Is Intestinal Gluconeogenesis a Key Factor in the Early Changes in Glucose Homeostasis Following Gastric Bypass?
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  • 作者:Mark Thomas Hayes (1)
    Jonathan Foo (1) (2)
    Vinko Besic (1)
    Yulia Tychinskaya (2)
    Richard Strawson Stubbs (1) (2)
  • 关键词:Intestinal gluconeogenesis ; Portal sensor ; Gastric bypass surgery ; Resolution of diabetes
  • 刊名:Obesity Surgery
  • 出版年:2011
  • 出版时间:June 2011
  • 年:2011
  • 卷:21
  • 期:6
  • 页码:759-762
  • 全文大小:93KB
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  • 作者单位:Mark Thomas Hayes (1)
    Jonathan Foo (1) (2)
    Vinko Besic (1)
    Yulia Tychinskaya (2)
    Richard Strawson Stubbs (1) (2)

    1. Wakefield Biomedical Research Unit, University of Otago, Wellington, New Zealand
    2. The Wakefield Clinic, Wakefield Hospital, Wellington, New Zealand
文摘
Background In 2008, Troy et al. hypothesised that under fasting conditions, intestinal gluconeogenesis generates glucose levels in the portal vein which trigger the portal sensor to change insulin resistance and that this mechanism contributes to the effects of Roux-en-Y gastric bypass (RYGB) surgery on type 2 diabetes mellitus (T2DM). In a recent paper, Kashyap et al. (Int J Obes 34(3):426-71, 2010) cited this hypothesis as a potential explanation for the early changes in insulin sensitivity and beta cell function seen after RYGB. We proposed a study to examine this possibility. Methods We simultaneously sampled fasting portal venous blood and central venous blood in 28 patients (eight diabetics and 20 non-diabetics) before and again six days after RYGB surgery in morbidly obese patients, for measurement of glucose levels. Results We found no significant difference in the glucose levels from the two sites either before or after RYGB in diabetic patients and a small, but significant difference in the post-operative glucose levels from non-diabetic patients (4.2 vs 4.0?mM, p-lt;-.0001). Conclusions Direct simultaneous measurement of fasting glucose in portal and central venous blood before and 6?days after RYGB provides no evidence to support the hypothesis that intestinal gluconeogenesis contributes to the resolution of T2DM seen after RYGB.

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