{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T15:19:39Z","timestamp":1789571979651,"version":"build-2803163510"},"reference-count":56,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T00:00:00Z","timestamp":1780963200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell Dev. Biol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Obesity impairs male reproductive function, yet effective protective strategies are limited. Compound 51 is a novel N-salicyloyl tryptamine derivative whose role in spermatogenic function is unknown. This study aimed to determine whether it protects against obesity-induced spermatogenic dysfunction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Employing a combined\n                      <jats:italic>in vivo<\/jats:italic>\n                      and\n                      <jats:italic>in vitro<\/jats:italic>\n                      approach, we first evaluated compound 51 in a high-fat diet-induced obese mouse model, assessing systemic metabolism, reproductive phenotype, and molecular changes in testes. To investigate the underlying cellular mechanisms suggested by the\n                      <jats:italic>in vivo<\/jats:italic>\n                      findings, parallel experiments were conducted in palmitic acid-injured TM4 Sertoli cells, focusing on insulin signaling and glycolytic function.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>In vivo<\/jats:italic>\n                      , compound 51 administration significantly improved body weight, semen quality, testicular\/epididymal morphology, and hormone levels (testosterone, follicle-stimulating hormone, inhibin B). It dose-dependently modulated apoptosis markers (downregulated Bax, upregulated Bcl-2\/PCNA), enhanced testicular insulin sensitivity (reduced insulin-like growth factor 1 (IGF1) and elevated its receptor IGF1R), and increased glycolytic enzyme expression (hexokinase 2, pyruvate kinase M2, lactate dehydrogenase A).\n                      <jats:italic>In vitro<\/jats:italic>\n                      , compound 51 promoted proliferation, improved insulin sensitivity, and enhanced glycolytic activity in PA-injured TM4 cells, thereby ameliorating Sertoli cell dysfunction.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Compound 51 ameliorates obesity-induced spermatogenic dysfunction by enhancing testicular insulin sensitivity and promoting glycolytic flux in Sertoli cells.<\/jats:p>\n                  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