About

Vala Hamidi is an Associate Clinical Professor in the Department of Medicine at UC San Diego. Her research focuses on endocrinology and metabolism, with notable contributions to the study of continuous glucose monitoring, postprandial IL6 reduction through chronic GLP1 therapy in obese humans with prediabetes, and the effects of GLP1 analogs mediated by interleukin-6 signaling in adipocytes. She has also investigated the impact of exenatide therapy on postprandial vasodilation in humans with prediabetes and reduced skeletal muscle phosphocreatine concentration in type 2 diabetic patients. Her work is characterized by a focus on diabetes care, endocrinology, and metabolic processes, with multiple publications derived from MEDLINE/PubMed and other sources. Vala Hamidi's research includes clinical trials and studies on the physiological and molecular mechanisms underlying diabetes and obesity, contributing to the understanding of therapeutic interventions and metabolic regulation.

Research topics

• Internal medicine
• Endocrinology
• Medicine
• Chemistry
• Biology
• Cell biology
• Biochemistry

Selected publications

• The Horizon Ahead

  Endocrinology and Metabolism Clinics of North America · 2026-05-01

  article1st author
  PublisherDOI

• 1578-P: Circulating Mitochondrial DNA Provides a Novel Biomarker for Hyperinsulinemia and Disease Severity in Type 2 Diabetes

  Diabetes · 2025-06-13

  article

  Introduction 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)

  PublisherDOI

• 269-OR: Glucagon Antagonism Improves Insulin Sensitivity and Increases Lean Body Mass in Patients with Type 1 Diabetes—A Twelve-Week Double-Blind, Randomized, Placebo-Controlled Trial

  Diabetes · 2025-06-13

  article

  Introduction 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)

  PublisherDOI

• Time in Tight Range for Patients With Type 1 Diabetes: The Time Is Now, or Is It Too Soon?

  Diabetes Care · 2024-04-19 · 27 citations

  editorialOpen access1st author
  PublisherOA PDFDOI

• 7068 Paraganglioma in Cyanotic Congenital Heart Disease

  Journal of the Endocrine Society · 2024-10-01

  articleOpen accessSenior author

  Abstract Disclosure: R. Lis: None. V. Hamidi: None. Paragangliomas arise from the non-chromaffin cells of the parasympathetic nervous system, which are composed of glomus cells. These function as chemoreceptors in response to hypoxia. Carotid body paragangliomas have been linked to conditions with chronic hypoxia. This was first seen in residents of high altitude locations in a case report presented by Saldana et. al and regression of a paraganglioma with resolution of hypoxia was reported by Gruber et. al. There have been few additional case reports of Paraganglioma in other hypoxic states. We present a rare case of a functional Paraganglioma in a patient with Cyanotic Congenital Heart Disease (CCHD).This is a 19 year old female with a history of CCHD due to double inlet left ventricle and transposition of the great arteries. Soon after birth, she had a fontan procedure. She subsequently developed fontan associated liver disease as well as chronic kidney disease, hypertension, sinus node dysfunction, and complete heart block. Her baseline oxygen saturation was 78-85%. Her heart rate was 40-49 beats per minute with upcoming plans for pacemaker placement. Her blood pressure ranged 90/50 to 150/80 mmHg on Amlodipine 5 mg and Lisinopril 2.5 mg. She routinely received abdominal imaging to monitor her liver disease. A liver MRI incidentally revealed a retroperitoneal mass concerning for a paraganglioma. Serum Normetanephrines were found to be 26.60 nmol/L (reference range less than 0.89). 24 hr Urine Norepinephrine was 1,187 ug/d (reference range 14-20). Further imaging was negative for additional sites of disease. Given her complete heart block, she was started on alpha blockade only prior to pacemaker placement. After the pacemaker was placed, she was started on beta blockade and underwent surgical resection of her paraganglioma. The pathology confirmed paraganglioma and mutation testing was negative for germline mutations including SDH, VHL, RET, NF1 mutations. Paragangliomas in patients with CCHD have been scarcely described in the literature given the rarity of both of these conditions. However, there is a relatively increased incidence of paragangliomas in the CCHD population due to chronic hypoxia triggering the hypoxia pathway. EPAS1 mutated HIF2alpha is often found to be the culprit in these patients. In addition, case reports have often described these patients to either be asymptomatic or have potential symptoms masked by their cardiac disease. Therefore, CCHD patients are at increased risk for paragangliomas and warrant additional awareness and regular screening. Screening has been proposed to start after 10 years of hypoxia in a case review by Agarwal et. al. as paraganglioma incidence in CCHD populations has not been seen before age 11. Incidence of recurrence is not yet widely studied, but significant concern for recurrence is warranted if the etiology of hypoxia is not reversed. Presentation: 6/3/2024

  PublisherOA PDFDOI

• Chronic GLP1 therapy reduces postprandial IL6 in obese humans with prediabetes

  Cardiovascular Endocrinology & Metabolism · 2024-01-04 · 1 citations

  articleOpen access1st author

  Single-dose glucagon-like peptide 1 (GLP1) therapy increases postprandial plasma IL6 levels in prediabetic, obese humans. GLP1-IL6 interactions underly multiple antidiabetic effects, but these may differ after acute versus chronic therapy. This study examines postprandial effects of GLP1 after chronic therapy. Seven humans (six Black) with prediabetes and obesity completed 6 weeks of exenatide extended release therapy. Then subjects returned for pre- and post-meal measurements of plasma IL6, GLP1, glucagon, and related inflammatory markers. Weight, which was measured before and after therapy, did not change. Plasma IL6 decreased from baseline to postmeal state ( = 0.016), with decreases in free fatty acids ( P < 0.001) and increases in insulin ( P = 0.002), glucose ( P < 0.0001), triglycerides ( P = 0.0178), and glucagon ( P = 0.018). Baseline GLP1 levels matched 6 weeks of therapy. The fall in postprandial plasma IL6, which contrasts with the increase after acute therapy, highlights the need for more investigation regarding the mechanisms of acute versus chronic GLP1-IL6 signaling.

  PublisherDOI

• Continuous Glucose Monitoring Time Below Range Predicts Impaired Epinephrine Response to Hypoglycemia in Patients With Type 1 Diabetes

  Diabetes Care · 2024 · 7 citations

  • Medicine
  • Internal medicine
  • Endocrinology
  PublisherOA PDFDOI

• Voice Outcomes From Direct Vocal Fold Testosterone Injections, a Case Report

  The Laryngoscope · 2023-01-03 · 5 citations

  articleOpen access

  Here we provide the first demonstration of targeted vocal fold testosterone injection to achieve voice masculinization in 2 transgender male patients. Successful voice outcome was achieved in 2-3 weeks, without side effects, and continues to be durable. Laryngoscope, 133:1211-1213, 2023.

  PublisherOA PDFDOI

• Anti-diabetic effects of GLP1 analogs are mediated by thermogenic interleukin-6 signaling in adipocytes

  Cell Reports Medicine · 2022 · 38 citations

  • Endocrinology
  • Internal medicine
  • Chemistry

  Mechanisms underlying anti-diabetic effects of GLP1 analogs remain incompletely understood. We observed that in prediabetic humans exenatide treatment acutely induces interleukin-6 (IL-6) secretion by monocytes and IL-6 in systemic circulation. We hypothesized that GLP1 analogs signal through IL-6 in adipose tissue (AT) and used the mouse model to test if IL-6 receptor (IL-6R) signaling underlies the effects of the GLP1-IL-6 axis. We show that liraglutide transiently increases IL-6 in mouse circulation and IL-6R signaling in AT. Metronomic liraglutide treatment resulted in AT browning and thermogenesis linked with STAT3 activation. IL-6-blocking antibody treatment inhibited STAT3 activation in AT and suppressed liraglutide-induced increase in thermogenesis and glucose utilization. We show that adipose IL-6R knockout mice still display liraglutide-induced weight loss but lack thermogenic adipocyte browning and metabolism activation. We conclude that the anti-diabetic effects of GLP1 analogs are mediated by transient upregulation of IL-6, which activates canonical IL-6R signaling and thermogenesis.

  PublisherOA PDFDOI

• 322-OR: SGLT2 Inhibition Has No Effect on the Counterregulatory Response to Hypoglycemia in Subjects with Type 1 Diabetes (T1D)

  Diabetes · 2021-06-01

  article

  Individuals with T1D have an ineffective glucagon response to low glucose levels which predisposes them to episodes of hypoglycemia. SGLT-2 inhibitors (SGLT2i) do not increase and may even reduce hypoglycemia in clinical trials, yet the mechanism is unknown. This trial was conducted to determine if SGLT2i improve the counterregulatory response (CR) to hypoglycemia.Subjects with T1D (n=22) received 4 weeks of SGLT2i (dapagliflozin 5 mg daily) and 4 weeks of placebo in a double-blind, random-order, cross-over study. After each phase, subjects underwent a hypoglycemic clamp. During 40 min of hypoglycemia (mean serum glucose 49 mg/dL) CR hormones were serially measured.There was no difference between treatment phases in glucagon or other CR hormones during hypoglycemia [Figure]. Mean ± SE (paired two-tailed t-test) during hypoglycemia for SGLT2i vs. Placebo were: Glucagon (15.4 ± 1.8 vs. 14.8 ± 2.1 pg/mL; P = 0.77), Epinephrine (216 ± 34 vs. 200 ± 28 pg/mL; P = 0.46), Norepinephrine (402 ± 39 vs. 381 ± 25 pg/mL; P = 0.51), GH (9.1 ± 1.3 vs. 8.4 ± 1.8 ng/mL; P = 0.60), and Cortisol (11.4 ± 1.1 vs. 10.3 ± 0.9 mcg/dL; P = 0.18).SGLT2i treatment has no effect on the CR hormone response to hypoglycemia in T1D. These data suggest that any reduction in hypoglycemia that occurs with these agents may be due to behavioral changes (e.g., lower insulin doses, less frequent bolusing), rather than a physiologic mechanism.View largeDownload slideView largeDownload slide DisclosureS. C. Boeder: Consultant; Self; Cecelia Health, Research Support; Self; Dexcom, Inc. D. G. Ines: None. E. R. Giovannetti: None. V. Hamidi: None. P. M. Burke: None. A. Armstrong: None. L. Carter: None. J. Pettus: Advisory Panel; Self; Novo Nordisk, Sanofi, Consultant; Self; Diasome Pharmaceuticals, Inc., Insulet Corporation, Lilly Diabetes, MannKind Corporation, Tandem Diabetes Care. FundingJDRF (2-SRA-2018-606-M-B)

  PublisherDOI

Frequent coauthors

• Absalon D. Gutierrez

  The University of Texas Health Science Center at Houston

  5 shared

• Zhan‐Guo Gao

  National Institute of Diabetes and Digestive and Kidney Diseases

  3 shared

• Amy Le

  Indiana University – Purdue University Indianapolis

  3 shared

• Mikhail G. Kolonin

  3 shared

• Kayla A. Riggs

  The University of Texas Southwestern Medical Center

  3 shared

• Karla Bermudez Saint Andre

  Houston Methodist

  3 shared

• Heinrich Taegtmeyer

  3 shared

• Sara Coverdale

  The University of Texas Health Science Center at Houston

  2 shared

Labs

• Vala HamidiPI