title: Effects of laparoscopic Roux-en-Y gastric bypass on glucose-6 phosphate dehydrogenase activity in obese type 2 diabetics.
abstract: BACKGROUND
  Glucose-6-phosphate dehydrogenase (G6PD) is the rate-limiting enzyme of the pentose phosphate pathway that provides the majority of NADPH required for lipid biosynthesis. G6PD overexpression has been implicated in insulin resistance, hyperlipidemia, and increased oxidative stress in animals. This study examines G6PD expression in obese diabetic and nondiabetic subjects pre- and post-laparoscopic Roux-en-Y gastric bypass (LRYGB).
  
  
  METHODS
  Patients undergoing LRYGB were recruited for the IRB-approved study and placed in either the diabetic (n = 11) or nondiabetic group (n = 16) (diabetic, HbA1c > 6.5%; nondiabetic, HbA1c < 6.0%). Blood samples were collected at baseline and throughout the first 3 postoperative months. Liver, adipose, and omental samples were taken during surgery. Results are expressed as mean ± SEM and were compared statistically using the Mann-Whitney test.
  
  
  RESULTS
  The two groups were not significantly different at baseline except for fasting glucose and HbA1c. G6PD activity (nm/min/mg protein) was significantly higher in red blood cells (RBCs) (3.12 ± 1.39 vs. 0.67 ± 0.14) and liver (17.23 ± 2.40 vs. 9.74 ± 2.18) in diabetics compared to nondiabetics. There was good correlation between increased liver G6PD activity and the severity of diabetes as measured by HbA1c (r (2) = 0.525) and fasting glucose (r (2) = 0.542). No significant difference was found in the adipose or omental G6PD expression. Both groups experienced a significant increase in G6PD blood activity shortly following surgery (1 week) followed by a reduction 3 months after surgery.
  
  
  CONCLUSIONS
  These results are the first ever seen in human subjects and demonstrate increased G6PD activity in diabetics compared to nondiabetics. These results suggest a correlation between G6PD activity and the severity of type 2 diabetes. The early increases in G6PD activity after LRYGB were unexpected and longer follow-up is needed to determine the effects of LRYGB on G6PD activity.
authors.affiliation: Department of Biomedical Sciences, University of South Alabama, College of Medicine, Mobile, AL, USA.
authors.forename: Andrew M
authors.initials: AM
authors.lastname: Schneider
authors.forename: Dhwajbahadur
authors.initials: D
authors.lastname: Rawat
authors.forename: L Steve
authors.initials: LS
authors.lastname: Weinstein
authors.forename: Sachin A
authors.initials: SA
authors.lastname: Gupte
authors.forename: William O
authors.initials: WO
authors.lastname: Richards
mesh_terms: D000273:Adipose Tissue / Q000201:enzymology; D000328:Adult; D003924:Diabetes Mellitus, Type 2 / Q000201:enzymology*; D004912:Erythrocytes / Q000201:enzymology; D005260:Female; D015390:Gastric Bypass / Q000379:methods*; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism*; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D010535:Laparoscopy / Q000379:methods*; D008099:Liver / Q000201:enzymology; D008297:Male; D008875:Middle Aged; D009767:Obesity, Morbid / Q000201:enzymology / Q000601:surgery*; D009852:Omentum / Q000201:enzymology
chemical_list: D005954:Glucosephosphate Dehydrogenase; D006442:Glycated Hemoglobin
references.citation: Mol Cell Biol. 2005 Jun;25(12):5146-57
references.pmid: 15923630
references.citation: Bioessays. 2004 Dec;26(12):1351-62
references.pmid: 15551269
references.citation: Endocrinology. 2011 Mar;152(3):793-803
references.pmid: 21248143
references.citation: Nutr Metab. 1975;19(1-2):45-54
references.pmid: 1226270
references.citation: Lancet. 2005 Sep 24-30;366(9491):1059-62
references.pmid: 16182882
references.citation: Diabetes. 1989 May;38(5):550-7
references.pmid: 2653926
references.citation: Eur J Endocrinol. 2003 Mar;148(3):293-300
references.pmid: 12611609
references.citation: Lancet. 2005 Oct 1;366(9492):1197-209
references.pmid: 16198769
references.citation: Diabetes. 2002 Jan;51(1):7-18
references.pmid: 11756317
references.citation: Curr Opin Investig Drugs. 2008 Sep;9(9):993-1000
references.pmid: 18729006
references.citation: J Gastrointest Surg. 2005 Nov;9(8):1112-6; discussion 1117-8
references.pmid: 16269382
references.citation: Nat Rev Mol Cell Biol. 2008 Mar;9(3):193-205
references.pmid: 18200017
references.citation: J Biol Chem. 1951 Nov;193(1):265-75
references.pmid: 14907713
references.citation: J Mol Med (Berl). 2002 Nov;80(11):696-702
references.pmid: 12436346
references.citation: J Clin Endocrinol Metab. 2003 Jul;88(7):3190-5
references.pmid: 12843164
references.citation: Gastroenterology. 2010 Aug;139(2):448-55
references.pmid: 20457158
references.citation: Free Radic Biol Med. 2009 Aug 1;47(3):219-28
references.pmid: 19230846
references.citation: Curr Pharm Des. 2006;12(26):3411-21
references.pmid: 17017935
references.citation: Ann Surg. 2010 Jun;251(6):1049-55
references.pmid: 20485144
references.citation: J Inherit Metab Dis. 2008 Jun;31(3):412-7
references.pmid: 18392752
references.citation: Endocrinology. 1992 Jan;130(1):43-52
references.pmid: 1727716
references.citation: J Clin Invest. 2005 May;115(5):1111-9
references.pmid: 15864338
references.citation: Cell Prolif. 2002 Jun;35(3):143-54
references.pmid: 12027950
references.citation: Diabetes Care. 2001 Feb;24(2):362-5
references.pmid: 11213893
references.citation: J Clin Invest. 2004 Dec;114(12):1752-61
references.pmid: 15599400
references.citation: Diabet Med. 2002 Jul;19(7):527-34
references.pmid: 12099954