Schafer Boeder
· Assistant Clinical ProfessorVerifiedUniversity of California, San Diego · Endocrinology and Metabolism
Active 2015–2025
About
Schafer Boeder is an Associate Clinical Professor in the Department of Medicine at UC San Diego. His research focuses on clinical diabetes, including glucose-lowering medications, glycemia, and cognitive outcomes, as evidenced by his involvement in the GRADE randomized clinical trial. He has contributed to studies on continuous glucose monitoring, insulin infusion safety, and the accuracy of glucose monitors in critically ill patients. His work also encompasses the development and evaluation of therapies for type 1 diabetes, such as SGLT2 inhibitors, glucagon receptor antagonists, and hepatoselective glucokinase activators. Dr. Boeder's research extends to understanding the impact of diabetes on COVID-19 severity, diabetic ketoacidosis risk, and the physiological responses to hypoglycemia. His publications demonstrate a significant contribution to advancing diabetes treatment and management through clinical trials and translational research.
Research topics
- Medicine
- Internal medicine
- Endocrinology
- Computer Science
- Intensive care medicine
- Gastroenterology
- Virology
Selected publications
Diabetes · 2025-06-13
articleIntroduction and Objective: This study compared accuracy and glycemic control using Dexcom G6 and G7 real-time continuous glucose monitors (rtCGM) integrated into an insulin infusion computer calculator (IICC) workflow for critically ill adult inpatients. Methods: A retrospective analysis evaluated 13 ICU patients using Dexcom G6 and 35 using G7, integrated into an institution-developed IICC workflow using a validation protocol. Accuracy was assessed by comparing matched rtCGM and point-of-care (POC) glucose values using mean absolute relative difference (MARD) and Surveillance Error Grid (SEG) analysis. Results: A total of 1,291 matched glucose pairs were analyzed for G7 and 758 for G6. G7 sensors demonstrated lower MARD (12.5% vs. 15.2%) and a higher percentage of values in SEG Zone A (86% vs. 76%). Both sensors showed high SEG accuracy, with 99.6% (G7) and 99.2% (G6) in the clinically acceptable Zone A+B (Figure). A lower mean glucose (142 vs. 151 mg/dL) and higher time in range (82.8% vs 79.3%) was achieved using G7 compared to G6. The G7 workflow also demonstrated lower time above range >180 mg/dL (14.5% vs. 20.5%). Despite low overall hypoglycemia rates, G7 workflow exhibited slightly higher time below range <70 mg/dL (0.5% vs. 0.18%) and marginally increased time <54 mg/dL (0.1% vs. 0.05%). Conclusion: G7 sensors demonstrated improved accuracy and glycemic performance compared to G6, with the exception of a slight increase in time spent below range. Disclosure E.R. Giovannetti: Advisory Panel; Eli Lilly and Company, Sanofi. R.O. Lee: None. R.L. Thomas: Research Support; REMD Therapeutics, Carmot Therapeutics. S.C. Boeder: Consultant; Cecelia Health. Advisory Panel; Novo Nordisk. Consultant; Lexicon Pharmaceuticals, Inc, Persperion Diagnostics. Research Support; Eli Lilly and Company, Carmot Therapeutics, Inc, REMD Therapeutics, Dexcom, Inc., Lexicon Pharmaceuticals, Inc. K. Kulasa: None. Funding Dexcom provided CGM sensors free of charge for this study.
Diabetes · 2025-06-13
articleIntroduction and Objective: Circulating cell-free mitochondrial DNA (cf-mtDNA) activates innate immunity and has been implicated in animal models of diabetes. This study aimed to assess how mitochondrial DNA levels correlate with diabetes disease state and hospitalization in humans. Methods: Using droplet digital PCR (ddPCR), we quantified plasma cf-mtDNA concentrations in 52 adults classified into 4 groups: non-diabetes (Non-DM), obesity without diabetes (ObND), outpatient Type 2 Diabetes (T2D) and hospitalized T2D (T2D-Hosp). ObND group participants had BMI >30 and hyperinsulinemia without hyperglycemia (~2-fold fasting insulin vs. Non-DM, p = 0.028). Results: Compared to Non-DM controls, logarithmic analysis revealed a progressive increase in plasma cf-mtDNA concentrations in ObND (p = 0.042), T2D (p = 0.006), and T2D-Hosp groups (p <0.001) (Figure). Conclusion: Here we show that cf-mtDNA is elevated in people with ObND or T2D compared to Non-DM controls. This effect is exacerbated by physiologic stress, with an additional ~3-fold increase in cf-mtDNA during hospitalization. Early cf-mtDNA elevation is detectable in obese patients with hyperinsulinemia before significant hyperglycemia develops. Plasma cf-mtDNA may thus provide a biomarker for early diagnosis and clinical severity in T2D. Disclosure R.L. Thomas: Research Support; REMD Therapeutics, Carmot Therapeutics. J.D. Garcia: None. A.J. Kumar: None. L. Carter: None. J.A. Masso-Silva: None. V. Hamidi: None. S.C. Boeder: Consultant; Cecelia Health. Advisory Panel; Novo Nordisk. Consultant; Lexicon Pharmaceuticals, Inc, Persperion Diagnostics. Research Support; Eli Lilly and Company, Carmot Therapeutics, Inc, REMD Therapeutics, Dexcom, Inc., Lexicon Pharmaceuticals, Inc. T.P. Ciaraldi: None. J.H. Pettus: None. M.L. Hepokoski: None. Funding R.L. Thomas: Altman Clinical and Translational Research Institute Pilot Project National Institutes of Health, CTSA Grant (UL1TR0014422); National Institute of Diabetes and Digestive and Kidney Diseases (P30 DK063491); Foundation for the National Institutes of Health T32 (2T32DK007044-41); National NIH K12 DiabDocs Program (K12DK133995)
Diabetes · 2025-06-13
article1st authorCorrespondingIntroduction and Objective: Glucagon has underappreciated effects on lipid, glucose, and amino acid metabolism. This study aimed to assess the comprehensive metabolic effects of glucagon antagonism in type 1 diabetes (T1D). Methods: 30 adults with T1D were randomized 1:1 to receive the glucagon receptor antagonist (GRA) volagidemab via once weekly subq injection for 12 weeks vs. placebo. A 2-stage hyperinsulinemic-euglycemic clamp (8 and 40 mU/m2/min) with indirect calorimetry was conducted at baseline and after 12-weeks to determine changes in insulin sensitivity and substrate oxidation. Results: GRA therapy decreased exogenous insulin use by 16% while maintaining glucose control (no Δ in A1c or CGM metrics). Compared to baseline, GRA decreased circulating FFA concentrations by 30% in the fasting state and 39% in the 1st stage of the insulin clamp, suggesting an increase in adipose tissue insulin sensitivity (p < 0.05). During the high dose step of the clamp, which is representative of skeletal muscle insulin action, glucose disposal increased by 33% (p = 0.052) and respiratory quotient by indirect calorimetry increased by 5% (p = 0.013). Thus, GRA therapy significantly increased glucose utilization and showed a strong trend toward improving skeletal muscle insulin sensitivity. Finally, bioimpedance data showed a significant increase in lean body mass of 1.5 kg after GRA therapy (p < 0.001) with no change in total body weight. As a potential explanation for this finding, GRA therapy significantly increased circulating amino acid concentrations (~2-fold) which may provide additional substrate for muscle tissue synthesis. Conclusion: GRA therapy decreased lipolysis, improved peripheral glucose disposal, increased glucose oxidation, and increased lean body mass. These data highlight the profound effects that glucagon action has on multiple aspects of metabolism that extend far beyond glucose control. Disclosure S.C. Boeder: Consultant; Cecelia Health. Advisory Panel; Novo Nordisk. Consultant; Lexicon Pharmaceuticals, Inc, Persperion Diagnostics. Research Support; Eli Lilly and Company, Carmot Therapeutics, Inc, REMD Therapeutics, Dexcom, Inc., Lexicon Pharmaceuticals, Inc. R.L. Thomas: Research Support; REMD Therapeutics, Carmot Therapeutics. V. Hamidi: None. E.R. Giovannetti: Advisory Panel; Eli Lilly and Company, Sanofi. A. Armstrong: None. L. Carter: None. T.P. Ciaraldi: None. J.H. Pettus: None. Funding Breakthrough T1D and the Helmsley Charitable Trust (3-SRA-2021-1066-M-B)
Journal of Diabetes Science and Technology · 2025-05-08 · 1 citations
articleOpen accessSenior authorCorrespondingBACKGROUND: Continuous glucose monitors (CGMs) are increasingly being used to guide glucose management in the hospital. However, uncertainty regarding their accuracy in this setting remains. METHODS: We conducted a nonrandomized, open-label, clinically blinded prospective trial of the Dexcom G6 Pro (G6P) and FreeStyle Libre Pro (FLP) in the inpatient setting among critically ill hospitalized patients (n = 40) requiring continuous intravenous insulin infusion. In parallel with CGM data, reference serum (Lab) glucose and point-of-care (POC) glucose values were obtained. On completion of the study, CGM and reference values were analyzed to assess CGM accuracy. RESULTS: A total of 1015 matched G6P-Lab pairs had a mean absolute relative difference (MARD) of 22.7%, 2369 G6P-POC pairs had an MARD of 22.9%, 1006 matched FLP-Lab pairs had an MARD of 25.2%, and 2353 FLP-POC pairs had an MARD of 27.0%. Both CGM systems demonstrated considerable inter-patient variability in sensor accuracy and tended to underestimate glucose in comparison with the reference values. Rarely were low reference values overestimated by either sensor. CONCLUSIONS: Factory-calibrated continuous glucose monitors may require accuracy validation and per-patient calibration for inpatient use in critically ill patients.
Endocrine Practice · 2025-06-23 · 4 citations
articleOpen accessSenior authorOBJECTIVE: Evaluate the integration of real-time CGM (rtCGM) into an insulin infusion computer calculator (IICC) to improve glycemic control, time efficiency, safety, and clinician workflow in the intensive care unit (ICU). METHODS: A retrospective analysis was conducted on 35 critically ill adult patients requiring insulin infusion in the surgical and medical ICUs. Dexcom G7 rtCGM values were integrated into an institution-developed IICC using an ongoing validation protocol, allowing for nonadjunctive CGM use. The accuracy of rtCGM was assessed by comparing matched CGM and point-of-care (POC) glucose values using mean absolute relative difference (MARD), surveillance error grid, and Parkes Error Grid analyses. CGM time-in-range metrics, clinician turnaround time for glucose monitoring, and nurse satisfaction were also evaluated. RESULTS: A total of 1291 matched glucose pairs were analyzed. The rtCGM system demonstrated a MARD of 12.5%, with 99.6% of the values falling within clinically acceptable error zones (A+B) on the Parkes Error Grid. Patients in the rtCGM-IICC protocol had mean glucose 141.9 mg/dL, with mean time in range (70-180 mg/dL) 82.8%, time above range (> 180 mg/dL) 14.5%, and time below range (< 70 mg/dL) 0.5%. Clinician time efficiency improved significantly, with POC testing requiring a mean turnaround time of nearly 5 minutes compared to 3-second CGM retrieval. All surveyed nurses (n = 20) reported rtCGM increased efficiency and improved safety and preferred rtCGM with POC over POC testing alone. CONCLUSION: Integrating rtCGM with an IICC protocol in the ICU enhances glycemic control, improves workflow efficiency, and reduces clinician workload while maintaining high accuracy.
Diabetes Technology & Therapeutics · 2024-03-05 · 15 citations
articleOpen access1st authorCorrespondingIntroduction: Sodium glucose cotransporter inhibitors may increase beta-hydroxybutyrate (BHB) in insulin-requiring patients. We determined factors associated with BHB changes from baseline (ΔBHB) and diabetic ketoacidosis (DKA) in patients with type 1 diabetes (T1D) receiving sotagliflozin as an insulin adjunct. Research Design and Methods: This post hoc analysis compared ΔBHB levels in adults with T1D receiving sotagliflozin 400 mg or placebo for 6 months. We evaluated clinical and metabolic factors associated with ΔBHB and used logistic regression models to determine predictors associated with BHB values >0.6 and >1.5 mmol/L (inTandem3 population; N = 1402) or with DKA events in a pooled analysis (inTandem1–3; N = 2453). Results: From baseline (median, 0.13 mmol/L), median fasting BHB increased by 0.04 mmol/L (95% confidence interval, 0.03–0.05; P < 0.001) at 24 weeks with sotagliflozin versus placebo; 67% of patients had no or minimal changes in BHB over time. Factors associated with on-treatment BHB >0.6 or >1.5 mmol/L included baseline BHB and sotagliflozin use. Age, insulin pump use, sotagliflozin use, baseline BHB, and ΔBHB were significantly associated with DKA episodes. Independent of treatment, DKA risk increased by 18% with each 0.1-mmol/L increase in baseline BHB and by 8% with each 0.1-mmol/L increase from baseline. Conclusion: Incremental increases in baseline BHB and ΔBHB were associated with a higher DKA risk independent of treatment. Adding sotagliflozin to insulin increased median BHB over 24 weeks in patients with T1D and was associated with increased DKA events. These results highlight the importance of BHB testing and monitoring and individualizing patient education on DKA risk, mitigation, identification, and treatment.
Diabetes Care · 2024-05-22 · 24 citations
articleOpen access1st authorOBJECTIVE: To examine the effects of insulin-adjunctive therapy with a sodium-glucose cotransporter 2 (SGLT2) inhibitor and a glucagon receptor antagonist (GRA) on glycemia, insulin use, and ketogenesis during insulinopenia in type 1 diabetes. RESEARCH DESIGN AND METHODS: In a randomized, double-blind, placebo-controlled, crossover trial we assessed the effects of adjunctive SGLT2 inhibitor therapy (dapagliflozin 10 mg daily) alone and in combination with the GRA volagidemab (70 mg weekly) in 12 adults with type 1 diabetes. Continuous glucose monitoring, insulin dosing, and insulin withdrawal tests (IWT) for measurement of glucose and ketogenesis during insulinopenia were completed during insulin-only (Baseline), SGLT2 inhibitor, and combination (SGLT2 inhibitor + GRA) therapy periods. RESULTS: Average glucose and percent time with glucose in range (70-180 mg/dL) improved with combination therapy versus Baseline and SGLT2 inhibitor (131 vs. 150 and 138 mg/dL [P < 0.001 and P = 0.01] and 86% vs. 70% and 78% [P < 0.001 and P = 0.03], respectively) without increased hypoglycemia. Total daily insulin use decreased with combination therapy versus Baseline and SGLT2 inhibitor (0.41 vs. 0.56 and 0.52 units/kg/day [P < 0.001 and P = 0.002]). Peak β-hydroxybutyrate levels during IWT were lower with combination therapy than with SGLT2 inhibitor (2.0 vs. 2.4 mmol/L; P = 0.048) and similar to levels reached during the Baseline testing period (2.1 mmol/L). Participants reported enhanced treatment acceptability and satisfaction with combination therapy. CONCLUSIONS: Glucagon antagonism enhances the therapeutic effects of SGLT2 inhibition in type 1 diabetes. Combination therapy improves glycemic control, reduces insulin dosing, and suggests a strategy to unlock the benefits of SGLT2 inhibitors while mitigating the risk of diabetic ketoacidosis.
Diabetes Care · 2024 · 7 citations
- Medicine
- Internal medicine
- Endocrinology
Acetazolamide Therapy and Kidney Function in Persons with Nonalbuminuric Diabetes Mellitus Type 1
Journal of the American Society of Nephrology · 2024-10-08 · 8 citations
articleOpen accessKey Points Low-dose acetazolamide reversibly lowered GFR in persons with type 1 diabetes mellitus, suggesting a possible role in relieving glomerular hyperfiltration. Low doses of acetazolamide were well tolerated in persons with type 1 diabetes. Background Sodium-glucose cotransporter-2 inhibitors (SGLT2is) lower the risk of kidney failure in persons with type 2 diabetes. The presumed mechanism of action is through greater delivery of sodium to the distal tubule and activation of tubuloglomerular feedback, which lowers GFR and intraglomerular pressure. SGLT2is are not approved for use in persons with type 1 diabetes because of the risk of diabetic ketoacidosis. Acetazolamide, a proximal tubule diuretic, delivers more sodium to the distal nephron and may activate tubuloglomerular feedback in a similar way to SGLT2is without a higher risk of diabetic ketoacidosis. The kidney effects and safety of acetazolamide in persons with type 1 diabetes have not been well studied. Methods We conducted a dose-escalation trial to determine the effects of three dosages of oral acetazolamide (62.5, 125, and 250 mg, all twice daily) in 12 persons with type 1 diabetes. Participants were treated for 2 weeks, followed by a 2-week washout period before exposure to the next dosage level. Blood and urine chemistries, as well as iohexol-measured GFR, were assessed before and after each treatment interval. We aimed to identify a dose that maximized measured GFR reductions while minimizing adverse effects. Results The mean age was 46±17 years, 100% were White, and 75% were female. The mean measured GFR was 89±18 ml/min per 1.73 m 2 at baseline. Acetazolamide reduced measured GFR by 15% (95% confidence interval [CI], 9 to 21), 14% (95% CI, 7 to 21), and 15% (95% CI, 10 to 21) after 2 weeks at the 62.5, 125, and 250 mg twice-daily dosage levels, respectively. The measured GFR reduction was fully reversed after each 2-week washout. Serum bicarbonate was reduced by 2.3, 4.2, and 4.4 mEq/L with escalating doses, and no episodes of hypokalemia (<3.5 mEq/L) were observed. Conclusions Among persons with type 1 diabetes and preserved kidney function, acetazolamide caused an acute, reversible reduction in measured GFR without effects on glucose metabolism. Clinical Trial registry name and registration number: Acetazolamide in Persons with Type 1 Diabetes, NCT05473364. Podcast This article contains a podcast at https://dts.podtrac.com/redirect.mp3/www.asn-online.org/media/podcast/JASN/2024_12_23_ASN0000000515.mp3
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
- 74 shared
Jeremy Pettus
University of California, San Diego
- 61 shared
John B. Buse
University of North Carolina at Chapel Hill
- 58 shared
Janet B. McGill
- 56 shared
Robin Goland
University of Michigan–Ann Arbor
- 56 shared
Maamoun Salam
Washington University in St. Louis
- 56 shared
Philip Raskin
The University of Texas Southwestern Medical Center
- 56 shared
Mallory Hillard
- 56 shared
Laura Young
Labs
Education
- 2006
Ph.D., Microbiology and Immunology
University of California, San Diego
- 2002
M.S., Microbiology and Immunology
University of California, San Diego
- 2000
B.S., Microbiology and Immunology
University of California, San Diego
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