About

Jeremy Pettus is an Associate Professor of Medicine at UC San Diego. His research focuses on diabetes, particularly the management and treatment of Type 1 Diabetes, including the use of technology such as continuous glucose monitoring and insulin delivery systems. He has contributed to studies on severe hypoglycemia, impaired awareness of hypoglycemia, and the efficacy of various therapeutic interventions in diabetes care. His work involves clinical trials and translational research aimed at improving glycemic control and reducing complications associated with diabetes. Pettus's research also explores the pathophysiology of diabetes-related vascular and immune mechanisms, as well as the development of novel therapeutic strategies to address these issues.

Research topics

• Medicine
• Endocrinology
• Internal medicine
• Intensive care medicine
• Computer Science
• Psychiatry
• Family medicine
• Cardiology
• Biology
• Biochemistry
• Cell biology
• Radiology
• Urology
• Virology
• Surgery

Selected publications

• Persistent Burden of Severe Hypoglycemia and Impaired Awareness of Hypoglycemia Among People with Type 1 Diabetes Despite Technology Use: A Follow-up Survey

  2026-02-26

  articleSenior author

  <p dir="ltr">Objective: To assess longitudinal trends in glycemic metrics, prevalence of severe hypoglycemic events (SHEs), impaired awareness of hypoglycemia (IAH), and technology use (continuous glucose monitoring [CGM], automated insulin delivery [AID]) in a real-world US cohort of adults with type 1 diabetes.</p><p dir="ltr">Research Design and Methods: This was a cross-sectional study of adults with type 1 diabetes conducted ~2 years after participants enrolled in the original retrospective observational study. Participants self-reported technology use, insulin delivery method, HbA1c, IAH, and SHEs. Change was assessed among these variables from the initial and follow-up study.</p><p dir="ltr">Results: Approximately 2 years after the original survey, 1,056 adults responded to the follow-up survey and were eligible for analysis (53% response rate; mean [SD] age: 46 [16] years; mean [SD] type 1 diabetes duration: 29 [16] years; 71% female; 97% White). Most reported using CGMs in the original study (91.8%) and at follow-up (94.4%), while the use of AID increased 17.7%. In the original study, 61.7% reported HbA1c <7% versus 67.4% at follow-up. Proportions of individuals with IAH and SHEs remained high at ~30% and ~20%, respectively, in both studies.</p><p dir="ltr">Conclusions: Although most participants used CGM and the use of AID increased, approximately one-third of respondents did not achieve HbA1c targets, ~20% continued to have SHEs in the last year, and ~30% had IAH. This highlights that while CGM and AID systems are a significant advancement, their use alone has not mitigated the risk of severe hypoglycemia and glucose management still remains suboptimal.</p><p><br></p>

  PublisherDOI

• Persistent Burden of Severe Hypoglycemia and Impaired Awareness of Hypoglycemia Among People with Type 1 Diabetes Despite Technology Use: A Follow-up Survey

  2026-02-26

  articleSenior author

  <p dir="ltr">Objective: To assess longitudinal trends in glycemic metrics, prevalence of severe hypoglycemic events (SHEs), impaired awareness of hypoglycemia (IAH), and technology use (continuous glucose monitoring [CGM], automated insulin delivery [AID]) in a real-world US cohort of adults with type 1 diabetes.</p><p dir="ltr">Research Design and Methods: This was a cross-sectional study of adults with type 1 diabetes conducted ~2 years after participants enrolled in the original retrospective observational study. Participants self-reported technology use, insulin delivery method, HbA1c, IAH, and SHEs. Change was assessed among these variables from the initial and follow-up study.</p><p dir="ltr">Results: Approximately 2 years after the original survey, 1,056 adults responded to the follow-up survey and were eligible for analysis (53% response rate; mean [SD] age: 46 [16] years; mean [SD] type 1 diabetes duration: 29 [16] years; 71% female; 97% White). Most reported using CGMs in the original study (91.8%) and at follow-up (94.4%), while the use of AID increased 17.7%. In the original study, 61.7% reported HbA1c <7% versus 67.4% at follow-up. Proportions of individuals with IAH and SHEs remained high at ~30% and ~20%, respectively, in both studies.</p><p dir="ltr">Conclusions: Although most participants used CGM and the use of AID increased, approximately one-third of respondents did not achieve HbA1c targets, ~20% continued to have SHEs in the last year, and ~30% had IAH. This highlights that while CGM and AID systems are a significant advancement, their use alone has not mitigated the risk of severe hypoglycemia and glucose management still remains suboptimal.</p><p><br></p>

  PublisherDOI

• Disentangling the Effects of Chromosomal Versus Hormonal Sex on Insulin Resistance

  Metabolism · 2026-03-05

  article
  PublisherDOI

• Persistent Burden of Severe Hypoglycemia and Impaired Awareness of Hypoglycemia Among People With Type 1 Diabetes Despite Technology Use: A Follow-up Survey

  Diabetes Care · 2026-02-26 · 1 citations

  articleOpen accessSenior author

  OBJECTIVE: To assess longitudinal trends in glycemic metrics, prevalence of severe hypoglycemic events (SHEs), impaired awareness of hypoglycemia (IAH), and technology use (continuous glucose monitoring [CGM], automated insulin delivery [AID]) in a real-world U.S. cohort of adults with type 1 diabetes. RESEARCH DESIGN AND METHODS: This was a cross-sectional study of adults with type 1 diabetes conducted ∼2 years after participants enrolled in the original retrospective observational study. Participants self-reported technology use, insulin delivery method, glycated hemoglobin (HbA1c), IAH, and SHEs. Change was assessed among these variables from the initial and follow-up study. RESULTS: Approximately 2 years after the original survey, 1,056 adults responded to the follow-up survey and were eligible for analysis (53% response rate; mean [SD] age: 46 [16] years; mean [SD] type 1 diabetes duration: 29 [16] years; 71% female; 97% White). Most reported using CGM in the original study (91.8%) and at follow-up (94.4%), while the use of AID increased 17.7%. In the original study, 61.7% reported HbA1c <7% vs. 67.4% at follow-up. Proportions of individuals with IAH and SHEs remained high at ∼30% and ∼20%, respectively, in both studies. CONCLUSIONS: Although most participants used CGM and the use of AID increased, approximately one-third of respondents did not achieve HbA1c targets, ∼20% continued to have SHEs in the last year, and ∼30% had IAH. This highlights that while CGM and AID systems are a significant advancement, their use alone has not mitigated the risk of severe hypoglycemia, and glucose management still remains suboptimal.

  PublisherOA PDFDOI

• The Role of Incretins in Obstructive Sleep Apnea “ <scp>GLP1RAs</scp> and <scp>GLP1RA</scp> / <scp>GIPRAs</scp> in <scp>OSA</scp> ”

  Journal of Diabetes · 2025-11-01

  articleOpen access

  Mechanisms of action and effects of GLP-1 receptor agonists and dual GLP-1/GIP receptor agonists on multiple organ systems relevant to obstructive sleep apnea and cardiometabolic health. Obstructive Sleep Apnea (OSA) is a highly prevalent condition characterized by upper airway collapse during sleep, causing intermittent desaturations and arousals from sleep [1]. OSA affects nearly ~1 billion people worldwide [2] and is associated with hypertension, congestive heart failure, type 2 diabetes (T2DM), and cerebrovascular disease. Importantly, OSA affects up to 90% of patients with T2DM, and acts as a cumulative and synergistic risk factor for cardiovascular disease (CVD) [1-5]. Conventional treatments like continuous positive airway pressure (CPAP), oral appliances, and upper airway surgery are limited by patient adherence, variable treatment response and incomplete efficacy. Recently, pharmacotherapy has gained great interest, particularly regarding incretins which are gastrointestinal hormones crucial to metabolic regulation. Although incretins have been known for ~100 years, the emergence of glucagon-like peptide 1 receptor agonists (GLP1RA) and glucose-dependent insulinotropic polypeptide receptor agonists (GIPRA) has had a major impact. Tirzepatide, a dual GLP1RA/GIPRA, has proven effective in treating OSA and offers a promising addition to conventional therapies [6]. These pharmacotherapies may be especially beneficial in patients with T2DM, where metabolic and sleep-related risks converge. Practitioners must be aware of the high burden of OSA, and the importance of timely diagnosis and management. The relationship between OSA and T2DM is multifaceted. OSA may contribute to insulin resistance through counter-regulatory hormones released with repetitive apneas, though evidence that treatment of OSA improves glycemic control is inconclusive [7-10]. Diabetes, in turn, may contribute to OSA through its effects on the control of breathing and/or pharyngeal neuromuscular function [11]. However, the role of diabetes-related neuromyopathy in upper airway muscles remains uncertain. Chronic hyperglycemia can lead to autonomic and peripheral neuropathy, which may impair neural control of upper airway dilator muscles. The resulting reduction in muscle tone and delayed reflex activation during sleep increases pharyngeal collapsibility, offering a potential mechanistic link between diabetes and OSA. Clinical studies have demonstrated an association between diabetic autonomic neuropathy and greater OSA severity, supporting this relationship [12]. Beyond glycemic control, both OSA and T2DM independently increase CVD risk. Specifically, OSA impairs endothelial function, whereas T2DM affects vascular smooth muscle and microcirculation. These overlapping processes suggest that treating both conditions may be required to decrease vascular risk. While most data have focused on T2DM, OSA is also a concern in T1DM. Despite lower rates of obesity in T1DM compared to T2DM, these patients still demonstrate a high prevalence of OSA, with some cohorts reporting rates up to 46% even among those with a normal BMI [7-10, 13]. These findings suggest that weight alone does not account for the high OSA burden. As in T2DM, OSA in T1DM independently predicts vascular disease. Additionally, patients with T1DM may be particularly sensitive to counter-regulatory hormones due to their insulin deficiency and inability to compensate [7, 8, 13]. Although substantial data have shown improvement in both T2DM and body weight with GLP1RA, people with type 1 DM and T2DM were excluded from SURMOUNT-OSA [6]. Because patients with T2DM experience less weight loss with GLP1RAs than those without T2DM, they may also derive less improvement in OSA from dual agonists like tirzepatide. Nevertheless, given their elevated vascular risk, patients with both OSA and T2DM may still derive substantial benefit. Similar questions remain in T1DM, where OSA is also common despite lower obesity rates, but data on treatment effects are lacking. Until more definitive evidence is available, clinicians should remain aware of these associations, which may already be clinically actionable. Given the high prevalence and clinical impact of OSA in DM, systematic screening is warranted. Patients who are obese, have central adiposity, resistant hypertension, or excessive daytime sleepiness are at particularly high risk and should be prioritized for evaluation. Other high-yield groups include those with poor glycemic control despite adherence to therapy, recurrent nocturnal hypoxemia, or unexplained cardiovascular or microvascular complications. Traditional tools like the STOP-BANG questionnaire and Berlin Questionnaire can aid in risk stratification, but their specificity is limited in patients with obesity and DM. Therefore, a low threshold for formal sleep evaluation is appropriate. Hypoglossal nerve stimulation (HGNS) is an additional type of surgery, in which an implanted device stimulates the hypoglossal nerve to control the tongue and prevent airway collapse during sleep. It has been approved as a treatment for moderate–severe OSA in CPAP-intolerant patients. HGNS reduces AHI and improves daytime sleepiness, with the highest efficacy in patients with BMI < 32 kg/m2, and without complete concentric palatal collapse [15]. Randomized trials have been reported preliminarily but remain unpublished. Weight loss is a key therapeutic strategy for OSA with two patterns of benefit [14-16]. Some suggest a threshold effect, where there is a substantial reduction in AHI once weight loss reaches a certain threshold. A meta-analysis found that a 20% reduction in BMI corresponded to a ~57% decrease in AHI, with diminishing returns beyond that point. Others support a dose–response relationship, with one study reporting that each 1-pound drop in weight, decreased AHI by ~1%. When combined with CPAP, weight loss provides additional benefit to AHI reductions [14]. In the INTERAPNEA randomized trial [17], patients receiving CPAP plus an 8-week lifestyle and weight-loss program had AHI reductions of 51% at 8 weeks and 57% at 6 months, compared with 27% and 30% in the CPAP-only group. This combined approach also yielded greater improvements in systolic blood pressure, body composition, and insulin resistance. Similarly, Chirinos [15] demonstrated that addressing both OSA and obesity together was more effective for reducing cardiometabolic risk than treating either condition alone. Weight loss in patients with OSA can be achieved through lifestyle modification, bariatric surgery, and pharmacotherapy. Lifestyle interventions are often first-line and consistently improve AHI and cardiometabolic health [15, 17-19], though long-term weight loss and adherence to modifications are often limited. Bariatric surgery (e.g., gastric bypass, sleeve gastrectomy, etc.) leads to greater and more durable weight loss than lifestyle interventions alone, with improvements in AHI, daytime sleepiness, and cardiometabolic outcomes [15, 17, 18, 20, 21]. However, up to 45% of patients have residual OSA despite weight loss, and others may experience weight regain or fat redistribution that contributes to recurrence [18]. Residual disease is more likely in those with older age, high preoperative BMI or AHI, or non-obesity factors. Glucagon-like peptide-1 receptor agonist (GLP1RA) and GLP-1/glucose-dependent insulinotropic polypeptide (GIP) receptor agonists are promising therapies for OSA, largely through their effects on weight loss and metabolism [6, 20-23]. GLP1RAs act centrally to reduce appetite through hypothalamic pathways and by dampening hedonic responses to food cues, leading to reduced intake and sustained weight loss. Dual agonists add GIP receptor activity, enhancing insulin secretion, improving adipocyte function, and increasing energy expenditure. Preclinical and clinical studies suggest that dual agonism produces greater reductions in food intake and body weight than GLP1RAs alone. In addition to these metabolic effects, dual agonists likely improve OSA through several mechanisms. As illustrated in Figure 1, their impact on glycemic control, insulin sensitivity, autonomic regulation, and central nervous system activity likely contribute to their observed benefits in OSA. GLP1RAs such as semaglutide and dual agonists such as tirzepatide consistently produce substantial weight loss, a key driver of OSA improvement. In the STEP trials, semaglutide achieved sustained weight reductions [20], while the SURMOUNT trials showed even greater effects with tirzepatide (15%–22.5% weight loss), superior to semaglutide in head-to-head comparison (20.2% vs. 13.7% at 72 weeks) [21]. Both agents also improved cardiometabolic health, including blood pressure, lipids, and glucose regulation, with tirzepatide generally yielding greater benefits [6, 20, 21]. These findings highlight the potential of incretin-based therapies as disease-modifying treatments for OSA by targeting obesity and metabolic dysfunction. In addition to the impact on weight loss and cardiometabolic outcomes, GLP1RA and dual agonists have shown efficacy in OSA. In the SCALE Sleep Apnea trial, adults with obesity and moderate to severe OSA who were unable to use CPAP received either liraglutide or placebo for OSA. Liraglutide led to a significant reduction in AHI, as well as increased weight loss over 32 weeks [22]. Building on this evidence, the SURMOUNT-OSA trials included two parallel phase 3 randomized controlled trials evaluating tirzepatide in adults with obesity and moderate-to-severe OSA. SURMOUNT-OSA trial 1 enrolled participants not using CPAP, whereas SURMOUNT-OSA trial 2 enrolled participants adherent to CPAP. Across both trials (n = 469), participants were randomized to the maximally tolerated dose of tirzepatide (10 or 15 mg) subcutaneously or placebo for 52 weeks. In both trials, tirzepatide significantly reduced AHI (by ~25–30/h), and led to substantial weight loss (~18%–20%), with improvements in systolic blood pressure, sleep apnea specific hypoxic burden, inflammatory markers, and patient-reported daytime and nighttime sleep outcomes [6]. The SURMOUNT-OSA trials demonstrated important benefits of tirzepatide for OSA with obesity, but several limitations affect generalizability. Participants were limited to individuals with obesity (BMI ≥ 30 kg/m2) and moderate-to-severe OSA, excluding those with mild OSA (AHI 5–15/h), T2DM, or lower BMI ranges. The follow-up period was 52 weeks, restricting conclusions about the long-term durability of AHI reductions, long-term effects on cardiovascular outcomes, and sustainability of weight loss. Data indicate that discontinuation of tirzepatide leads to significant weight regain, suggesting that its use for OSA may require prolonged or indefinite therapy [23]. However, the long-term safety profile of tirzepatide with extended use remains unknown, and potential long-term adverse effects warrant further investigation. Finally, SURMOUNT-OSA did not compare active treatments e.g., tirzepatide vs. CPAP, limiting insights into comparative effectiveness. Future studies should evaluate whether combining tirzepatide with PAP therapy yields additive benefits. Nevertheless, SURMOUNT-OSA provides the first high-quality evidence that pharmacologic therapy can meaningfully reduce OSA severity, opening the door to new disease-modifying strategies. These findings highlight the potential of incretin-based therapies to complement or extend beyond conventional approaches, particularly for patients with obesity-related OSA who struggle with CPAP. Given the strong association between T2DM and OSA, future studies are clearly needed to define the role of these agents in patients with T2DM, where the potential benefits for both metabolic and sleep outcomes may be greatest. Future research should aim to address several issues. Long-term randomized controlled trials are needed to evaluate whether tirzepatide-induced improvements in OSA are widely generalizable and translate into reductions in validated cardiovascular outcomes and durable AHI improvements beyond 1 year. Comparative effectiveness trials directly assessing tirzepatide, CPAP, and combination therapy could define optimal treatment strategies. Mechanistic studies integrating imaging, upper airway physiology, and biomarker assessments may help elucidate causal pathways. Given concerns about sarcopenia, future studies could address methods to limit loss of skeletal muscle using resistance exercise, altering protein intake, androgen modulators and/or medications such as bimagrumab. GLP1RAs and dual receptor agonists represent a highly promising approach to OSA management, addressing both the underlying metabolic drivers of the disease and upper airway obstruction. Evidence demonstrates that pharmacologic weight loss can lead to clinically meaningful reductions in AHI and improved patient-reported outcomes. All authors contributed significantly to this work in accordance with the guidelines of the International Committee of Medical Journal Editors (ICMJE). Ana Lucia Fuentes: conceptualization, literature review, drafting of the manuscript, and critical revision for intellectual content. Gurleen Dhami: literature review, data organization, and drafting of manuscript sections. Jeremy Pettus: conceptualization, subject-matter expertise in incretin-based therapies, and critical revision of the manuscript. Praveen Akuthota: conceptualization and critical revision of the manuscript. Atul Malhotra: conceptualization, supervision, subject-matter expertise in sleep and OSA, critical revision of the manuscript, and overall project oversight. The authors declare no conflicts of interest. Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.

  PublisherOA PDFDOI

• Authors' Reply: Acetazolamide and Renal Hemodynamics: Interplay between Tubuloglomerular Feedback and Renin-Angiotensin-Aldosterone System Adaptation

  Journal of the American Society of Nephrology · 2025-05-12

  article

  We thank Drs. Ito and Mori for their thoughtful letter1 regarding our recent JASN manuscript “Acetazolamide Therapy and Kidney Function in Persons with Nonalbuminuric Diabetes Mellitus Type 1,” considering the potential consequences of longer-term use of acetazolamide for kidney protection.2 We believe that the pathways described are elegant, important, and worthy of investigation. We were careful to highlight that this study was very short term, reflecting kidney changes over 2 weeks, and that longer-term studies are needed to address many of the cautions raised by Drs. Ito and Mori. We highlight that effects (and then blunting) of natriuresis and activation for the renin-angiotensin-aldosterone system would seem to also be at play for sodium-glucose cotransporters, and yet these medications have profound kidney benefits above and beyond use of renin-angiotensin-aldosterone system inhibitors.3 We are also familiar with the basic evidence that induction of ammonia production due to acidosis may enhance complement activation and might theoretically contribute to kidney injury over the long term. However, driven primarily by this hypothesis, multiple randomized trials have tested whether delivery of sodium bicarbonate may provide kidney protection. The results of these studies have been conflicting, without clear benefit.4,5 Overall, we are at an early stage with regard to using acetazolamide for an indication to preserve kidney function. These and other exciting and important hypotheses require detailed investigation in future work.

  PublisherDOI

• A vascular-associated fibroblastic cell controls pancreatic islet immunity

  Cell Reports · 2025-08-29

  articleOpen access

  The immune protection of pancreatic β cells has three layers: anatomical, with their distribution in 1 million islets; central, with the thymic deletion of β cell-specific T cells; and peripheral, with inhibitory cellular networks. The failure of the latter leads to most spontaneous type 1 diabetes and all diabetes induced by checkpoint inhibitor therapy. Because CD4 T cells initiate disease, major histocompatibility complex (MHC) class II-expressing cells are central to the onset. In non-diabetic mouse and human islets, two such cells were detected outside of the islet boundaries near the efferent post-capillary venules: one related to the vasculature and a fibroblast referred to as a "vascular-associated fibroblast" (VAF). Functionally, primary VAFs spontaneously presented islet antigens to CD4 T cells and expressed high levels of inhibitory B7 receptors and no costimulatory receptors. VAFs induced anergy in primary pre-activated anti-islet CD4 T cells. VAFs are likely important to protect the endocrine pancreas from autoimmunity.

  PublisherDOI

• Reflecting on a Year at the Helm of Diabetes Care.

  UNC Libraries · 2025-01-17

  articleOpen access

  A year has passed since we were given the responsibility of leading Diabetes Care. In 2023, perhaps the most momentous highlight for all of us from a health perspective has been the sense that we are on the better side of recovery from the coronavirus disease 2019 (COVID-19) pandemic.

  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

  articleSenior author

  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 &amp;lt; 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 &amp;lt; 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

• UTE MRI technical developments and applications in osteoporosis: a review

  Frontiers in Endocrinology · 2025-02-06 · 7 citations

  reviewOpen access

  Osteoporosis (OP) is a metabolic bone disease that affects more than 10 million people in the USA and leads to over two million fractures every year. The disease results in serious long-term disability and death in a large number of patients. Bone mineral density (BMD) measurement is the current standard in assessing fracture risk; however, the majority of fractures cannot be explained by BMD alone. Bone is a composite material of mineral, organic matrix, and water. While bone mineral provides stiffness and strength, collagen provides ductility and the ability to absorb energy before fracturing, and water provides viscoelasticity and poroelasticity. These bone components are arranged in a complex hierarchical structure. Both material composition and physical structure contribute to the unique strength of bone. The contribution of mineral to bone's mechanical properties has dominated scientific thinking for decades, partly because collagen and water are inaccessible using X-ray based techniques. Accurate evaluation of bone requires information about its components (mineral, collagen, water) and structure (cortical porosity, trabecular microstructure), which are all important in maintaining the mechanical integrity of bone. Magnetic resonance imaging (MRI) is routinely used to diagnose soft tissue diseases, but bone is "invisible" with clinical MRI due to its short transverse relaxation time. This review article discusses using ultrashort echo time (UTE) sequences to evaluate bone composition and structure. Both morphological and quantitative UTE MRI techniques are introduced. Their applications in osteoporosis are also briefly discussed. These UTE-MRI advancements hold great potential for improving the diagnosis and management of osteoporosis and other metabolic bone diseases by providing a more comprehensive assessment of bone quantity and quality.

  PublisherDOI

Frequent coauthors

• E. Diaz

  Medical University of South Carolina

  257 shared

• M. Mullen

  242 shared

• Robin Goland

  University of Michigan–Ann Arbor

  180 shared

• Jamie Diner

  172 shared

• Naji Younes

  Milken Institute

  172 shared

• Robert R. Henry

  Medical University of South Carolina

  149 shared

• Melissa Lee

  Otterbein University

  146 shared

• Mary Ann Banerji

  143 shared

Education

• Ph.D., Molecular and Computational Biology

  University of California, San Diego

  2005

• M.S., Molecular and Computational Biology

  University of California, San Diego

  2001

• B.S., Biology

  University of California, San Diego

  1998