# Bariatric and metabolic surgery improves glycolipid metabolism via bile acid regulation and intestinal barrier repair in T2DM patients **Authors:** Jingjing Zhang, Shadike Apaer, Shuo Zhang, Guanyou Liang, Tao Li, Xinling Cao PMC · DOI: 10.5937/jomb0-58245 · Journal of Medical Biochemistry · 2026-01-06 ## TL;DR Bariatric surgery improves blood sugar and fat metabolism in diabetes patients by regulating bile acids and repairing the gut barrier. ## Contribution This study identifies bile acid regulation and intestinal barrier repair as key mechanisms behind the metabolic benefits of bariatric surgery in T2DM patients. ## Key findings - Bariatric surgery significantly reduced weight and improved glucose-lipid metabolism in T2DM patients. - Surgery altered bile acid-related enzyme activity, with decreased CYP7A1 and increased FXR and FGF19. - Intestinal barrier markers D-LA and Zonulin decreased post-surgery, indicating improved gut function. ## Abstract To observe the changes in bile acid synthase activity, conjugation enzyme gene and intestinal mucosal barrier function (D-LA, Zonulin, MFG-E8) in patients with type 2 diabetes mellitus (T2DM) after bariatric and metabolic surgery (BMS), and to provide an objective opinion on the clinical optimisation of BMS. 127 patients with T2DM who had received BMS treatment at our hospital from October 2023 to August 2024 were included in the study, and weight loss glucose-lipid metabolism was detected before surgery and 6 months after surgery. Furthermore, the study quantified the expression levels of key enzymes involved in bile acid synthesis and conjugation (CYP7A1, CYP27A1, FXR, FGF19) and markers indicative of intestinal mucosal barrier function (D-LA, Zonulin, MFG-E8). After BMS, the patient's weight was significantly reduced, and glucolipid metabolism was significantly improved (P< 0.05). In addition, CYP7A1 was decreased, and FXR and FGF19 were elevated in patients after surgery (P < 0.05). Regarding the intestinal mucosal barrier function, D-LA and Zonulin were reduced in patients after surgery (P< 0.05). MFG-E8 was not significantly altered. BMS can effectively improve glucose-lipid metabolism and reduce body weight in T2DM patients, and its mechanism is related to regulating bile acid metabolism and promoting the recovery of intestinal barrier function. ## Linked entities - **Genes:** CYP7A1 (cytochrome P450 family 7 subfamily A member 1) [NCBI Gene 1581], CYP27A1 (cytochrome P450 family 27 subfamily A member 1) [NCBI Gene 1593], NR1H4 (nuclear receptor subfamily 1 group H member 4) [NCBI Gene 9971], FGF19 (fibroblast growth factor 19) [NCBI Gene 9965] - **Diseases:** type 2 diabetes mellitus (MONDO:0005148), T2DM (MONDO:0005148) ## Full-text entities - **Genes:** GAPDH (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 2597] {aka G3PD, GAPD, HEL-S-162eP}, TJP1 (tight junction protein 1) [NCBI Gene 7082] {aka ZO-1}, FASN (fatty acid synthase) [NCBI Gene 2194] {aka FAS, OA-519, SDR27X1}, NR1H4 (nuclear receptor subfamily 1 group H member 4) [NCBI Gene 9971] {aka BAR, FXR, HRR-1, HRR1, PFIC5, RIP14}, CYP27A1 (cytochrome P450 family 27 subfamily A member 1) [NCBI Gene 1593] {aka CP27, CTX, CYP27}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, MFGE8 (milk fat globule EGF and factor V/VIII domain containing) [NCBI Gene 4240] {aka BA46, EDIL1, HMFG, HsT19888, MFG-E8, MFGM}, GPBAR1 (G protein-coupled bile acid receptor 1) [NCBI Gene 151306] {aka BG37, GPCR19, GPR131, M-BAR, TGR5}, FAS (Fas cell surface death receptor) [NCBI Gene 355] {aka ALPS1A, APO-1, APT1, CD95, FAS1, FASTM}, FGF19 (fibroblast growth factor 19) [NCBI Gene 9965], SLC27A5 (solute carrier family 27 member 5) [NCBI Gene 10998] {aka ACSB, ACSVL6, BACS, BAL, FACVL3, FATP-5}, CYP8B1 (cytochrome P450 family 8 subfamily B member 1) [NCBI Gene 1582] {aka CP8B, CYP12, CYPVIIIB1}, HP (haptoglobin) [NCBI Gene 3240] {aka HP2ALPHA2, HPA1S}, PCK2 (phosphoenolpyruvate carboxykinase 2, mitochondrial) [NCBI Gene 5106] {aka PEPCK, PEPCK-M, PEPCK2, mtPCK2}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, CYP7A1 (cytochrome P450 family 7 subfamily A member 1) [NCBI Gene 1581] {aka CP7A, CYP7, CYPVII}, CLDN4 (claudin 4) [NCBI Gene 1364] {aka CPE-R, CPER, CPETR, CPETR1, WBSCR8, hCPE-R}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R} - **Diseases:** T2DM (MESH:D003924), cognitive impairments (MESH:D003072), endotoxemia (MESH:D019446), gastrointestinal disorders (MESH:D005767), insulin resistance (MESH:D007333), weight loss (MESH:D015431), obesity (MESH:D009765), function (MESH:D003291), metabolic disorders (MESH:D008659), hyperglycemia (MESH:D006943), gastroesophageal reflux (MESH:D005764), inflammation (MESH:D007249), DM (MESH:D003920), malignancies (MESH:D009369), psychiatric (MESH:D001523), alcohol or drug abuse (MESH:D019966), glucose metabolism disorders (MESH:D044882) - **Chemicals:** UDCA (MESH:D014580), SYBR Green (MESH:C098022), lipid (MESH:D008055), glucose (MESH:D005947), Bile acid (MESH:D001647), BMS (-), lithocholic acid (MESH:D008095), TRIzol (MESH:C411644), glycogen (MESH:D006003), glycolipid (MESH:D006017), cholesterol (MESH:D002784), vitamin D (MESH:D014807), DCA (MESH:D003840), D-LA (MESH:D019344), TG (MESH:D014280) - **Species:** Homo sapiens (human, species) [taxon 9606] ## Full text _Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12967183/full.md ## Figures 4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12967183/full.md ## References 32 references — full list in the complete paper: https://tomesphere.com/paper/PMC12967183/full.md --- Source: https://tomesphere.com/paper/PMC12967183