{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T05:15:17Z","timestamp":1783574117993,"version":"3.55.0"},"reference-count":87,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T00:00:00Z","timestamp":1783555200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100017699","name":"Galecto","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100017699","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Physiol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Metabolic syndrome (MetS) is an increasingly prevalent condition characterized by visceral obesity, insulin resistance, dyslipidemia, hypertension, and chronic low-grade inflammation. Impaired preadipocyte differentiation contributes to metabolic disturbances, inflammation, and mitochondrial dysfunction. Galectin-3 (Gal-3) plays a key role in promoting visceral adipose tissue (VAT) inflammation, fibrosis, and mitochondrial impairment. In a preclinical rabbit model of MetS, treatment with the Gal-3 inhibitor selvigaltin reduced VAT mass, indicating potential therapeutic value. This study seeks to clarify how selvigaltin influences the metabolic function of differentiation induction medium (DIM)-induced adipocytes mitochondria, potentially offering a new strategy for treating MetS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Male New Zealand White rabbits were housed individually under standard conditions. Following one week on a regular diet (RD), they were randomly assigned to one of the following groups for 12 weeks: RD with vehicle, high-fat diet (HFD) with vehicle, or HFD with selvigaltin (0.3, 1.0, or 5.0 mg\/kg), administered orally once daily, five days a week, starting from week 9. Visceral adipose tissue (VAT) was collected, and preadipocytes were isolated and induced to differentiate\n                      <jats:italic>in vitro<\/jats:italic>\n                      into DIM-differentiated adipocytes. Subsequent experiments examined mitochondrial dynamics and morphology, superoxide production, oxygen consumption, lipid droplets formation, and target genes mRNA expression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>HFD in rabbits induces features of metabolic syndrome, including increased visceral fat, mitochondrial dysfunction, oxidative stress, and lipid accumulation in visceral adipose tissue. Treatment with Gal-3 inhibitor selvigaltin reversed many of these changes, specifically, improving DIM-differentiated adipocytes mitochondrial morphology and dynamics, reducing oxidative stress and lipid droplet size. Furthermore, the HFD induced upregulation of inflammatory markers (COX2, IL-1\u03b2, IL-6, TLR2, TLR4, TNF\u03b1) and immune cell polarization transcription factors (GATA3, TBX21), all noticeably decreased by selvigaltin treatment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>This study highlights mitochondrial dysfunction as a key factor in VAT impairment. In DIM-differentiated adipocytes, selvigaltin improves mitochondrial structure, dynamics, and function, reduces oxidative stress and lipid droplet size, and lowers the mRNA expression of proinflammatory-related genes. It also promotes a shift toward a healthier, more metabolically active adipocyte phenotype. Selvigaltin restores mitochondrial health, suggesting its potential as a therapeutic option for metabolic disorders involving VAT dysfunction. Further studies are needed to confirm its clinical relevance.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fphys.2026.1710592","type":"journal-article","created":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T04:20:03Z","timestamp":1783570803000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Galectin-3 inhibitor selvigaltin dosed therapeutically in vivo in a rabbit model of metabolic syndrome induced by high-fat diet: effects on rabbit differentiated adipocytes"],"prefix":"10.3389","volume":"17","author":[{"given":"Gabriele","family":"Acciai","sequence":"first","affiliation":[{"name":"Department of Experimental and Clinical Biomedical Sciences \u201cMario Serio\u201d, University of Florence","place":["Florence, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paolo","family":"Comeglio","sequence":"additional","affiliation":[{"name":"Department of Experimental and Clinical Biomedical Sciences \u201cMario Serio\u201d, University of Florence","place":["Florence, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandra","family":"Filippi","sequence":"additional","affiliation":[{"name":"Department of Neurosciences, Psychology, Drug Research and Child Health (NEUROFARBA), University of Florence","place":["Florence, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ilaria","family":"Cellai","sequence":"additional","affiliation":[{"name":"Department of Experimental and Clinical Biomedical Sciences \u201cMario Serio\u201d, University of Florence","place":["Florence, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Rapizzi","sequence":"additional","affiliation":[{"name":"Department of Experimental and Clinical Biomedical Sciences \u201cMario Serio\u201d, University of Florence","place":["Florence, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tommaso","family":"Mello","sequence":"additional","affiliation":[{"name":"Department of Experimental and Clinical Biomedical Sciences \u201cMario Serio\u201d, University of Florence","place":["Florence, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian","family":"Holyer","sequence":"additional","affiliation":[{"name":"Galecto Biotech AB","place":["Copenhagen, Denmark"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fredrik R.","family":"Zetterberg","sequence":"additional","affiliation":[{"name":"Galecto Biotech AB","place":["Copenhagen, Denmark"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrea","family":"Galli","sequence":"additional","affiliation":[{"name":"Department of Experimental and Clinical Biomedical Sciences \u201cMario Serio\u201d, University of Florence","place":["Florence, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linda","family":"Vignozzi","sequence":"additional","affiliation":[{"name":"Department of Experimental and Clinical Biomedical Sciences \u201cMario Serio\u201d, University of Florence","place":["Florence, Italy"]},{"name":"Interuniversity Consortium \u201cIstituto Nazionale Biostrutture e Biosistemi\u201d (INBB)","place":["Rome, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert J.","family":"Slack","sequence":"additional","affiliation":[{"name":"Galecto Biotech AB","place":["Copenhagen, Denmark"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mario","family":"Maggi","sequence":"additional","affiliation":[{"name":"Department of Experimental and Clinical Biomedical Sciences \u201cMario Serio\u201d, University of Florence","place":["Florence, Italy"]},{"name":"Interuniversity Consortium \u201cIstituto Nazionale Biostrutture e Biosistemi\u201d (INBB)","place":["Rome, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,7,9]]},"reference":[{"key":"B57","doi-asserted-by":"publisher","DOI":"10.3389\/fendo.2023.1141303","article-title":"Effects of allicin on human Simpson-Golabi-Behmel syndrome cells in mediating browning phenotype","volume":"14","author":"Ali","year":"2023","journal-title":"Front. 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