About

Dr. Jaume Amengual is from Palma de Mallorca, Spain. He obtained his PhD in 2009 at the University of the Balearic Islands in Spain. Following his doctoral studies, he was a post-doctoral fellow at Case Western Reserve University from 2009 to 2013 and at New York University from 2013 to 2015. In 2016, he became a Research Assistant Professor at the School of Medicine at NYU, where he worked until 2017. In 2018, he joined the Department of Food Science and Human Nutrition at the University of Illinois Urbana-Champaign. His research focuses on food science and human nutrition, contributing to the understanding of lipid secretion and its role in health conditions such as atherosclerosis.

Research topics

• Biology
• Chemistry
• Biochemistry
• Medicine
• Immunology
• Endocrinology
• Internal medicine
• Food science
• Pharmacology
• Chromatography
• Cell biology

Selected publications

• From the Discovery of Essential Growth Factors to Modern Nutrition: 150 Years of Nutrition Science

  ACS Nutrition Science · 2026-05-04

  article1st authorCorresponding

  Over the past one hundred fifty years, nutritional science has evolved from the identification of essential nutrients responsible for classic deficiencies into a multidisciplinary field. Landmark discoveries in biochemical nutrition resulted in numerous Nobel laureates but also reshaped past and current global health policies and clinical practices. Despite these advances, fundamental aspects of nutrition remain dubious to the general public, even though the diet is a constant and unavoidable component of our daily life. In commemoration of the American Society of Chemistry’s 150th anniversary, this perspective reflects on the major conceptual advances that have shaped the nutrition science field over the past century and a half. It also explores the limitations of current paradigms and considers emerging directions that are likely to redefine how nutrition is studied and applied in the decades ahead.

  PublisherDOI

• From lipoprotein metabolism to blood clotting: Highlights of the 2025 Fredrickson lipid research conference

  Journal of Lipid Research · 2026-04-16

  articleOpen access

  The biannual Fredrickson Lipid Research conference took place in person in Milwaukee, Wisconsin, from September 3-5, 2025. Each conference highlights the most advanced basic and translational research in lipids and lipoprotein metabolism. As with each Fredrickson Lipid Research conference, the overall theme is focused on "Lipid Metabolism, Lipoproteins, and Atherosclerosis," and this year included a special scientific session exploring the connections between Blood Clotting and Lipid Metabolism. This session underscored ongoing research aimed at explaining the mechanisms by which dyslipidemia alters the coagulation system and drives thrombotic cardiovascular disease. Other scientific session themes at the conference included Biomarkers in Cardiovascular Diseases, Efferocytosis and Inflammation, Regulation of Lipoproteins, Adipocyte Plasticity in Cardiometabolic Diseases, and Novel Therapeutic Strategies for Atherosclerosis. From the six moderated scientific sessions, invited speakers provided summaries of their work to showcase their contributions to the lipid and lipoprotein metabolism fields. This review article aims to serve as a resource for readers to learn more about ongoing research in lipid and lipoprotein metabolism and to encourage future studies and collaborations that advance the field.

  PublisherDOI

• Hepatic SEC16B regulates lipid homeostasis by coordinating VLDL secretion and lipid droplet expansion

  Journal of Clinical Investigation · 2026-04-24

  articleOpen access

  The liver plays a critical role in lipid homeostasis, where lipids are either secreted as very-low-density lipoproteins (VLDL) or stored in lipid droplets (LDs). However, the regulatory mechanisms governing these two interconnected processes remain poorly understood. Here, we demonstrate that SEC16B functions as a lipid-responsive regulator in the liver, promoting VLDL secretion and LD expansion to handle lipid flux and maintain lipid homeostasis. Genome-wide association studies have identified single-nucleotide polymorphisms in SEC16B to be highly associated with serum lipid levels in humans. Hepatic Sec16b deficiency decreases serum lipid levels by impairing VLDL secretion through mechanisms that are at least partially independent of microsomal triglyceride transfer protein (MTP)-mediated ApoB lipidation and COPII-mediated intracellular trafficking. SEC16B partially localizes at ER-LD contact sites and promotes LD expansion by facilitating the targeting of ER proteins to LDs. More importantly, suppression of Sec16b dramatically lowers serum lipid levels and reduces atherosclerotic lesion size in Ldlr null mice. These data reveal a mechanism that coordinates VLDL and LD metabolism and suggest SEC16B as a potential therapeutic target for atherosclerosis treatment.

  PublisherDOI

• Introducing <i>ACS Nutrition Science</i> to the Growing ACS Family

  ACS Nutrition Science · 2026-01-20 · 1 citations

  article1st authorCorresponding
  PublisherDOI

• Exercise Training Induces a Hepatic Memory that Synchronizes the Lipid Delivery to Skeletal Muscle

  Physiology · 2026-05-01

  article

  Endurance exercise is a powerful non-pharmacological strategy to improve metabolic health, but how these benefits persist after training stops remains poorly defined. Emerging studies point to the establishment of a muscle memory of exercise that can enhance muscle growth. The liver is central coordinator of whole-body metabolism, and adaptative responses in exercised muscle depend on effective hepatic metabolic support. Nevertheless, whether an analogous memory exists in the liver has not yet been determined. Here, we tested how endurance training induces a persistent hepatic metabolic memory capable of protecting against the metabolic consequences of an obesogenic diet. Eight-week-old male mice were fed either a control diet (CD; 10% kcal from fat) or a high-fat diet (HFD; 45% kcal from fat) and assigned to sedentary (SED, static cages) or endurance training (voluntary wheel running; VWR). Mice underwent 4-week training (4wk), 4-week detraining (8wk), and 4-week retraining periods (12wk). Timed-exercise CD-fed controls were used to isolate the effects of prior training. Metabolic health, tissue morphology, and transcriptomics were assessed at each time point. In HFD-fed mice, endurance retraining robustly reduced adiposity, significantly improved HOMA-IR, enhanced hepatic gluconeogenic regulation, and suppressed hepatic lipid accumulation. Hepatic transcriptomic analysis revealed that endurance retraining strongly activated hepatic protein and lipid secretory pathways independently from diet. Transcription factor prediction and comparative analysis between endurance retrained and exercise-naïve controls identified the PPARα/RXR–BMAL1/CLOCK/NPAS2 axis as a main pathway associated with the memory. Among the hepatic memory targets, retraining prominently induced carboxylesterase (Ces) gene expression and release, assessed by plasma CES activity, and improved plasma lipid profiles by raising HDL-C and lowering total triglycerides and LDL-C. Using Ldlr-knockout mice, we show that CES proteins directly associate with circulating lipoproteins primarily LDL particles and is inversely correlated with LDL-C levels. Moreover, retraining markedly increased hepatic, plasma, and muscle phosphatidylcholine (PC/LPC) species, which are known circadian lipids that stimulate skeletal muscle fatty acid oxidation. This hepatic PPARα–circadian secretory axis might provide a link for the coordinated response required for the exercise memory that enhances systemic lipid and glucose homeostasis. Our findings point to endurance exercise as an important factor that imprints a hepatic metabolic memory, reactivated upon retraining to protect against diet-induced metabolic dysfunction. This abstract was presented at the American Physiology Summit 2026 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

• EcoHIV Infection Promotes Atherosclerosis Progression in LDLR-Deficient Mice

  Arteriosclerosis Thrombosis and Vascular Biology · 2025-09-04

  articleOpen accessSenior author

  BACKGROUND: People with HIV are at higher risk of atherosclerotic cardiovascular disease than uninfected individuals; however, the molecular mechanisms behind this association remain elusive due to the lack of suitable animal models. METHODS: To study the impact of HIV on atherosclerotic cardiovascular disease, we infected the atheroprone Ldlr −/− mice with the chimeric virus EcoHIV. RESULTS: In comparison to uninfected controls, EcoHIV infection increased the ratio of circulating inflammatory monocytes, monocyte recruitment, and CD68 + content in the atherosclerotic lesion. These changes occurred independently of alterations in plasma lipid profile or lesion size between groups. Lesions of EcoHIV-infected mice displayed greater vulnerability to rupture, as determined by increased necrotic core area and CD38 + content, and reduced presence of collagen compared with uninfected mice. Last, we report the presence of active viral replication of EcoHIV in the atherosclerotic lesion. CONCLUSIONS: Our data suggest that EcoHIV infection in Ldlr −/− mice resembles the pathogenesis of atherosclerotic cardiovascular disease in people with HIV. Our findings have therapeutic implications for people with HIV, a vulnerable population with an elevated risk of cardiovascular disease.

  PublisherOA PDFDOI

• Does sweet turn sour? How aspartame aggravates atherosclerosis in a preclinical model

  Cell Metabolism · 2025-05-01 · 1 citations

  letterSenior author
  PublisherDOI

• Recent advances in carotenoid absorption, distribution, and elimination

  Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · 2025-04-28 · 2 citations

  reviewOpen accessSenior author

  Carotenoids are a class of pigments with antioxidant properties synthesized by photosynthetic and heterotrophic organisms. Humans can store carotenoids in their intact form or cleave them enzymatically to apocarotenoids such as vitamin A, a hormone-like nutrient with crucial roles in gene expression and vision. Clinical and preclinical studies suggest that the consumption of diets rich in carotenoids attenuate cardiometabolic diseases, some types of cancer, neurodegenerative disorders, and inflammatory conditions. The bioactive properties of carotenoids depend, at least in part, on their accumulation in target tissues. However, the pathways that drive carotenoid absorption, delivery, and accumulation in tissues remain largely uncharacterized. This review provides a critical overview of the experimental models utilized to monitor carotenoid homeostasis in mammals. We also delve into recent findings concerning carotenoid intestinal uptake, bodily distribution, cellular uptake, and intracellular trafficking. Finally, we discuss the physiological relevance of a fecal carotenoid elimination pathway that operates independently of carotenoid enzymatic cleavage. Establishing the players governing carotenoid biodistribution and elimination is essential to maximize the bioactive properties of carotenoids in humans to prevent chronic diseases.

  PublisherDOI

• The Role of Extracellular Vesicles in Vitamin A Secretion in Macrophages

  Current Developments in Nutrition · 2025-05-01

  articleOpen access

  serve as a potential strategy to promote cardiovascular health.

  PublisherOA PDFDOI

• β-carotene accelerates the resolution of atherosclerosis in mice

  eLife · 2024-01-11

  preprintOpen accessSenior author

  Abstract β-carotene oxygenase 1 (BCO1) catalyzes the cleavage of β-carotene to form vitamin A. Besides its role in vision, vitamin A regulates the expression of genes involved in lipid metabolism and immune cell differentiation. BCO1 activity is associated with the reduction of plasma cholesterol in humans and mice, while dietary β-carotene reduces hepatic lipid secretion and delays atherosclerosis progression in various experimental models. Here we show that β-carotene also accelerates atherosclerosis resolution in two independent murine models, independently of changes in body weight gain or plasma lipid profile. Experiments in Bco1-/- mice implicate vitamin A production in the effects of β-carotene on atherosclerosis resolution. To explore the direct implication of dietary β-carotene on regulatory T cells (Tregs) differentiation, we utilized anti-CD25 monoclonal antibody infusions. Our data show that β-carotene favors Treg expansion in the plaque, and that the partial inhibition of Tregs mitigates the effect of β-carotene on atherosclerosis resolution. Our data highlight the potential of β-carotene and BCO1 activity in the resolution of atherosclerotic cardiovascular disease.

  PublisherOA PDFDOI

Frequent coauthors

• Edward A. Fisher

  New York University

  81 shared

• Ivan Pinos

  University of Illinois Urbana-Champaign

  57 shared

• Donald Molina

  University of Illinois Urbana-Champaign

  51 shared

• Patrick McQueen

  New York University

  50 shared

• Johana Coronel

  Columbia University

  50 shared

• M. Luisa Bonet

  Centro de Investigación Biomédica en Red

  49 shared

• Asma’a Albakri

  University of Jordan

  47 shared

• Amparo Blanco

  University of Illinois Urbana-Champaign

  46 shared

Labs

• Amengual LabPI