Excess glucose shapes mitochondrial metabolism and redox state in human primary white adipocytes.
Herbers E., Moisio K., Torregrosa-Muñumer R., Karppinen JE., Heinonen S., van der Kolk BW.
Laboratory Study with a reported sample of 6, published in Free Radic Biol Med (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
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Free Radic Biol Med (2026)
- Country
- United States
- Reported sample size
- 6
- Source database
- PubMed
- PMID
- 42242596
- DOI
- 10.1016/j.freeradbiomed.2026.05.321
Abstract (original English)
Mitochondrial dysfunction in white adipose tissue (WAT) is a hallmark of obesity, yet nutrient-driven responses in adipocytes remain poorly defined, partly due to widespread use of supra-physiological glucose-rich media in in vitro adipocyte models. We used integrated transcriptomics, fluxomics, and functional analyses to assess how glucose availability shapes mitochondrial metabolism and redox status during human adipocyte differentiation. Primary human adipocytes (n = 6 donors) were differentiated in commonly used media containing high glucose (DMEM/F12, 17.6 mM; DMEM/HG, 25 mM), physiological glucose (LG, 5.5 mM), or galactose (Gal, 25 mM). High-glucose conditions were associated with a shift from oxidative phosphorylation toward glycolysis, reduced mitochondrial biogenesis, NADH accumulation, and elevated mitochondrial reactive oxygen species, accompanied by impaired insulin sensitivity, reduced adiponectin secretion, together with transcriptional signatures of inflammatory and stress-associated responses. Fluxomics revealed altered pyruvate flux, enhanced anaplerotic pathways, and upregulated anabolic programs. In contrast, LG and Gal conditions preserved mitochondrial and redox features, more closely resembling characteristics of healthy WAT. Collectively, these data define a metabolic phenotype, in which supra-physiological glucose is associated with redox imbalance and
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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