Fig. 4: HMGA1 promotes lipid accumulation.

a Pathway analysis of differentially enriched metabolites in IECs from Hmga1^flox/flox mice as compared with those in IECs from Hmga1^△IEC mice. b Untargeted metabolomics was used to identify metabolites in IECs from Hmga1^△IEC and Hmga1^flox/flox mice. The heatmaps showed significantly up-regulated metabolites (left panel) and down-regulated metabolites (right panel) in IECs from Hmga1^△IEC mice. c Neutral lipids was assessed by oil red O staining in HMGA1-overexpressed HT-29 cells (Scale bar = 20 μm). d The relative levels of triglycerides, total cholesterol, and free fatty acids in HMGA1-overexpressed HT-29 cells. e Nile red staining of HMGA1-overexpressed HT-29 cells (Scale bar = 20 μm). n = 3. f, g Lipogenesis in the colorectum (CRC) from control and AOM/DSS-induced Rosa26^Hmga1/+ and Hmga1^IEC-OE/+ mice was determined by oil red O staining (f) (Scale bar = 20 μm) and nile red staining (g) (Scale bar = 50 μm) using frozen sections. n = 12. h HMGA1 overexpression and control HT-29 cells were cultured in glucose free DMEM in the presence of [U-¹³C] glucose (2 g/L) for 6 h. Saturated and monounsaturated FFAs labeled by ¹³C were analyzed using UHPLC-QTOF-MS-based nontargeted metabolomics. Data are presented as mean ± SD. Statistical significance was determined by two-tailed unpaired t-test (d, e, f, h) or hypergeometric test (a). Representative data from 3 independent experiments. IECs: intestinal epithelial cells. Source data are provided as a Source Data file.