Insulin-stimulated glucose uptake is impaired in senescent human adipocytes
Alexandersson I., Palmgren H., Uhrbom M., Oscarsson J., Boucher J.
Laboratory Study, published in Front Endocrinol (Lausanne) (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Laboratory Study
- Journal
- Front Endocrinol (Lausanne) (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41924527
- PMCID
- PMC13035520
- DOI
- 10.3389/fendo.2026.1795654
Abstract (original English)
Background Cell senescence, a state of cell cycle arrest induced by intrinsic or extrinsic stress, is linked to aging and aging-associated diseases. Senescence markers are elevated in adipose tissue with age and in obesity. Recently, it was shown that human mature adipocytes can undergo senescence in response to hyperinsulinemia. However, the functional consequences of adipocyte cell senescence remain poorly understood. Methods To study the impact of cellular senescence on human adipocyte function, we induced senescence in differentiated primary human preadipocytes (referred to as human adipocytes) using nutlin-3a, doxorubicin and etoposide. Expression of senescence markers, insulin receptor signaling, response to lipolytic stimuli and insulin mediated glucose uptake were investigated. Results The senescence-inducing compounds increased expression of senescence markers p21, p53, activity of senescence-associated β-galactosidase (SA-βgal) and secretion of senescence-associated secreted factors (SASP). We showed that insulin-stimulated glucose uptake, but not basal glucose uptake, was significantly reduced in senescent adipocytes. Insulin receptor signaling was largely unaffected, while expression of insulin receptor signaling proteins and especially GLUT4 expression were reduced. Expression of some adipocyte marker genes, including ADIPOQ, LEP , PNPLA2, LIPE and PPARγ2 , and sec
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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