About

Dr. Laurie J. Goodyear is a Senior Investigator at the Joslin Diabetes Center and a Professor of Medicine at Harvard Medical School. Her laboratory's long-standing goal is to elucidate the molecular basis for the benefits of exercise on health. Her research focuses on understanding how regular physical activity can improve glycemic control, lipid profiles, and reduce the risk of cardiovascular disease, Alzheimer’s disease, and other complications, especially in individuals with obesity and type 2 diabetes. Her group has been at the forefront of basic and translational research, investigating cell systems, rodent models, and human subjects to determine mechanisms underlying these effects. Her lab's current major focus areas include studying adipose tissue and muscle as critical mediators of exercise-induced improvements in glucose tolerance and metabolism, exploring the mechanisms by which maternal and paternal exercise influence offspring metabolic health, and identifying novel circulating factors induced by exercise that facilitate tissue-to-tissue communication to enhance tissue and metabolic function. Her extensive experience encompasses exercise physiology, muscle and adipose tissue physiology, intracellular signaling mechanisms, and in vivo metabolism. Throughout her career, she has trained over 100 post-doctoral fellows, junior faculty, graduate, and undergraduate students, contributing significantly to the field of metabolic health and exercise science.

Research topics

• Biology
• Medicine
• Internal medicine
• Cell biology
• Endocrinology
• Bioinformatics
• Genetics
• Psychology
• Biochemistry
• Chemistry
• Physical therapy
• Physical medicine and rehabilitation

Selected publications

• Novel Mechanisms Mediating the Beneficial Effects of Exercise on Metabolic Health

  Japanese Journal of Physical Fitness and Sports Medicine · 2026-01-01

  articleOpen access1st authorCorresponding

  Regular physical activity is essential for the prevention and treatment of metabolic diseases, yet the mechanisms for these beneficial effects are only poorly understood.The goal of the Goodyear laboratory is to elucidate the molecular mechanisms by which exercise improves health.This lecture discussed several of the seminal findings from the Goodyear lab in many critical areas of exercise biology.

  PublisherOA PDFDOI

• Author Correction: The cold-induced lipokine 12,13-diHOME promotes fatty acid transport into brown adipose tissue

  Nature Medicine · 2026-01-01

  articleOpen access
  PublisherOA PDFDOI

• Multi-omic responses to acute exercise in abdominal subcutaneous adipose tissue of sedentary adults: findings from MoTrPAC

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-09

  articleOpen access

  Exercise induces widespread health benefits across multiple tissues, yet the acute molecular responses in human adipose tissue remain poorly defined. The Molecular Transducers of Physical Activity Consortium (MoTrPAC) profiled temporal molecular changes in abdominal subcutaneous adipose tissue (ASAT) following a single bout of exercise. Healthy sedentary adults were randomized to endurance (EE), resistance (RE), or control (CON) groups. ASAT biopsies were collected pre-exercise and at 45min, 4hr, and 24hr post-exercise, followed by transcriptomic, proteomic, phosphoproteomic, and metabolomic analyses. EE and RE elicited distinct, time-resolved molecular programs involving angiogenesis, extracellular matrix remodeling, mitochondrial metabolism, substrate utilization, and circadian regulation. Phosphoproteomics revealed acute changes in cytoskeletal and branched-chain amino acid metabolism proteins associated with glycemic control. Temporal metabolomic shifts were cell-type-specific. Finally, we identified candidate adipose-derived exerkines with predicted endocrine actions. This multi-omic map of acute ASAT responses offers insight into adipose-specific mechanisms by which exercise promotes metabolic health.

  PublisherDOI

• Advances in Adipose Tissue Biology

  Endocrine Reviews · 2025-09-07 · 4 citations

  articleOpen accessSenior author

  Adipose tissue has emerged as a central regulator of human physiology, with its dysfunction driving the global rise in obesity-associated diseases, such as type 2 diabetes, cardiovascular and liver diseases, and several cancers. Once thought to be inert, adipocytes are now recognized as dynamic, responsive cells essential for energy homeostasis and interorgan communication, including the brain. Distinct adipose depots support specialized functions across development, sex, and aging. Technologies like single-cell RNA sequencing are unraveling depot-specific mechanisms, with the potential of identifying new therapeutic targets. This review highlights major scientific advancements leading to our current appreciation of the pivotal role of adipose tissue in health and disease. Many key discoveries in this field have been catalyzed by National Institutes of Health funding, particularly through the National Institute of Diabetes, Digestive and Kidney Diseases, now celebrating its 75th anniversary.

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• Rejuvenation of white adipose tissue in a longitudinal heterochronic transplantation model

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-29

  articleOpen access

  Exposure to a younger system can induce organismal rejuvenation, yet whether all tissues can be rejuvenated and by what mechanisms remains understudied. We performed heterochronic and isochronic transplantation of subcutaneous white adipose tissue (WAT) between young and old mice and longitudinally tracked changes in biological age. Transplantation accelerated tissue aging, and the molecular age of grafts shifted toward that of the host. Most importantly, old WAT was rejuvenated in a young body. Epigenetic and transcriptomic clocks revealed a reduction of predicted age, accompanied by coordinated activation of canonical and previously unrecognized thermogenic pathways. Molecular rejuvenation was further supported by architectural changes toward a youthful state, including reduced lipid droplet size and decreased cellular heterogeneity. Mitochondrial abundance and morphology remained unchanged, while collagen deposition increased. These results demonstrate that WAT biological age is partially reversible and identify molecular and cellular features underlying its rejuvenation.

  PublisherDOI

• Exercise training remodels inter-organ endocrine networks

  Molecular Metabolism · 2025-07-21 · 3 citations

  articleOpen access

  Exercise induces organism-wide molecular adaptations, partly mediated by humoral factors released in response to acute and chronic physical activity. However, the extent and specificity of endocrine effects from training-induced secreted factors remain unclear. Here, we applied systems genetics approaches to quantify inter-organ endocrine networks using multi-tissue transcriptomics and proteomics data collected from endurance-trained rats in The Molecular Transducers of Physical Activity Consortium (MoTrPAC). Eight weeks of endurance training significantly altered both the magnitude and specificity of endocrine effects across multiple origin-target tissue pairs. Subcutaneous white adipose tissue emerged as a key endocrine regulator impacted by training, while extracellular matrix-derived factors were identified as globally regulated secretory features in trained vs sedentary animals. Notably, secretory Wnt signaling factors were identified as key mediators of exercise-induced endocrine adaptations in multiple tissues. Our systems genetics framework provides an unprecedented atlas of inter-organ communication significantly remodeled by endurance exercise, serving as a valuable resource for novel exerkine discovery. • Exercise training remodels endocrine networks across 16 tissues, with subcutaneous white adipose tissue emerging as a key origin of secreted factors. • Systems genetics analysis using QENIE (Quantitative Endocrine Network Interaction Estimation) and GD-CAT (Gene-Derived Correlations Across Tissues) identifies secretory extracellular matrix proteins and Wnt signaling factors as central mediators of inter-organ communication induced by endurance training. • This study provides a multi-tissue atlas of exercise-induced endocrine interactions, serving as a resource for novel exerkine discovery and mechanistic investigation.

  PublisherDOI

• Sequentially Constrained Randomization in Preclinical Animal Studies

  Function · 2025-01-01

  articleOpen access

  Randomization is a key component to scientific inquiry as it facilitates unbiased estimation of treatment effects via balancing of measured and unmeasured prognostic variables across treatment groups. Recent reports have noted that randomization is lacking in animal studies, threatening internal validity. Animal studies often involve rodents (mice or rats) sent in small batches to laboratories or bred on site in litters. Randomizing half of each batch to treatment and half to control (simple randomization) is a viable strategy to implementing randomization in animal studies, however experimenters may be concerned about chance imbalances, given the smaller sample sizes utilized in animal studies, in key prognostic variables, eg, baseline weight. Constrained randomization, wherein key prognostic factors are balanced within each batch, may offer benefits over simple randomization, especially if it were sequential, ie, could take balance of previous batches into account when randomly assigning treatment in current batch. Adjusting for prognostic variables in a statistical model is a way to address imbalances, independent of choice of randomization scheme. In simulations designed to mimic realistic scenarios, all methods of randomization tested led to unbiased treatment effect estimation, with model adjustment reducing standard errors and improving statistical power in all scenarios. Treatment effects in unadjusted and adjusted models were nearly an order of magnitude closer to each other in sequentially constrained randomization compared to simple randomization, yielding more robust findings.

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• TRB3 Regulates Beige Fat Formation in Response to Exercise and Beta-adrenergic Receptor Agonist

  Physiology · 2025-05-01

  article

  Brown adipose tissue (BAT) and a recently identified brown-like adipocyte, beige fat, have been implicated as anti-obese and anti-diabetic tissues due to their ability to dissipate energy as heat by the expression of UCP1. Recent studies have demonstrated that BAT found in adult humans is composed of beige fat and that its activity is significantly increased in response to exercise training and β-adrenergic receptor (β-AR) agonist administration. However, the signaling molecules that regulate beige fat activity during exercise and β-AR activation have not yet been elucidated. TRB3 has been shown to regulate differentiation and metabolism in multiple tissues but the role of the protein in beige fat has not been studied. For this study we tested the hypothesis that TRB3 inhibits beige fat formation and activity, and that inhibition of TRB3 improves beige fat function. In order to examine the role of TRB3 on beige fat formation and function, we injected wild type mice with either saline or CL316,243, a β3-AR agonist, at 1 mg/kg daily for 6 days. TRB3 expression was significantly decreased in the inguinal fat from CL316,243 injected mice compared to saline injected mice by 63%, which was associated with increased UCP1 expression by 249%. We also trained wild type mice in the wheel cages for 8 weeks and found that TRB3 expression was significantly decreased in the inguinal fat from trained mice compared to controls by 42%, whereas UCP1 expression was increased by 84%. We next investigated if knockout of TRB3 promotes exercise training- and β3-AR-induced beige fat formation and found that inguinal fat UCP1 expression was further increased in TRB3KO mice compared to controls after 6 days of CL316,243 injection and 8 week exercise training by 215% and 311%, respectively. Consistent with these findings, TRB3KO mice were cold resistant (rectal temperature at 4°C for 2 hrs: 34.3°C ± 0.4 vs. 35.7°C ± 0.1). These data demonstrate that TRB3 regulates exercise- and β3-AR-induced beige fat formation and activity. 1R16GM149457-01A1 This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

  PublisherDOI

• A consensus guide to preclinical indirect calorimetry experiments

  Nature Metabolism · 2025-09-24 · 14 citations

  reviewOpen access
  PublisherOA PDFDOI

• Type 2 Diabetes and Obesity Alter Exercise Training-Induced Transcriptional Adaptations to Subcutaneous White Adipose Tissue

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-12

  preprintOpen accessSenior authorCorresponding

  Abstract White adipose tissue (WAT) dysfunction contributes to obesity-associated metabolic disease and type 2 diabetes (T2D). Rodent studies have demonstrated that exercise training improves WAT function, but molecular studies investigating exercise training effects on WAT in humans have been limited, particularly in the context of metabolic disease. Here, we defined the subcutaneous WAT (scWAT) transcriptome in middle-aged adults (10 male, 19 female) that were classified by lower BMI (<27 kg/m 2 ), higher BMI (≥27 kg/m 2 ), and T2D status before and after a 10-week endurance exercise regimen. At baseline, 624 genes were significantly upregulated and 112 genes downregulated in the scWAT from higher BMI participants compared to lower BMI. There was a spectrum of pathway dysregulation in scWAT in higher BMI individuals, ranging from increased markers of extracellular matrix (ECM) deposition and inflammation to decreased circadian rhythm gene expression. In people with T2D, there were additional transcriptomic differences such as translation-related pathways, selenoamino acid metabolism, and proteoglycans. Exercise training had robust effects on the transcriptome regardless of metabolic status, and notably, for the high BMI and T2D groups, training reversed several of the detrimental gene expression patterns in a cell-type-specific manner. These beneficial exercise-induced transcriptomic adaptations significantly correlated with lower levels of free fatty acids and blood pressure, particularly in participants with higher BMI and T2D. By integrating our exercise training-modulated genes with GWAS meta-analysis of physical activity, genes influenced by exercise training in the higher BMI group showed a significant enrichment in genetic associations of exercise traits in the population. A circadian rhythm-related transcription factor NR1D1 was enriched in enhancers linked with both the exercise differentially expressed genes (DEGs) and GWAS signals, suggesting a link between the circadian rhythm and training-induced adaptations. These findings demonstrate that obesity and T2D result in marked, progressive alterations in cell-type specific gene transcription in scWAT, while endurance exercise training reverses many of the metabolic disease-associated adaptations. Identification of novel molecular pathways regulated by exercise training can lead to therapeutic targets for obesity and metabolic disease.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01AR045670

  NIH · $5.1M · 2013

• Exercise Regulation of Glucose Homeostasis

  NIH · $7.3M · 2013–2028

• Training Grant in Diabetes and Metabolism

  NIH · $13.0M · 1977–2027

• NIH Grant R01DK112283

  NIH · $1.2M · 2020

• Administrative Core

  NIH · $20.3M · 1997–2027

Frequent coauthors

• Michael F. Hirshman

  Joslin Diabetes Center

  578 shared

• Nobuharu Fujii

  Tokyo Metropolitan University

  189 shared

• Nicolas Musi

  154 shared

• Roeland J.W. Middelbeek

  136 shared

• Kristin I. Stanford

  The Ohio State University

  117 shared

• Rong Tian

  University of Washington

  95 shared

• Kei Sakamoto

  University of Copenhagen

  94 shared

• Jørgen F. P. Wojtaszewski

  University of Copenhagen

  86 shared