title: Alleviation of podocyte injury: the possible pathway implicated in anti-inflammation of alpha-lipoic acid in type 2 diabetics.
abstract: OBJECTIVE
  The objective of this study is to observe the effect of alpha-lipoic acid (ALA) on Pod injury by anti-inflammation and explore its possible renal protective mechanism.
  
  
  METHODS
  A total of 36 cases with type 2 diabetes with microalbuminuria and fasting plasma glucose (FPG) levels less than 9 mmol/L and glycated hemoglobin A1c (HbA1c) ≤9.0 % were recruited to be treated with ALA (600 mg, daily) for 6 months (group DA). Another 30 healthy individuals were chosen as normal controls (group NC). The levels of serum creatinine (Cr), FPG, and HbA1c were detected; blood pressure was recorded; and early morning urine samples (corrected for urinary Cr) were collected for the examination of urinary monocyte chemoattractant protein-1 (MCP-1), transforming growth factor-β1 (TGF-β1), podocalyxin (PCX), nephrin, albumin and Cr in group NC and group DA at the baseline and the sixth month.
  
  
  RESULTS
  The excretions of urinary MCP-1, TGF-β1, PCX, nephrin and albumin to Cr ratio (abbreviated as UMCR, UTCR, UPCR, UNCR and UACR respectively) were significantly increased in group DA compared with group NC (all P < 0.01), and after 6-month treatment, all indexes mentioned above decreased markedly (P < 0.05), while FPG and HbA1c had no obvious changes. Additionally, there was a positive correlation between UMCR, UTCR with UPCR, UNCR and UACR, respectively (all P < 0.01).
  
  
  CONCLUSIONS
  Anti-inflammation of ALA in vivo and local kidney is implicated in the protection of glomerular Pod injury in patients with type 2 diabetes.
authors.affiliation: Department of Endocrinology, Anhui Provincial Hospital Affiliated to Anhui Medical University, Hefei, 230001, China.
authors.forename: Xi-He
authors.initials: XH
authors.lastname: Bao
authors.forename: Jiang
authors.initials: J
authors.lastname: Xu
authors.forename: Yan
authors.initials: Y
authors.lastname: Chen
authors.forename: Chun-Lin
authors.initials: CL
authors.lastname: Yang
authors.forename: Shan-Dong
authors.initials: SD
authors.lastname: Ye
mesh_terms: D000328:Adult; D000418:Albumins / Q000032:analysis; D000893:Anti-Inflammatory Agents / Q000737:chemistry; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000652:urine; D003404:Creatinine / Q000097:blood / Q000652:urine; D003924:Diabetes Mellitus, Type 2 / Q000276:immunology*; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007249:Inflammation; D008297:Male; D008565:Membrane Proteins / Q000652:urine; D008875:Middle Aged; D009000:Monocytes / Q000166:cytology; D050199:Podocytes / Q000166:cytology / Q000473:pathology*; D012795:Sialoglycoproteins / Q000652:urine; D015398:Signal Transduction; D008063:Thioctic Acid / Q000737:chemistry*; D053773:Transforming Growth Factor beta1 / Q000652:urine
chemical_list: D000418:Albumins; D000893:Anti-Inflammatory Agents; D001786:Blood Glucose; D018932:Chemokine CCL2; D003404:Creatinine; D006442:Glycated Hemoglobin; D008565:Membrane Proteins; D012795:Sialoglycoproteins; D008063:Thioctic Acid; D053773:Transforming Growth Factor beta1; C111835:CCL2 protein, human; C517652:hemoglobin A1c protein, human; C113267:nephrin; C001643:podocalyxin