bims-mimead Biomed News
on Adipose tissue and metabolic disease
Issue of 2026–06–14
eleven papers selected by
Rachel M. Handy, University of Guelph and Universiteit Mastricht
  1. Chronic viral infection aggravates white adipose tissue dysfunction and liver pathology in obesity.
  2. Semaglutide-induced loss of skeletal muscle mass is blunted by co-administration of ketone esters.
  3. IL-6 Activity is Required for Maximal Catecholamine Release During High-Intensity Exercise in Men.
  4. 17β-estradiol mitigates ovariectomy-induced defects in mitochondrial bioenergetics and redox balance after VML injury in female mice.
  5. Effect of an acute prolonged overnight fast on skeletal muscle insulin and anabolic sensitivity in healthy men.
  6. A subphenotype of obesity with reduced enteroendocrine GLP-1 synthesis and enhanced tirzepatide response.
  7. Cell-type-specific proximity labeling of organ secretomes reveals energy balance-dependent proteomic remodeling.
  8. High Basal Skeletal Muscle Glucose Uptake in Normoglycemic and Hyperinsulinemic Overweight Men is Coupled With an Increase in the Alanine-Glucose Cycling.
  9. Endurance exercise elicits temporal and sexual dimorphic multi-omics remodeling of liver metabolism revealed by MoTrPAC.
  10. Feasibility, reproducibility, and cold-induced energy expenditure using whole-room calorimetry in adults and children.
  11. Exercise Snacks in Adults Living With Obesity: Protocol for a Randomized Feasibility Trial.
  1. Mol Metab. 2026 Jun 09. pii: S2212-8778(26)00078-5. [Epub ahead of print] 102394
    Chronic viral infection aggravates white adipose tissue dysfunction and liver pathology in obesity.
    Katarzyna M Luda, Marianne Agerholm, Si Brask Sonne, Dipsikha Biswas, Lisa DeCamp, Russell G Jones, Allan Randrup Thomsen, Benjamin Anderschou Holbeck Jensen, Jan Pravsgaard Christensen, Kei Sakamoto.
      White adipose tissue (WAT) plays a central role in maintaining systemic metabolic homeostasis by buffering lipid flux throughout the body. Impairment of this lipid-buffering capacity is a hallmark of obesity and has also been observed during chronic viral infection. Such dysfunction is closely associated with ectopic fat accumulation, particularly in the liver. We hypothesized that the coexistence of obesity and chronic viral infection exacerbates WAT dysfunction, thereby promoting liver pathology. However, the specific response of obese WAT to chronic viral infection - and its downstream impact on liver health - remains to be explored. To investigate this interaction, we employed a model of chronic viral infection in mice using lymphocytic choriomeningitis virus (LCMV) clone 13. In obese hosts, chronic infection caused sustained WAT depletion and progressive weight loss, accompanied by a reduction of Tim-4+ eWAT-resident macrophages and features reminiscent of lipodystrophy and aggravated metabolic dysfunction-associated steatotic liver disease (MASLD). Depletion of CD8+ T cells, the key mediators of LCMV-driven weight loss in lean mice, only modestly attenuated weight loss and did not ameliorate liver pathology in obese mice. Likewise, therapeutic interventions including TNF-α blockade and glycemic control with metformin did not reverse infection-induced weight loss; moreover, TNF-α blockade failed to improve liver pathology. Collectively, these findings reveal a previously unrecognized crosstalk between WAT and the liver in infection-driven MASLD, highlight distinct responses in WAT of obese mice compared to their lean counterpart, and underscore the increased susceptibility to virus-induced metabolic complications in obesity.
    Keywords:  MASLD; Obesity; adipose–liver crosstalk; viral infection; white adipose tissue (WAT)
    DOI:  https://doi.org/10.1016/j.molmet.2026.102394
  2. JCI Insight. 2026 Jun 09. pii: e201810. [Epub ahead of print]
    Semaglutide-induced loss of skeletal muscle mass is blunted by co-administration of ketone esters.
    Yasser Abuetabh, Mya A Schmidt, Masaaki Naganuma, Ramana Vaka, Mahmoud A El-Ghiaty, Shelly Braun, Ethan A Kwan, Matthieu Cp Zolondek, Darius Sahid, Laibah Khan, Rajat K Shandal, Ashley L Trudeau, Yaning Li, Sufyan O Malik, Qiuyu Sun, Danica K Roth, Daniela Y Morales-Llamas, Jody L Levasseur, Mourad Ferdaoussi, Richard P Fahlman, Jason Rb Dyck.
      While glucagon-like peptide-1 receptor agonists (GLP-1RAs) like semaglutide are effective in treating obesity, up to 45% of the resulting weight loss can be attributed to skeletal muscle loss. Given the critical role of skeletal muscle in health and mobility, this may have long-term adverse consequences. Herein we investigated whether oral ketone ester supplementation could prevent semaglutide-induced muscle loss and explored the underlying molecular mechanisms. Obese, glucose-intolerant mice received vehicle, semaglutide, or semaglutide plus a β-hydroxybutyrate-generating ketone ester for three weeks. Body composition, muscle strength, and endurance were assessed longitudinally. Semaglutide monotherapy reduced lean mass, impaired muscle strength, and suppressed mitochondrial gene expression while elevating atrophy-related genes in skeletal muscle samples. Co-administration with ketone ester preserved skeletal muscle mass and function without compromising fat loss. Mechanistically, ketone ester co-treatment prevented semaglutide-induced changes in mitochondrial and atrophy-related gene expression, suggesting mitochondrial defects and impaired ketone metabolism contribute to GLP-1RA-induced muscle loss. Together, these findings demonstrate that ketone ester supplementation can maintain muscle mass and performance during semaglutide-driven weight loss. These preclinical findings support ketone therapy as a promising strategy to counteract the sarcopenia-promoting effects of GLP-1RAs and warrant clinical evaluation to assess its translational potential.
    Keywords:  Metabolism; Muscle biology; Obesity
    DOI:  https://doi.org/10.1172/jci.insight.201810
  3. Mol Metab. 2026 Jun 10. pii: S2212-8778(26)00079-7. [Epub ahead of print] 102395
    IL-6 Activity is Required for Maximal Catecholamine Release During High-Intensity Exercise in Men.
    Andreas K Ziegler, Tim Schauer, Sara F Myrup, Gerrit van Hall, Bente K Pedersen, Jesper F Christensen, Helga Ellingsgaard.
      High-intensity exercise triggers a coordinated activation of metabolic, endocrine, and immune pathways, yet the mechanisms integrating these responses remain incompletely understood. Interleukin-6 (IL-6), released during exercise, has been proposed as a systemic signal linking skeletal muscle activity to whole-body stress responses. We tested whether exercise-induced IL-6 is required for full sympathoadrenal activation and immune cell mobilization during intense exercise in humans. Healthy young men received the IL-6 receptor (IL-6R) antibody tocilizumab prior to high-intensity interval exercise. IL-6R blockade reduced circulating epinephrine by ∼50%, lowered plasma glucose levels, and attenuated lactate accumulation, resulting in a smaller decline in blood pH. Immune cell mobilization was selectively impaired, with reduced recruitment of lymphocytes, CD8+ T cells, CD56ˆbright natural killer (NK) cells, monocytes, neutrophils, and dendritic cells, while CD4+ T cells, CD56ˆdim NK cells, and B cells were unaffected. Although upstream hypothalamic-pituitary-adrenal (HPA)-axis hormones corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) were unchanged, adrenocorticotropic hormone (ACTH) was significantly reduced and associated with pH and catecholamine responses in the control condition. A lower lactate-to-pyruvate ratio during IL-6R blockade suggests enhanced pyruvate oxidation as a potential upstream mechanism. These findings position IL-6 as an integrative metabolic signal that mediates organ crosstalk and amplifies the HPA and sympathoadrenal response during high-intensity exercise. By linking skeletal muscle metabolic stress to endocrine activation, glucose regulation, and immune cell mobilization, IL-6 appears to coordinate the complex systemic fight-or-flight response to intense physical exertion.
    Keywords:  Epinephrine; Exercise; Glucose; Immune System; Interleukin-6; Tocilizumab
    DOI:  https://doi.org/10.1016/j.molmet.2026.102395
  4. Am J Physiol Cell Physiol. 2026 Jun 11.
    17β-estradiol mitigates ovariectomy-induced defects in mitochondrial bioenergetics and redox balance after VML injury in female mice.
    Junwon Heo, David L Miller, Jessica R Hoffman, Reese M Groover, Sarah M Greising, Jarrod A Call.
      Volumetric muscle loss (VML) is characterized by an irrecoverable loss of skeletal muscle mass, persistent functional deficits, and metabolic dysfunction. A disrupted cellular redox homeostasis is one attribute of this metabolic dysfunction and can lead to excessive reactive oxygen species (ROS) emissions and chronic oxidative stress. The primary objective of this study was to define the role of ovarian hormones, specifically 17β-estradiol (17β-E2), in driving mitochondrial bioenergetic and redox balance after VML injury. Female C57BL/6J mice were randomized into experimental and control groups (VML-sham OVX, VML-OVX, and VML-OVX-E2). A time course of ROS emissions and antioxidant buffering capacity (AoxBC) for VML-injured muscles was established across the first 60 days post-injury (dpi) in ovary-intact females. Ovariectomy (OVX) was performed prior to injury to deplete ovarian hormones, and 17β-E2 was administered via continuous-release pellets to investigate the effects of hormone loss and repletion on ROS emissions and mitochondrial bioenergetics. The long-term effects of 17β-E2 were evaluated to determine whether restoring redox led to sustained redox balance long-term. Transcriptomic analyses were conducted to explore molecular mechanisms of 17β-E2 benefit after VML. In intact females, ROS emissions were greater during the first 14-dpi, but AoxBC recovered more rapidly than previously observed in males. OVX exacerbated VML-induced metabolic dysfunction, resulting in less AoxBC, greater ROS emissions, and an early suppression of mitochondrial gene networks. 17β-E2 repletion attenuated ROS emissions and improved AoxBC at 7-dpi, and led to greater mitochondrial respiratory capacity, conductance, and bioenergetic efficiency out to 60-dpi. Chronic 17β-E2 depletion resulted in impaired glucose tolerance and greater adiposity, which were mitigated by 17β-E2 treatment. Transcriptomic analyses suggest that 17β-E2 contributes to resolving inflammation and enforcing a temporal decoupling of cellular expansion and mitochondrial maturation after VML injury.
    Keywords:  Estrogen Receptors; Metabolic Flexibility; Muscle Trauma; Regenerative Medicine; Sex as a Biological Variable (SABV)
    DOI:  https://doi.org/10.1152/ajpcell.00282.2026
  5. J Nutr. 2026 Jun 07. pii: S0022-3166(26)00309-3. [Epub ahead of print] 101660
    Effect of an acute prolonged overnight fast on skeletal muscle insulin and anabolic sensitivity in healthy men.
    Joanne E Mallinson, Mia Keeton, Aline Nixon, Abhishek Sheth, Robert Jones, Pardeep Pabla, Joan M G Senden, Luc J C van Loon, Kostas Tsintzas.
       BACKGROUND: Repeated prolonged overnight fasting enhances anabolic sensitivity and preserves myofibrillar protein synthesis. Whether a single fasting episode can enhance dietary protein-derived amino acid incorporation into skeletal muscle protein remains unclear.
    OBJECTIVE: To investigate the effect of a single 16-hour versus 10-hour overnight fast on postprandial insulin and anabolic sensitivity in humans.
    METHODS: Randomized, cross-over study. On 2 occasions, healthy participants (n=9; age 22.6±3.5 y; BMI 24.0±2.5 kg·m-2; HOMA-IR 1.00±0.54) ingested a liquid meal, which consisted of specifically produced, intrinsically [1-13C]phenylalanine labelled milk protein (0.35 g·kg-1 body mass, bm) and dextrose (0.8 g·kg-1 bm), dissolved in 6 mL·kg-1 bm water, after either a 10-hour (Control) or 16-hour (Long OF) overnight fast. Skeletal muscle and blood samples were obtained before, during, and 3 hours after meal ingestion.
    RESULTS: Postprandial incorporation of dietary protein-derived [1-13C]phenylalanine into myofibrillar protein did not differ between Control and Long OF (0.018±0.005 vs. 0.022±0.005 Mole Percent Excess (MPE), ds=0.22, P=0.56). Forearm branched amino acid uptake iAUC [Δ (95% CI) 103 (-1618 to 1823) μmol.min-1.180min, ds=0.05, P=0.892] and glucose uptake [Δ (95% CI) 24.7 (to -25.3 to 74.8) μmol.min-1, η2p=0.16, P=0.280] also did not differ between treatments, but the postprandial serum insulin response [Δ (95% CI) -7.4 (-14.4 to -0.4) mIU.L-1, η2p=0.42, P=0.042] was lower in Long OF.
    CONCLUSIONS: A single prolonged overnight fast does not enhance postprandial skeletal muscle insulin sensitivity or dietary protein-derived amino acid incorporation into skeletal muscle protein in healthy, young adults. Whether susceptible populations such as older, insulin resistant individuals, may benefit from a more prolonged overnight fast warrants investigation.
    CLINICAL TRIAL REGISTRY NUMBER: ClinicalTrials.gov Identifier NCT05420181 URL OF REGISTRATION: https://clinicaltrials.gov/study/NCT05420181?term=overnight%20fasting%0AKostas%20Tsintzas&rank=1.
    Keywords:  anabolic sensitivity; fasting; insulin sensitivity; protein metabolism; skeletal muscle
    DOI:  https://doi.org/10.1016/j.tjnut.2026.101660
  6. Gastroenterology. 2026 Jun 05. pii: S0016-5085(26)06942-8. [Epub ahead of print]
    A subphenotype of obesity with reduced enteroendocrine GLP-1 synthesis and enhanced tirzepatide response.
    Alexander L Ticho, Alison N McRae, Lizeth Cifuentes, Thomas Fredrick, Diego Anazco, Maria A Espinosa, Juan M Garcia Cordova, Michael Romanos, Jose Villamarin, Stephen Johnson, Ryan Lennon, Maria D Hurtado Andrade, Jun Chen, Michael Camilleri, Andres J Acosta.
       BACKGROUND & AIMS: Obesity is a heterogeneous disease characterized by different pathophysiological and behavioral traits that influence response to GLP-1-based therapies. We previously identified an obesity phenotype characterized by fast gastric emptying and increased postprandial hunger. We aimed to elucidate pathophysiologic mechanisms in this phenotype by evaluating plasma enteroendocrine hormones and mucosal gene expression, and to evaluate treatment response to tirzepatide across subphenotypes.
    METHODS: 483 adults with obesity underwent solid meal gastric emptying (SGE) by scintigraphy, postprandial appetite assessment using visual analog scale (VAS), and plasma enteroendocrine hormone profiling. Gaussian mixed modeling identified phenotypic clusters. Associations with plasma short-chain fatty acids (SCFAs) and fecal metagenomics were explored. A separate cohort (n=31) underwent colonic mucosal biopsies with quantification of GCG (GLP-1) and PYY mRNA. Retrospective evaluation of weight loss in participants treated with tirzepatide among each cluster was performed (n=61).
    RESULTS: Three clusters were identified based on SGE and GLP-1. One cluster demonstrated fast SGE, increased postprandial hunger, and discordantly low postprandial GLP-1 (termed dc-GE/GLP-1; n=130, 26.9%), as well as lower plasma PYY and CCK. dc-GE/GLP-1 showed higher plasma SCFA levels, without significant differences in fecal microbial composition. Compared with concordant clusters (c-GE/GLP-1; n=353, 73.1%), dc-GE/GLP-1 had decreased mucosal mRNA expression of GCG (GLP-1) and PYY. At 6-months of tirzepatide, dc-GE/GLP-1 was associated with greater weight loss compared with c-GE/GLP-1 (21.5% vs 11.7%).
    CONCLUSIONS: We identified a subphenotype of obesity with fast gastric emptying and discordantly low GLP-1 plasma levels, reduced mucosal hormone synthesis, and enhanced weight loss to tirzepatide. Further studies are needed to identify mechanisms contributing to GLP-1 deficiency in this subphenotype of obesity.
    Keywords:  appetite regulation; enteroendocrine cells; gastric emptying; precision medicine
    DOI:  https://doi.org/10.1053/j.gastro.2026.05.019
  7. Cell Rep. 2026 Jun 11. pii: S2211-1247(26)00585-1. [Epub ahead of print]45(6): 117507
    Cell-type-specific proximity labeling of organ secretomes reveals energy balance-dependent proteomic remodeling.
    Kaja Plucińska, Charlotte R Wayne, Henry Sanford, Boby Mathew, Nathalie Ropek, Stephanie M Adaniya, Corey Model, Nicolás Gómez-Banoy, Ksenia Morozova, Xiongwen Cao, Jeffrey M Friedman, Ken H Loh, Paul Cohen, Ekaterina V Vinogradova.
      Intercellular communication is critical for maintaining organismal metabolic homeostasis. Here, we develop a method enabling temporally controlled, cell-type-specific labeling of secreted and membrane proteins in key metabolic tissues. The method employs a genetically encoded proximity-labeling strategy by targeting a Cre-dependent TurboID ligase to the endoplasmic reticulum (ER) in ES cell-derived mice. The expression of TurboID in hepatocytes, adipocytes, and B lymphocytes enabled the characterization of cell type-specific ER proteomes at baseline and in response to fasting, inflammation, and dietary obesity, revealing tissue- and perturbation-specific changes and augmenting our understanding of how the proteomes of individual tissues change to regulate systemic energy balance. This comprehensive resource represents an important advance toward understanding both how cell-to-cell communication changes in response to energy balance and how it contributes to these alterations. This method is broadly applicable and provides a means for identifying biomarkers and therapeutic targets across a wide range of tissues.
    Keywords:  CP: metabolism; ER proteomics; TurboID; inflammation; obesity; plasma proteomics; proximity labeling
    DOI:  https://doi.org/10.1016/j.celrep.2026.117507
  8. Diabetes. 2026 Jun 11. pii: db250860. [Epub ahead of print]
    High Basal Skeletal Muscle Glucose Uptake in Normoglycemic and Hyperinsulinemic Overweight Men is Coupled With an Increase in the Alanine-Glucose Cycling.
    Laura Hjort Blicher, Leanne Hodson, Kieran Smith, Bjørn Hald, Birgitte Andersen, Fredrik Karpe.
       ARTICLE HIGHLIGHTS: This study investigated glucose metabolism in the forearm during fasting and postprandial states, comparing overweight men with lean men. We sought to understand how glucose is metabolized to prevent hyperglycemia in insulin-resistant obese men and the implications of increased basal glucose uptake in this population. Our findings reveal that overweight men exhibit elevated basal glucose uptake in the face of increased insulin concentrations and, unlike lean men, very limited basal lactate output. The overweight group demonstrated increased alanine release, suggesting a pathway toward enhanced hepatic gluconeogenesis.
    DOI:  https://doi.org/10.2337/db25-0860
  9. Cell Rep. 2026 Jun 08. pii: S2211-1247(26)00494-8. [Epub ahead of print]45(6): 117416
    Endurance exercise elicits temporal and sexual dimorphic multi-omics remodeling of liver metabolism revealed by MoTrPAC.
    MoTrPAC study group
      The mechanisms by which exercise modulates liver metabolism are poorly understood. Leveraging data from molecular transducers of physical activity consortium (MoTrPAC), we analyzed liver adaptations across 1, 2, 4, and 8 weeks of exercise in male and female rats using multi-omics approaches. Female livers displayed a progressive increase in oxidative phosphorylation (OXPHOS) protein complexes, while male livers showed an increased acetylation of OXPHOS, tricarboxylic acid cycle, and fatty acid oxidation enzymes. Mechanistic examination revealed that these sex-specific acetylation events are partially mediated by carnitine acetyltransferase. Exercise enhanced liver cholesterol and bile acid synthesis, reducing liver lipid metabolites in males after 8 weeks of exercise. Male rats had higher fecal cholesterol and cholic acid levels, indicating a sex-specific mechanism of lipid excretion with exercise. Eight weeks of training reduced markers related to hepatic stellate cell activation and fibrosis in both sexes. This study highlights the sexual dimorphic and temporal molecular signatures by which exercise modulates liver metabolism to provide hepatoprotective effects.
    Keywords:  CP: metabolism; CrAT; bile acids; endurance exercise; lipids; liver; metabolism; mitochondria; omics
    DOI:  https://doi.org/10.1016/j.celrep.2026.117416
  10. J Endocr Soc. 2026 Jul;10(7): bvag102
    Feasibility, reproducibility, and cold-induced energy expenditure using whole-room calorimetry in adults and children.
    Paige Cheveldayoff, Bader Alamri, Dongdong Wang, Rogelio Cruz Gonzalez, Aaron C Q Thomas, Norm Konyer, Michael D Noseworthy, Hertzel C Gerstein, Zubin Punthakee, Gregory R Steinberg, Katherine M Morrison.
       Context: To understand energy balance, whole-room indirect calorimetry (WRIC) allows for accurate measurement of energy expenditure (EE).
    Objective: To examine the relationship between cold-induced resting EE and brown adipose tissue (BAT) activity measured by magnetic resonance imaging (MRI) and to evaluate WRIC system (WRICS) performance and feasibility of use in children and adults.
    Methods: The WRICS was equipped with a Promethion High-Definition Room Calorimetry System. Technical validation utilized nitrogen (N2) and carbon dioxide (CO2) gas infusions. Healthy adults (n = 21) and children aged 8-17 years (n = 17) attended two 4-hour WRIC visits (one week apart) and one MRI visit. Resting EE at 25 °C (REE25) was compared between visits and to REE at 18 °C (REE18). Recruitment and completion rates were examined. BAT activity was assessed by MRI as the decline in supraclavicular proton density fat fraction during 18 °C cold exposure.
    Results: Gas infusion testing confirmed high accuracy (respiratory exchange ratio [RER] = 0.99; 95% CI 0.991-0.996). Study completion rates were high (adults: 20/21; children: 17/18). REE25 over a 10-minute period was consistent between visits (adults: 1.68 ± 0.462 vs 1.66 ± 0.301 kcal/min, P = 0.77; children: 1.50 ± 0.358 vs 1.58 ± 0.348 kcal/min, P = .25). Cold exposure increased fasting EE by 0.21 kcal/min (adults) and 0.14 kcal/min (children). BAT activity was correlated with REE18 in adults (r = 0.49, P = .04).
    Conclusion: WRICS use was feasible in adults and children. Changes in EE during cold (ie, cold-induced thermogenesis) were measurable and related to BAT activity, supporting the usefulness of this system in the assessment of EE in response to interventions in adults and children.
    Keywords:  BAT activity; cold exposure; energy expenditure; indirect calorimetry; obesity; pediatrics
    DOI:  https://doi.org/10.1210/jendso/bvag102
  11. JMIR Res Protoc. 2026 Jun 12. 15 e100108
    Exercise Snacks in Adults Living With Obesity: Protocol for a Randomized Feasibility Trial.
    Seth F McCarthy, Ella Harness, Noah Mulkewich, Roderick E Sandilands, Alexis Marcotte-Chénard, Hashim Islam, Douglas L Richards, Kenneth Madden, Joel Singer, Mary Jung, Martin J Gibala, Jonathan P Little.
       Background: Rates of obesity worldwide continue to increase and are associated with myriad health risks and socioeconomic burdens. Exercise is a traditional treatment for adults with obesity to increase physical activity levels, improve cardiorespiratory fitness, and reduce cardiometabolic risk. However, many people living with obesity do not engage in enough physical activity to achieve health benefits and often cite a perceived lack of time, lack of access to equipment, and stigma as barriers. "Exercise snacks" are short (~1 min) isolated bouts of vigorous exercise performed sporadically throughout the day that may be a viable strategy to improve fitness and cardiometabolic health. It is unknown whether exercise snacks are a feasible option in the real world for people living with obesity.
    Objective: This study aims to conduct a pilot randomized clinical trial (RCT) to determine the feasibility and preliminary efficacy of a 12-week smartphone app-supported exercise snacks intervention with behavior change counseling for improving cardiorespiratory fitness and other indices of cardiometabolic health in previously inactive adults living with obesity.
    Methods: A 2-site, parallel arm, RCT will be conducted in Kelowna and Hamilton, Canada. Eighty inactive adults living with obesity will be randomized to an exercise snacks or stretching/mobility exercise comparator group for 12 weeks. The former will complete 4 × 1-minute bouts of vigorous exercise at least 5 days per week, and the latter will perform mobility or stretching exercises using the same schedule. Interventions will be delivered through a customized smartphone mobile app and will be tailored to the participants' schedules via onboarding counseling sessions, with ongoing telephone check-in call support at weeks 1, 2, 4, and 8. This pilot RCT will focus on feasibility as reflected by rates of recruitment, adherence, and dropout. We will also assess cardiorespiratory fitness, anthropometric markers, and routine blood health markers (eg, glucose, insulin) at baseline and postintervention.
    Results: This study is funded through the Heart & Stroke Foundation of Canada Grants-in-Aid program (2024/2025). Recruitment began on July 18, 2025 (Kelowna) and in November 2025 (Hamilton). As of March 31, 2026, we have enrolled 65 participants (University of British Columbia Okanagan, n=51; McMaster University, n=14). Data analysis will begin once all enrolled participants have completed the trial, and we expect to publish the results of the trial in winter 2027.
    Conclusions: This study will test an RCT protocol, provide evidence on the feasibility of exercise snacks in inactive adults living with obesity, and report preliminary effect size estimates for their ability to improve cardiometabolic health.
    Keywords:  behavior counselling; cardiorespiratory fitness; exercise; obesity; physical activity
    DOI:  https://doi.org/10.2196/100108
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