ArticleCell death & disease2024
Advanced glycation end-products accelerate amyloid deposits in adipocyte's lipid droplets.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Brazilin attenuates methylglyoxal‑induced endothelial injury by enhancing eIF5A hypusination and inhibiting the AMPK/mTOR‑mediated autophagy/apoptosis axisInternational journal of molecular medicine · 2026Article
- Advanced glycation end products drive blood-brain barrier lipid dysregulation via RAGE-ABCA1 signaling to promote neurovascular dysfunction in Alzheimer's disease.Molecular psychiatry · 2026Article
- β-Hydroxybutyrate attenuates glycation-induced structural destabilization and amyloidogenic aggregation in human serum albumin.Biochemistry and biophysics reports · 2026Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adipose tissue dysfunction is central to insulin resistance, and the emergence of type 2 diabetes (T2D) is associated with elevated levels of carbonyl metabolites from glucose metabolism. In this study, using methylglyoxal (MGO) and glycolaldehyde (GAD) carbonyl metabolites induced protein glycation, leading to misfolding and β-sheet formation and generation of advanced glycation end products (AGEs). The formed AGEs compromise adipocytes activity. Microscopic and spectroscopic assays were used to examine the impact of MGO and GAD on lipid droplet-associated proteins. The results provide information about how these conditions lead to the appearance of glycated and amyloidogenic proteins formation that hinders metabolism and autophagy in adipocytes. We measured the beneficial effects of metformin (MET), an anti-diabetic drug, on misfolded protein as assessed by thioflavin (ThT) spectroscopy and improved autophagy, determined by LC3 staining. In vitro findings were complemented by in vivo analysis of white adipose tissue (WAT), where lipid droplet-associated β-amyloid deposits were predominantly linked to adipose triglyceride lipase (ATGL), a lipid droplet protein. Bioinformatics, imaging, biochemical and MS/MS methods affirm ATGL's glycation and its role in β-sheet secondary structure formation. Our results highlighted the pronounced presence of amyloidogenic proteins in adipocytes treated with carbonyl compounds, potentially reshaping our understanding of adipocyte altered activity in the context of T2D. This in-depth exploration offers novel perspectives on related pathophysiology and underscores the potential of adipocytes as pivotal therapeutic targets, bridging T2D, amyloidosis, protein glycation, and adipocyte malfunction.
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