Ketosis leads to increased methylglyoxal production on the Atkins diet

被引:48
作者
Beisswenger, BGK
Delucia, EM
Lapoint, N
Sanford, RJ
Beisswenger, PJ
机构
[1] Dartmouth Coll Sch Med, Dept Med, Endocrinol Sect, Hanover, NH 03756 USA
[2] Dartmouth Coll Sch Med, Dept Med, Sect Diabet & Metab, Hanover, NH 03756 USA
来源
MAILLARD REACTION: CHEMISTRY AT THE INTERFACE OF NUTRITION, AGING, AND DISEASE | 2005年 / 1043卷
关键词
Atkins diet; ketosis; methylglyoxal; acetone; acetol;
D O I
10.1196/annals.1333.025
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In the popular and widely used Atkins diet, the body burns fat as its main fuel. This process produces ketosis and hence increased levels of Phydroxybutyrate (BOB) acetoacetate (AcAc) and its by-products acetone and acetol. These products are potential precursors of the glycotoxin methylglyoxal. Since methylglyoxal and its byproducts are recognized as a significant cause of blood vessel and tissue damage, we measured methylglyoxal, acetone, and acetol in subjects on the Atkins diet. We found that by 14-28 days, methylghyoxal levels rose 1.67-fold (P = 0.039) and acetol and acetone levels increased 2.7and 6.12-fold, respectively (P = 0.012 and 0.028). Samples from subjects with ketosis showed even greater increases in methylglyoxal (2.12-fold), as well as acetol and acetone, which increased 4.19- and 7.9-fold, respectively; while no changes were seen in samples from noncompliant, nonketotic subjects. The increase in methylglyoxal implies that potential tissue and vascular damage can occur on the Atkins diet and should be considered when choosing a weight-loss program.
引用
收藏
页码:201 / 210
页数:10
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