ENDOPLASMIC RETICULUM STRESS MARKERS EXPRESSION LEVELS IN LEPTIN RESISTANCE DEVELOPMENT

dc.contributor.authorIsaqjonova Moxinur Nodirjon qizi
dc.date.accessioned2025-12-29T18:00:22Z
dc.date.issued2025-10-29
dc.description.abstractThis review explores the link between endoplasmic reticulum (ER) stress and leptin resistance in obesity, with a focus on women. ER dysfunction activates stress markers such as XBP1, CHOP, and GRP78, disrupting leptin signaling and promoting metabolic imbalance. Chronic overnutrition induces sustained ER stress, impairing hypothalamic and peripheral leptin pathways. Elevated expression of these markers correlates with obesity severity and metabolic dysfunction, particularly in females due to hormonal and fat distribution differences. Understanding these molecular mechanisms may guide the development of targeted therapies for obesity-related disorders.
dc.formatapplication/pdf
dc.identifier.urihttps://webofjournals.com/index.php/5/article/view/5319
dc.identifier.urihttps://asianeducationindex.com/handle/123456789/24933
dc.language.isoeng
dc.publisherWeb of Journals Publishing
dc.relationhttps://webofjournals.com/index.php/5/article/view/5319/5350
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/4.0
dc.sourceWeb of Medicine: Journal of Medicine, Practice and Nursing ; Vol. 3 No. 10 (2025): WOM; 215-218
dc.source2938-3765
dc.subjectLeptin, obesity, stress, xbp1, chop, grp78, resistance, adipose, gene, expression, women, cytokines, hormone, er, metabolism.
dc.titleENDOPLASMIC RETICULUM STRESS MARKERS EXPRESSION LEVELS IN LEPTIN RESISTANCE DEVELOPMENT
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.typePeer-reviewed Article

item.page.files

item.page.filesection.original.bundle

pagination.showing.labelpagination.showing.detail
loading.default
thumbnail.default.alt
item.page.filesection.name
qizi_2025_endoplasmic_reticulum_stress_markers_exp.pdf
item.page.filesection.size
330.28 KB
item.page.filesection.format
Adobe Portable Document Format

item.page.collections