About

Rohit Loomba is a Professor of Medicine at UC San Diego, with a focus on hepatology and gastroenterology. His educational background includes an MBBS (MD) from the Armed Forces Medical College in India, and postgraduate training through residencies and fellowships at St. Luke's Hospital and UC San Diego, respectively. His research primarily centers on non-alcoholic fatty liver disease (NAFLD), metabolic dysfunction-associated steatohepatitis (MASH), and related liver conditions. He is involved in clinical trials and research activities aimed at non-invasive screening, diagnosis, and treatment of liver diseases, including the development of biomarkers and therapeutic options for NAFLD and MASH. Dr. Loomba has contributed to understanding the epidemiology, genetics, and clinical management of liver diseases, and his work includes leadership roles in multiple NIH-funded projects.

Research topics

• Medicine
• Internal medicine
• Gastroenterology
• Pathology
• Computer Science
• Biology
• Political Science
• Radiology
• Bioinformatics
• Endocrinology
• Computational biology
• Biochemistry
• Artificial Intelligence
• Chemistry
• Computer Security
• Genetics
• Zoology
• Classics
• Environmental health
• Art history
• Nursing
• History
• Gerontology
• Intensive care medicine

Selected publications

• 1263 PERFORMANCE AND RISK OF FALSE NEGATIVES IN CLINICAL PATHWAYS TO IDENTIFY ADVANCED FIBROSIS IN METALD AND ALD

  Gastrointestinal Endoscopy · 2026-05-01

  article
  PublisherDOI

• Su2096 GAPS IN GUIDELINE-CONCORDANT STATIN THERAPY AND ASSOCIATIONS WITH FIBROSIS SEVERITY AMONG PATIENTS AT RISK FOR MASLD

  Gastrointestinal Endoscopy · 2026-05-01

  article
  PublisherDOI

• 1079 A CELL FREE DNA METHYLATION-BASED LIQUID BIOPSY FOR SEMAGLUTIDE WEIGHT-LOSS RESPONSE IN AT-RISK MASH

  Gastrointestinal Endoscopy · 2026-05-01

  article1st authorCorresponding
  PublisherDOI

• Clinical Use of Noninvasive Testing for Liver Fibrosis in Metabolic Dysfunction-Associated Steatotic Liver Disease

  Clinical Gastroenterology and Hepatology · 2026-04-01

  articleSenior author
  PublisherDOI

• Su2096 GAPS IN GUIDELINE-CONCORDANT STATIN THERAPY AND ASSOCIATIONS WITH FIBROSIS SEVERITY AMONG PATIENTS AT RISK FOR MASLD

  Gastroenterology · 2026-05-01

  article
  PublisherDOI

• Editorial: Gene Silencing Therapy for a New Era of Pancreatitis Prevention. Authors' Reply

  Alimentary Pharmacology & Therapeutics · 2026-04-21

  article1st authorCorresponding

  We commend Dr Petrov for a thoughtful and forward-looking editorial that reframes pancreatitis prevention as a longitudinal, mechanistically informed discipline rather than a purely episodic, hospital-based endeavour [1]. The rising global burden of acute pancreatitis (AP) [2], together with its increasingly recognised long-term sequelae, underscores the urgency of advancing prevention strategies beyond their historically narrow scope. As highlighted in the editorial, recurrent AP remains understudied. The emerging evidence that recurrent AP confers long-term risk [3-5] substantially elevates its clinical importance and strengthens the case for earlier, proactive intervention. We agree that targeting hypertriglyceridaemia (HTG) represents a biologically compelling and clinically actionable approach to primary prevention in selected populations. Apolipoprotein C-III (APOC3) occupies a central regulatory position in triglyceride (TG) metabolism through inhibition of both lipoprotein lipase-dependent and lipoprotein lipase-independent lipolysis and clearance of triglyceride-rich lipoproteins (TRL) [6]. Genetic [7], mechanistic [6] and clinical data [8-11] collectively support APOC3 as a rational therapeutic target in conditions characterised by severe or refractory HTG. The study with plozasiran, an siRNA therapeutic now approved as Redemplo in the United States, Canada and China as an adjunct to diet to reduce TGs in adults with familial chylomicronaemia syndrome (FCS), represents an important conceptual and clinical advance [12]. Despite its modest sample size—inevitable in rare disease research—the magnitude and rapidity of TG lowering, coupled with the known associated reduction in pancreatitis risk, provide a strong rationale for broader investigation. The inclusion of patients without genetically confirmed familial chylomicronaemia syndrome (FCS) further strengthens the evidence of the therapeutic implications extending beyond monogenic disease. At the same time, the field would benefit from thoughtful delineation of the populations most likely to derive benefit from triglyceride-lowering interventions aimed at pancreatitis prevention. While very severe HTG is a well-established risk factor for pancreatitis, the TG thresholds, trajectories and modifiers that meaningfully influence the risk of its recurrence in more heterogeneous clinical settings remain incompletely defined. Future trials will therefore need to balance mechanistic ambition with pragmatic design, incorporating appropriate baseline risk stratification and clinically relevant endpoints. Of interest, studies with plozasiran that are powered for pancreatitis-related endpoints—not solely lipid parameters—are in process and will be essential to establishing clinical utility. In this context, the editorial serves as a timely and constructive call to action, and successful integration into clinical practice will depend on rigorous clinical investigation, careful patient selection and sustained collaboration across gastroenterology, lipidology, cardiology and endocrinology. Rohit Loomba: conceptualization, writing – original draft, writing – review and editing. Enrique de-Madaria: writing – review and editing. Elham Afghani: writing – review and editing. Vikesh K. Singh: writing – review and editing. Nicholas J. Leeper: conceptualization, writing – original draft, writing – review and editing. The authors' declarations of personal and financial interests are unchanged from those in the original article [12]. This work was supported by Arrowhead Pharmaceuticals. The authors declare no conflicts of interest. This article is linked to Loomba et al. papers. To view these articles, visit https://doi.org/10.1111/apt.70662 and https://doi.org/10.1111/apt.70623. The data that support the findings of this study are available from the corresponding author upon reasonable request.

  PublisherDOI

• Global Longitudinal Assessment of <scp>MASLD</scp> Using Magnetic Resonance Elastography ( <scp>GOLDMINE</scp> ): A Multi‐Center, International Prospective Cohort Study of Imaging Biomarkers in <scp>MASLD</scp> Clinical Outcomes

  Alimentary Pharmacology & Therapeutics · 2026-04-22 · 3 citations

  articleSenior authorCorresponding

  BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) exhibits marked heterogeneity in fibrosis progression and liver-related outcomes. Liver biopsy is not feasible for longitudinal risk stratification at scale, creating a need for validated non-invasive biomarkers, particularly imaging biomarkers, that can predict clinically meaningful disease progression and liver-related outcomes. AIMS: To describe the design and rationale of the GOLDMINE study, established to determine whether non-invasive imaging biomarkers predict MASLD progression and liver-related clinical outcomes. METHODS: GOLDMINE is an investigator-initiated, multi-centre, international longitudinal cohort enrolling up to 1000 adults with either biopsy-proven MASLD or MASLD cirrhosis across the full fibrosis spectrum. Participants are recruited from 15 sites in the US and 4 international sites (Japan, Singapore and France). At baseline, participants undergo clinical phenotyping, vibration-controlled transient elastography, and advanced magnetic resonance imaging (MRI), including proton-density-fat-fraction and magnetic resonance elastography (MRE). MRI (and biospecimen banking) is repeated at 2-year intervals (years 2 and 4), with annual follow-up visits for up to 10 years. Baseline liver histology is centrally processed, digitized and reviewed by a single expert hepatopathologist; all MRI/MREs are centrally interpreted. RESULTS: The prespecified clinical outcomes include progression to cirrhosis, clinically significant portal hypertension, major adverse liver-related outcomes (ascites, hepatic encephalopathy, portal hypertensive bleeding, liver transplantation/qualification), hepatocellular carcinoma, major adverse cardiovascular events, and all-cause mortality, with independent central adjudication of all events. CONCLUSIONS: GOLDMINE establishes a rigorously phenotyped MASLD cohort integrating centralized histology, advanced MRI-based biomarkers, longitudinal biobanking, and adjudicated outcomes, providing a platform to validate imaging and blood-based prognostic biomarkers in MASLD.

  PublisherDOI

• 1079 A CELL FREE DNA METHYLATION-BASED LIQUID BIOPSY FOR SEMAGLUTIDE WEIGHT-LOSS RESPONSE IN AT-RISK MASH

  Gastroenterology · 2026-05-01

  article1st authorCorresponding
  PublisherDOI

• 1263 PERFORMANCE AND RISK OF FALSE NEGATIVES IN CLINICAL PATHWAYS TO IDENTIFY ADVANCED FIBROSIS IN METALD AND ALD

  Gastroenterology · 2026-05-01

  article
  PublisherDOI

• Factors associated with protection from MASLD in type 2 diabetes: A prospective study integrating longitudinal MRI/MRE and stable isotope tracing

  JHEP Reports · 2026-01-08

  articleOpen accessSenior author

  Background & Aims: Type 2 diabetes is one of the strongest risk factors for the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD). In this study, we aimed to identify factors associated with protection from MASLD in a prospective cohort of individuals with type 2 diabetes. Methods: This prospective study included 148 individuals with type 2 diabetes who underwent advanced liver phenotyping using MRI and MRE techniques at baseline and 2-year follow-up. Protection from MASLD was defined as the absence of hepatic steatosis (MRI-proton density fat fraction <5%) and significant fibrosis (MRE <3 kPa) at both time points. Factors associated with protection from MASLD were assessed using Firth's penalized logistic regression. Regularized logistic regression models were fitted as complementary analyses. Results: lipogenesis in those free from MASLD. Conclusions: Managing modifiable risk factors, such as body weight and lipid profile, may be critical for preventing MASLD development in individuals with type 2 diabetes. Impact and implications: lipogenesis may underlie this protective phenotype. These findings suggest that managing modifiable risk factors, such as body weight and lipid profile, may be critical for preventing MASLD development and progression in individuals with type 2 diabetes.

  PublisherDOI

Recent grants

• NIH Grant K23DK090303

  NIH · $721k · 2015

• Novel IL-23 inhibitor for the treatment of alcohol associated liver disease

  NIH · $3.7M · 2020–2026

• QUS Technology for Diagnosis and Grading of Hepatic Steatosis in NAFLD

  NIH · $680k · 2015–2020

• Non-invasive screening of diabetics for advanced fibrosis due to NAFLD

  NIH · $1.7M · 2020–2025

• QUS Technology for Diagnosis and Grading of Hepatic Steatosis in NAFLD

  NIH · $2.7M · 2015–2022

Frequent coauthors

• Claude B. Sirlin

  The University of Texas Southwestern Medical Center

  367 shared

• Arun J. Sanyal

  Virginia Commonwealth University

  345 shared

• Kris V. Kowdley

  206 shared

• Daniel Q. Huang

  National University Health System

  183 shared

• Kathryn J. Fowler

  179 shared

• Brent A. Neuschwander‐Tetri

  178 shared

• Tania Kamphaus

  Foundation for the National Institutes of Health

  166 shared

• Roberto A. Calle

  166 shared

Education

• M.D.

  University of California, San Diego

• B.S.

  University of California, San Diego