.60, 1.2) with glimepiride (P<0.0001). Thereafter, weight decreased in all groups. Weight gain within the first six months was associated with increased risk of HbA1c>7.5%, with modest differences by treatment, and with subsequent CVD (HR 1.03 [1.005, 1.06]). Weight gain at 1 year was associated with increased risk of HbA1c>7.5% (HR 1.05 [1.04, 1.07]) and kidney disease (HR 1.03 [1.01, 1.06]). Baseline weight, but not weight gain, was associated with new-onset neuropathy. Weight gain was associated with lower diabetes treatment satisfaction.</p><p dir="ltr">Conclusions: Liraglutide and sitagliptin were associated with initial weight loss and glargine and glimepiride with slight weight gain followed by weight loss in metformin-treated T2D. Weight gain was associated with worsening glycemia and increased risk of cardiovascular and kidney outcomes largely independent of treatment. </p>
Circulation · 2024-02-12 · 21 citations
articleOpen accessBACKGROUND: Cardiovascular disease is a major cause of morbidity and mortality in patients with type 2 diabetes. The effects of glucose-lowering medications on cardiovascular outcomes in individuals with type 2 diabetes and low cardiovascular risk are unclear. We investigated cardiovascular outcomes by treatment group in participants randomly assigned to insulin glargine, glimepiride, liraglutide, or sitagliptin, added to baseline metformin, in GRADE (Glycemia Reduction Approaches in Type 2 Diabetes: A Comparative Effectiveness Study). METHODS: A total of 5047 participants with a mean±SD age of 57.2±10.0 years, type 2 diabetes duration of 4.0±2.7 years, and low baseline prevalence of cardiovascular disease (myocardial infarction, 5.1%; cerebrovascular accident, 2.0%) were followed for a median of 5 years. Prespecified outcomes included between-group time-to-first event analyses of MACE-3 (composite of major adverse cardiovascular events: cardiovascular death, myocardial infarction, and stroke), MACE-4 (MACE-3+unstable angina requiring hospitalization or revascularization), MACE-5 (MACE-4+coronary revascularization), MACE-6 (MACE-5+hospitalization for heart failure), and the individual components. MACE outcomes and hospitalization for heart failure in the liraglutide-treated group were compared with the other groups combined using Cox proportional hazards models. MACE-6 was also analyzed as recurrent events using a proportional rate model to compare all treatment groups. RESULTS: We observed no statistically significant differences in the cumulative incidence of first MACE-3, MACE-4, MACE-5, or MACE-6, or their individual components, by randomized treatment group. However, when compared with the other treatment groups combined, the liraglutide-treated group had a significantly lower risk of MACE-5 (adjusted hazard ratio, 0.70 [95% CI, 0.54–0.91]; P =0.021), MACE-6 (adjusted hazard ratio, 0.70 [95% CI, 0.55–0.90]; P =0.021), and hospitalization for heart failure (adjusted hazard ratio, 0.49 [95% CI, 0.28–0.86]; P =0.022). Compared with the liraglutide group, significantly higher rates of recurrent MACE-6 events occurred in the groups treated with glimepiride (rate ratio, 1.61 [95% CI, 1.13–2.29]) or sitagliptin (rate ratio 1.75; [95% CI, 1.24–2.48]). CONCLUSIONS: This comparative effectiveness study of a contemporary cohort of adults with type 2 diabetes, largely without established cardiovascular disease, suggests that liraglutide treatment may reduce the risk of cardiovascular events in patients at relatively low risk compared with other commonly used glucose-lowering medications. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01794143.
Diabetes Obesity and Metabolism · 2023-03-31 · 41 citations
articleOpen accessAbstract Aim To determine the effects of astaxanthin treatment on lipids, cardiovascular disease (CVD) markers, glucose tolerance, insulin action and inflammation in individuals with prediabetes and dyslipidaemia. Materials and Methods Adult participants with dyslipidaemia and prediabetes ( n = 34) underwent baseline blood draw, an oral glucose tolerance test and a one‐step hyperinsulinaemic‐euglycaemic clamp. They were then randomized ( n = 22 treated, 12 placebo) to receive astaxanthin 12 mg daily or placebo for 24 weeks. Baseline studies were repeated after 12 and 24 weeks of therapy. Results After 24 weeks, astaxanthin treatment significantly decreased low‐density lipoprotein (−0.33 ± 0.11 mM) and total cholesterol (−0.30 ± 0.14 mM) (both P < .05). Astaxanthin also reduced levels of the CVD risk markers fibrinogen (−473 ± 210 ng/mL), L‐selectin (−0.08 ± 0.03 ng/mL) and fetuin‐A (−10.3 ± 3.6 ng/mL) (all P < .05). While the effects of astaxanthin treatment did not reach statistical significance, there were trends toward improvements in the primary outcome measure, insulin‐stimulated, whole‐body glucose disposal (+0.52 ± 0.37 mg/m 2 /min, P = .078), as well as fasting [insulin] (−5.6 ± 8.4 pM, P = .097) and HOMA2‐IR (−0.31 ± 0.16, P = .060), suggesting improved insulin action. No consistent significant differences from baseline were observed for any of these outcomes in the placebo group. Astaxanthin was safe and well tolerated with no clinically significant adverse events. Conclusions Although the primary endpoint did not meet the prespecified significance level, these data suggest that astaxanthin is a safe over‐the‐counter supplement that improves lipid profiles and markers of CVD risk in individuals with prediabetes and dyslipidaemia.
Frequent coauthors
- 407 shared
Robert R. Henry
Medical University of South Carolina
- 174 shared
Devjit Tripathy
The University of Texas Health Science Center at San Antonio
- 172 shared
Nicolas Musi
- 172 shared
Ralph A. DeFronzo
- 170 shared
George A. Bray
Louisiana State University
- 170 shared
Dawn C. Schwenke
Phoenix VA Health Care System
- 161 shared
Peter D. Reaven
Phoenix VA Health Care System
- 159 shared
Abbas E. Kitabchi
Education
- 1997
M.D., Medicine
University of California, San Diego
- 1993
B.S., Biology
University of California, San Diego
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