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Proteomics Data of Kaempferol Treatment on Podocytes in High Glucose Models.

ABSTRACT: Proteomic analysis of podocyte alterations in high glucose models, combined with statistical assessment of differential protein restoration following kaempferol intervention, facilitates screening for potential diabetic nephropathy biomarkers. KEGG and GO enrichment analyses reveal multiple autophagy-related signaling pathways, indicating that kaempferol may alleviate high-glucose-induced podocyte injury through autophagy regulation.

ORGANISM(S): Mus Musculus

SUBMITTER: Hua Zheng

PROVIDER: PXD068234 | iProX | Tue Sep 09 00:00:00 BST 2025

REPOSITORIES: iProX

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Project description:Background: Systemic glucose homeostasis is affected by adipose cell function. Still, the cellular events preceding the onset of insulin resistance in adipocytes are not yet resolved. To capture the immediate cellular changes during diet-induced expansion of cell volume and number, we characterized the initial changes in mature adipocytes during a short high fat diet (HFD) intervention. Methods: C57BL6/J male mice were fed chow diet, and switched to HFD for 2, 4, 6 or 14 days. Systemic glucose clearance was assessed by glucose tolerance test. Adipose tissue was dissected for RNA seq analysis and cell size distribution analyzed using coulter counter technique. Insulin response in isolated adipocytes was measured by glucose uptake and Western blotting of insulin signaling intermediates. Confocal microscopy was used to assess autophagic flux in cells pre-incubated with rapamycin and chloroquine. Results: Switching to HFD was accompanied by an immediate adipose cell size expansion followed by recruitment of new adipocytes. Despite an increase in both basal and insulin-stimulated glucose uptake in adipocytes, we observed a progressive decrease in insulin-stimulated activation of Protein Kinase B (PKB) Ser473, PKB Thr308 and Akt substrate of 160 (AS160) Tyr642, and onset of systemic insulin-resistance already after two days. Moreover, RNA-seq analysis of adipose tissue revealed marked changes in gene expression at day four, of which the most significant included genes directly involved in autophagy (Trp53Inp2 and Beclin1). Enhanced autophagy was observed in isolated adipocytes from HFD-fed mice, detected as an increased density of LC3-positive puncta by confocal microscopy, and increase of LC3II. Conclusions: HFD rapidly caused impaired insulin signal transduction in adipocytes, while both basal and insulin-stimulated glucose uptake increased, which support the concept of spare signaling. Interestingly, our data suggests autophagy as one of the early cellular events that could contribute to insulin resistance.

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Proteomics Data of Kaempferol Treatment on Podocytes in High Glucose Models.

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