bims-mimead 2025-11-16 papers

bims-mimead

Biomed News

on Adipose tissue and metabolic disease

Issue of 2025–11–16
eleven papers selected by
Rachel M. Handy, University of Guelph

Global mapping of RNA N6-methyladenosine (m6A) in human subcutaneous and visceral adipose tissue reveals novel targets that correlate with clinical variables of obesity.
ATGL-mediated lipolysis is essential for myocellular mitochondrial function, mitochondria-lipid droplet interaction and mitochondrial network connectivity.
Glyoxalase 1 is a pro-adipogenic gene.
miR-432 Exacerbates Obesity-Induced Dysregulation of Glucose and Lipid Homeostasis.
Impaired mitochondrial ketone body oxidation in insulin resistant states.
Rapid cell turnover to model adipocyte size distribution.
Crosstalk Between Obesogenic Diet and Estrogen Drives Distinct Microbiota Profiles in Ovariectomized Mice.
Mutation in IR or IGF1R produces features of long-lived mice while maintaining metabolic health.
Assessing the interaction of the UCP system and fatty acids on epicardial adipose tissue mitochondrial respiration.
Protocol for in vivo assessment of glucose metabolism in mouse models.
Roux-en-Y Gastric Bypass Improves Insulin Response and Secretion of GLP-1 and PYY in Response to Postprandial Acute Exercise.

Biomark Res. 2025 Nov 12. 13(1): 146

Global mapping of RNA N6-methyladenosine (m6A) in human subcutaneous and visceral adipose tissue reveals novel targets that correlate with clinical variables of obesity.

Torunn Rønningen, Yong Zeng, Mai Britt Dahl, Junbai Wang, Tina Visnovska, Tone Møller Tannæs, Lars la Cour Poulsen, Akin Cayir, Stina Ingrid Alice Svensson, Marius Svanevik, Jens Kristoffer Hertel, Jøran Hjelmesæth, Jon A Kristinsson, Tom Mala, Matthias Blüher, Housheng Hansen He, Tone Gretland Valderhaug, Yvonne Böttcher.

   BACKGROUND: Obesity is a major health challenge and fat accumulation in visceral depots is more strongly associated with metabolic comorbidities than deposition in subcutaneous depots. Epitranscriptomic regulation of gene expression by N6-methyladenosine (m6A) influences various aspects of RNA metabolism, however the m6A methylome in human adipose tissue and its relationship with fat distribution has not yet been investigated in detail.
METHODS: In this study, we performed epitranscriptomic mapping of m6A in intra-individually paired samples of subcutaneous (SAT) and omental visceral adipose tissue (OVAT) from women with normal weight (BMI ≤25, n = 3) and obesity (BMI ≥35, n = 10) using meRIP-seq (discovery cohort). We further investigated differential m6A methylation for specific target genes in a larger cohort of individuals with obesity (n = 72, validation cohort) using meRIP-qPCR. meRIP-seq was performed for primary adipocytes from a subset of the patients (n = 4) to account for cell type specific differences.
RESULTS: We here provide the first global map of m6A in human adipose tissue in paired samples of SAT and OVAT. We show an overall high overlap in m6A sites between individuals and depots, but also distinct depot-specific differences. We identify 339 target genes showing depot-specific m6A methylation. Depot-specific methylation was validated for selected sites in SEMA3A, SNAP47 and PPP1R9A in a larger validation cohort. We additionally identify differentially methylated targets between lean individuals and individuals with obesity, including TSC22D1, FMNL2 and IL1R1. By combining data from primary adipocytes with data from corresponding bulk adipose tissue, we identified a higher number of genes containing m6A in non-adipocyte cells in OVAT compared to SAT. Mechanistically, we show for selected targets that m6A affects RNA lifetime in pre-adipocyte cell culture models. Importantly, m6A methylation in selected targets correlates with clinically important variables related to obesity, fat distribution and glucose metabolism.
CONCLUSIONS: We identify a catalogue of novel targets showing adipose tissue depot specific m6A methylation, with potential as biomarkers in metabolic disease. Our findings underscore the regulatory role of m6A in obesity and provide valuable insights for future research. The datasets generated represent a significant resource for further insight in adipose tissue biology and its implications for metabolic health.

Keywords:  Adipose tissue; Epitranscriptomics; Fat distribution; N6-methyladenosine; Obesity

DOI:  https://doi.org/10.1186/s40364-025-00857-0
Biochim Biophys Acta Mol Cell Biol Lipids. 2025 Nov 10. pii: S1388-1981(25)00111-8. [Epub ahead of print]1871(1): 159703

ATGL-mediated lipolysis is essential for myocellular mitochondrial function, mitochondria-lipid droplet interaction and mitochondrial network connectivity.

Anne Gemmink, Tineke van de Weijer, Gert Schaart, Gernot F Grabner, Esther Kornips, Kèvin Knoops, Rudolf Zechner, Martina Schweiger, Matthijs K C Hesselink.

  Defects in Adipose tissue TriGlyceride Lipase (ATGL)-mediated myocellular lipid droplet (LD) lipolysis results in mitochondrial dysfunction of unknown origin, which can be rescued by PPAR agonists. Here we examine if ATGL-mediated lipolysis is required to maintain mitochondrial network connectivity and function. Moreover, we explored if the functional implications of ATGL deficiency for mitochondrial network dynamics and function can be alleviated by promoting PPARα and/or PPARδ transcriptional activity. To this end, we cultured human primary myotubes from patients with neutral lipid storage disease with myopathy (NLSDM), a rare metabolic disorder caused by a mutation in the gene encoding for ATGL. These myotubes possess dysfunctional ATGL and compromised LD lipolysis. In addition, mitochondria-LD contact, mitochondrial network connectivity, and mitochondrial membrane potential were affected. Using a humanized ATGL inhibitor in myotubes (cultured form healthy donors) revealed similar results. Upon stimulating PPARδ transcriptional activity, mitochondrial respiration improved by more than 50 % in human primary myotubes from healthy lean individuals. This increase in respiration was dampened in myotubes with dysfunctional ATGL. Stimulation of PPARδ transcriptional activity had no effect on mitochondria-LD contacts, mitochondrial network connectivity, and mitochondrial membrane potential. Our results demonstrate that dysfunctional ATGL results in compromised mitochondrial-LD contacts and mitochondrial network connectivity, and that functional ATGL is required to improve mitochondrial respiratory capacity upon stimulation of PPARδ transcriptional activity.

Keywords:  ATGL; Lipid droplets; Microscopy; Mitochondrial networks; NLSDM; PPAR transcriptional activity; Skeletal muscle

DOI:  https://doi.org/10.1016/j.bbalip.2025.159703
J Biol Chem. 2025 Nov 07. pii: S0021-9258(25)02778-4. [Epub ahead of print] 110926

Glyoxalase 1 is a pro-adipogenic gene.

Marissa N Trujillo, Wei-Chen Zhang, Emely A Hoffman, Naoya Kitamura, Aiden M Phoebe, James J Galligan.

  Diabetes is one of the most prevalent and wide-spread diseases, with the majority of cases stemming from prolonged obesity. Obesity occurs through the expansion of adipose tissue in an unhealthy and dysfunctional manner, where patients develop inflammation and insulin resistance. Diabetic patients have increased levels of the reactive glycolytic by-product, methylglyoxal (MGO), and its resulting post-translational modifications (PTMs) compared to non-diabetic patients. To combat this, cells are equipped with the glyoxalase cycle, consisting of two enzymes, glyoxalase 1 (GLO1) and GLO2, to reduce the levels of MGO. Previous work has identified a putative role for MGO in the pathologies associated with obesity. We thus sought to interrogate the role of GLO1 in the context of adipogenesis using GLO1 knockout (GLO1-/-) 3T3-L1 preadipocytes. These cells have elevated, physiologically relevant, levels of MGO and MGO-derived PTMs. When differentiated to mature adipocytes, GLO1-/- cells fail to accumulate lipid, despite significant elevations in MGO. We also show a restoration of MGO-derived PTMs in GLO1-/- cells following differentiation. Proteomic analysis reveals significant enrichment in glycolytic and TCA cycle enzymes in WT cells compared to GLO1-/- cells after differentiation. Lastly, immunoblotting shows decreased AKT phosphorylation and reduced glucose uptake in differentiated GLO1-/- cells. Taken together, our data identifies a putative pro-adipogenic role for GLO1 and MGO in adipogenesis.

Keywords:  GLO1; Glyoxalase; glycation; glycerol; methylglyoxal

DOI:  https://doi.org/10.1016/j.jbc.2025.110926
Diabetes. 2025 Nov 11. pii: db250295. [Epub ahead of print]

miR-432 Exacerbates Obesity-Induced Dysregulation of Glucose and Lipid Homeostasis.

Cuizhe Wang, Yanting Hou, Meixiu Zhang, Jingzhou Wang, Xiaolong Chu, Maodi Liang, Chaoyue Sun, Jianxin Xie, Jun Zhang, Cong-Yi Wang.

miRNAs are key regulators of metabolic homeostasis, yet their role in obesity-associated dysfunction remains incompletely understood. Here, we identify miR-432 as a driver of systemic metabolic dysregulation. Serum miRNA profiling revealed a positive correlation between miR-432 expression and obesity/type 2 diabetes mellitus. Functionally, adipose-specific miR-432 exacerbated high-fat diet-induced obesity and insulin resistance. Similarly, hepatic-specific miR-432 aggravated hepatic steatosis and systemic glucose dysregulation, while skeletal muscle-specific miR-432 disrupted glucose homeostasis without affecting body composition. Mechanistically, miR-432 disrupted insulin sensitivity by inhibiting the PIK3R3/AKT pathway and perturbed lipid homeostasis by suppressing the PIK3R3/PPAR-α axis. Notably, obesity-induced miR-432 upregulation was predominantly localized in adipocytes and driven by the CDK5/PPAR-γ axis. Furthermore, adipocyte-derived exosomal miR-432 was identified as a mediator of systemic metabolic dysfunction, facilitating intertissue cross talk in obesity. Collectively, our data demonstrate that miR-432 exacerbates obesity-induced dysregulation of glucose and lipid metabolism.
ARTICLE HIGHLIGHTS: miR-432 overexpression in adipose tissue, liver, and skeletal muscle exacerbates high-fat diet-induced disruption of metabolic homeostasis. miR-432 impairs glucose homeostasis by suppressing the PIK3R3/AKT pathway and disrupts lipid homeostasis via inhibition of the PIK3R3/PPAR-α axis or directly suppressing PPAR-α. Obesity-induced elevation of miR-432 is predominantly localized in adipocytes and driven by the CDK5/PPAR-γ axis. Adipocyte-derived exosomal miR-432 mediates systemic metabolic dysfunction, establishing an intertissue regulatory network.

DOI: https://doi.org/10.2337/db25-0295
EBioMedicine. 2025 Nov 11. pii: S2352-3964(25)00451-7. [Epub ahead of print]122 106007

Impaired mitochondrial ketone body oxidation in insulin resistant states.

Elric Zweck, Sarah Piel, Johannes W Schmidt, Daniel Scheiber, Martin Schön, Sabine Kahl, Volker Burkart, Bedair Dewidar, Ricarda Remus, Alexandra Chadt, Hadi Al-Hasani, Lucia Mastrototaro, Hug Aubin, Udo Boeken, Artur Lichtenberg, Jörg Distler, Amin Polzin, Malte Kelm, Ralf Westenfeld, Robert Wagner, Patrick Schrauwen, Julia Szendroedi, Michael Roden, Cesare Granata.

   BACKGROUND: Reduced mitochondrial respiratory function has been implicated in metabolic disorders like type 2 diabetes (T2D), obesity, and metabolic dysfunction-associated steatotic liver disease (MASLD), which are tightly linked to insulin resistance and impaired metabolic flexibility. However, the contribution of the ketone bodies (KBs) β-hydroxybutyrate (HBA) and acetoacetate (ACA) as substrates for mitochondrial oxidative phosphorylation (OXPHOS) in these insulin resistant states remains unclear.
METHODS: Targeted high-resolution respirometry protocols were applied to detect the differential contribution of HBA and ACA to OXPHOS capacity in heart, skeletal muscle, kidney, and liver of distinct human or murine cohorts with T2D, obesity, and MASLD.
FINDINGS: In humans with T2D, KB-driven mitochondrial OXPHOS capacity was ∼30% lower in the heart (p < 0.05) and skeletal muscle (p < 0.05) compared to non-diabetic controls. The relative contribution of KBs to maximal OXPHOS capacity in T2D was also lower in both the heart (∼25%, p < 0.05) and skeletal muscle (∼50%, p < 0.05). Similarly, in kidney cortex from high-fat diet-induced obese mice, both the absolute and relative contribution of KBs to OXPHOS capacity was ∼15% lower (p < 0.05). Finally, hepatic HBA-driven mitochondrial OXPHOS capacity was 29% lower (p < 0.05) in obese humans with hepatic steatosis compared to humans without.
INTERPRETATION: Mitochondrial KB-driven OXPHOS capacity is impaired in insulin resistant states in various organs in absolute and relative terms, likely reflecting impaired mitochondrial metabolic flexibility. Our data suggest that KB respirometry can provide a sensitive readout of impaired mitochondrial function in diabetes, obesity, and MASLD.
FUNDING: German Research Foundation, German Diabetes Center, German Federal Ministry of Health, Ministry of Culture and Science of the state of North Rhine-Westphalia, German Federal Ministry of Education and Research, German Center for Diabetes Research, German Heart Foundation, German Diabetes Society, Christiane-and-Claudia Hempel Foundation, European Community and Schmutzler Stiftung.

Keywords:  Diabetes mellitus; Ketone bodies; MASLD; Mitochondrial respiration; Obesity

DOI:  https://doi.org/10.1016/j.ebiom.2025.106007
J Theor Biol. 2025 Nov 10. pii: S0022-5193(25)00295-4. [Epub ahead of print] 112311

Rapid cell turnover to model adipocyte size distribution.

Louis Fostier, Aloïs Dauger, Romain Yvinec, Magali Ribot, Chloe Audebert, Hedi Soula.

  White adipose tissue, composed of adipocyte cells, primarily stores energy as lipid droplets. The size of adipocytes varies significantly within the tissue according to the amount of stored lipids. A striking observation is that the adipocyte size distribution is bimodal, and thus, this tissue is lacking a characteristic size. We propose a novel dynamical model, based on a partial differential equation, to represent the adipocyte size distribution. The model assumes continuous adipocyte growth, with a velocity dependent on cell radius and extracellular lipid availability, together with constant rates of cell recruitment and death. We prove the existence and local stability of a unique stationary solution for a broad range of growth velocity functions. Choosing a parcimonious formulation, we show that only three parameters are enough to describe adipocyte size distributions measurements in rats. These parameters are robustly estimated through approximate Bayesian computation, and the model demonstrates excellent agreement with experimental data. This mechanistic, three-parameter framework offers a new and interpretable approach to characterizing adipocyte size distributions.

Keywords:  Adipocyte size distribution; Parameter estimation; Partial differential equation modeling; Stationary solution; White adipocyte tissue

DOI:  https://doi.org/10.1016/j.jtbi.2025.112311
Physiol Genomics. 2025 Nov 14.

Crosstalk Between Obesogenic Diet and Estrogen Drives Distinct Microbiota Profiles in Ovariectomized Mice.

Taylor B Scheidl, Jessica L Wager, Jane Shearer, Jennifer A Thompson, Chunlong Mu.

  The menopausal transition is associated with an increased obesity risk, which can be ameliorated by hormone replacement therapy. However, the independent and interactive effects of obesity and menopause on the gut microbiota, along with the influence of hormone therapy, remain poorly understood. To address this, this study employed a mouse model using sham-operated and ovariectomized mice, with or without high-fat diet-induced obesity, to disentangle the roles of menopause and obesity. Ovariectomized mice on a high-fat diet were further treated with estradiol to assess the regulatory effects of hormone supplementation on the gut microbiota. The results showed that obesity and ovariectomy altered the relative abundances of 29 and 7 genera, and 243 and 99 amplicon sequence variants, respectively, indicating a stronger impact of obesity on gut microbial composition. Notably, ovariectomy increased the abundance of Faecalibaculum and enriched microbial taxa capable of producing estrogen-metabolizing enzymes, including Bifidobacterium and Dubosiella species, as well as the predicted abundance of the estrobolome enzyme β-glucuronidase. Estradiol supplementation increased the relative abundance of Bacteroides and decreased Akkermansia, both of which possess distinct β-glucuronidase subtypes. It also reduced the species Faecalibaculum rodentium that positively associated with adiposity. Together, these findings highlight the distinct and significant impacts of obesity and menopause on the gut microbiota and suggest that estrogen supplementation modulates microbial features linked to metabolic health. These results further implicate the potential of modulating the gut microbiota to improve postmenopausal health outcomes.

Keywords:  Gut microbiota; Hormone therapy; Menopause; Metabolic health; Obesity

DOI:  https://doi.org/10.1152/physiolgenomics.00184.2025
JCI Insight. 2025 Nov 11. pii: e189683. [Epub ahead of print]

Mutation in IR or IGF1R produces features of long-lived mice while maintaining metabolic health.

Ulalume Hernández-Arciga, Jun Kyoung Kim, Jacob L Fisher, Alexander Tyshkovskiy, Alibek Moldakozhayev, Catherine Hall, Souvik Ghosh, Yashvandhini Govindaraj, Ian J Sipula, Jake Kastroll, Diana Cooke, Jinping Luo, Jonathan K Alder, Stacey J Sukoff Rizzo, Gene P Ables, Eunhee Choi, Vadim N Gladyshev, Michael J Jurczak, Marc Tatar, Andrey A Parkhitko.

  Insulin/insulin growth factor signaling is a conserved pathway that regulates lifespan. Yet, long-lived loss-of-function mutants often produce insulin-resistance, slow growth, and impair reproduction. Recently, a gain-of-function mutation in the kinase insert domain (KID) of the Drosophila insulin/IGF receptor was seen to dominantly extend lifespan without impairing insulin-sensitivity, growth and reproduction. This substitution occurs within residues conserved in mammalian insulin receptor (IR) and insulin growth factor-1 receptor (IGF-1R). We produced two knock-in mouse strains that carry the homologous KID Arg/Cys substitution in murine IR or IGF-1R, and we replicated these genotypes in human cells. Cells with heterodimer receptors of IR or IGF-1R induce receptor phosphorylation and phospho-Akt when stimulated with insulin or IGF. Heterodimer receptors of IR fully induce pERK but ERK was less phosphorylated in cells with IGF-1R heterodimers. Adults with a single KID allele (producing heterodimer receptors) have normal growth and glucose regulation. At four months, these mice variably display hormonal markers that associate with successful aging counteraction, including elevated adiponectin, FGF21, and reduced leptin and IGF-1. Livers of IGF-1R females show decreased transcriptome-based biological age, which may point toward delayed aging and warrants an actual lifespan experiment. These data suggest that KID mutants may slow mammalian aging while they avoid the complications of insulin resistance.

Keywords:  Aging; Glucose metabolism; Insulin; Metabolism

DOI:  https://doi.org/10.1172/jci.insight.189683
Eur J Clin Invest. 2025 Nov 15. e70149

Assessing the interaction of the UCP system and fatty acids on epicardial adipose tissue mitochondrial respiration.

Diana Santos, Ana Burgeiro, Ana Catarina R G Fonseca, Cândida Dias, Teresa Cunha-Oliveira, Aryane Oliveira, João Laranjinha, António Canotilho, Gonçalo Coutinho, David Prieto, Pedro Antunes, Manuel Antunes, Eugenia Carvalho.

   BACKGROUND: Epicardial adipose tissue (EAT) exhibits brown-like features, including the expression of uncoupling protein 1 (UCP1). EAT interacts dynamically with cardiac cells to modulate local cardiac tissue physiology and metabolic function. No studies have evaluated the impact of UCP1 inhibition on oxidative phosphorylation (OXPHOS) in fresh EAT explants. This study aimed to determine the unique bioenergetic characteristics of fresh EAT explants by comparing it to subcutaneous adipose tissue (SAT). Furthermore, the key impact of UCP1 inhibition on EAT respiration and how this process is influenced by the presence of type 2 diabetes mellitus (DM) or coronary artery disease (CAD), was also evaluated.
METHODS: EAT and SAT biopsies were collected from 205 (151 male and 51 female) study participants, undergoing cardiac surgery. Participants were stratified according to the presence/absence of DM or CAD. Markers of mitochondrial content and bioenergetics were evaluated.
RESULTS: EAT demonstrated a higher bioenergetic activity compared to SAT, in both nicotinamide adenine dinucleotide (NADH)-linked and fatty acid oxidation (FAO)-linked OXPHOS. Importantly, UCP1 inhibition with guanosine 5'-diphosphate (GDP), flattens the differences between the tissues in the NADH-linked OXPHOS; in contrast these differences were potentiated in the FAO-linked OXPHOS. Minor differences in mitochondrial content and respiration were observed when subjects were stratified according to either DM or CAD.
CONCLUSIONS: This study emphasizes the important bioenergetic differences between EAT and SAT, which are crucial in the context of the local cardiomyocyte metabolism, as well as the impact of UCP1 inhibition in EAT. A deeper understanding of the unique characteristics of EAT and its metabolic micro-environment may provide valuable insights into the cardiovascular disease pathologies.

Keywords:  cardiovascular disease; epicardial adipose tissue; fatty acid oxidation; mitochondrial respiration; uncoupling protein 1

DOI:  https://doi.org/10.1111/eci.70149
STAR Protoc. 2025 Nov 07. pii: S2666-1667(25)00598-2. [Epub ahead of print]6(4): 104192

Protocol for in vivo assessment of glucose metabolism in mouse models.

Titaya Lerskiatiphanich, Cedric S Cui, John D Lee.

  Metabolic disturbances are common in motor neuron disease (MND), and elucidating their mechanisms may reveal therapies. Here, we present a protocol to assess glucose homeostasis in mice, including glucose tolerance, insulin tolerance, and glucagon challenge tests. We describe steps for fasting, intraperitoneal injections, and serial blood glucose measurements. The protocol also includes plasma collection for catecholamine analysis using matrix-assisted laser desorption ionization (MALDI) mass spectrometry imaging and immunofluorescence of pancreatic hormones, enabling comprehensive metabolic profiling in aged and neurodegenerative mouse models. For complete details on the use and execution of this protocol, please refer to McDonald et al.1 and McDonald et al.2.

Keywords:  Metabolism; Metabolomics; Neuroscience

DOI:  https://doi.org/10.1016/j.xpro.2025.104192
Obes Surg. 2025 Nov 14.

Roux-en-Y Gastric Bypass Improves Insulin Response and Secretion of GLP-1 and PYY in Response to Postprandial Acute Exercise.

Saulo Gil, Igor Hisashi Murai, Wagner S Dantas, Carlos Alberto Abujabra Merege-Filho, Alice Erwig Leitão, Carolina Ferreira Nicoletti, Alisson Padilha de Lima, Fabiana Benatti, Roberto de Cleva, Marco Aurélio Santo, John P Kirwan, Bruno Gualano, Hamilton Roschel.

   BACKGROUND: The acute exercise-mediated changes in metabolic, immunomodulatory, and gut hormones are blunted by excessive adiposity. We investigated whether bariatric surgery improves the acute postprandial exercise response in terms of glucose metabolism, gut hormones, and inflammatory markers in women with severe obesity.
METHODS: Thirteen women (age: 37 ± 7; BMI: 47.6 ± 5.6) underwent an exercise session (resistance training plus aerobic exercise) before and 3 months after surgery. Blood samples were collected at baseline, immediately and 30 min after exercise to analyze glucose, insulin, inflammatory markers, and gut hormones.
RESULTS: Post-surgery, glucose levels decreased immediately (P = 0.0011) and 30 min after exercise (P = 0.0160), but AUC remained similar (181.0 vs. 166.8 mg/dL x min-1, P = 0.1980) between conditions. Insulin response to postprandial exercise did not change after surgery (all P > 0.05), but AUC was reduced post-surgery (60.7 vs. 26.3 µU/mL x min-1, P = 0.0457). No changes occurred in Glucagon-Like Peptide-1 (GLP-1) and Peptide YY (PYY) pre-surgery exercise (all P > 0.05); however, both parameters were increased immediately (P = 0.0180 and P = 0.0020, respectively) and 30 min post-exercise (P = 0.0380 and P = 0.0360, respectively) after surgery. AUC for GLP-1 (2.3 vs. 14.5 pg/mL x min-1, P = 0.0075) and PYY (9.9 vs. 224.2 pg/mL x min-1, P = 0.0004) were increased post-surgery. Surgery did not affect Pancreatic Polypeptide (PP) or Gastric Inhibitory Polypeptide (GIP) responses to postprandial exercise. Both parameters were elevated immediately (all P < 0.05) and 30 min post-exercise (all P < 0.05), regardless of surgery. PP (549.6 vs. 261.7 pg/mL x min-1, P = 0.0457) and GIP (610.6 vs. 429.1 pg/mL x min-1, P = 0.0260) AUC was lower post- vs. pre-surgery. No changes were observed for ghrelin levels and inflammatory markers (all P > 0.05).
CONCLUSIONS: Bariatric surgery improves the secretion of GLP-1 and PYY in response to postprandial acute exercise in parallel with enhanced peripheral insulin response.

Keywords:  Bariatric surgery; Exercise ; Metabolism

DOI:  https://doi.org/10.1007/s11695-025-08327-0