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Low-carb and Mediterranean diets beat low-fat for weight-loss,lipid changes at two years
HbA1c
LoFat 0.4% Med 0.5% LoCarb 0.9% fBG (1 yr, 2 yr mg/dL) LoFat Med -23.6, -32.8 LoCarb -18.1, 1.2 *But why the reduction of HbA1c behaved differently from fasting plasma glucose and HOMA-IR, so that it was larger in low-carb group than in the Med group, is a mystery to me, too. *Perhaps people familiar with diabetes could have some kind of explanation or speculation about this? Is it possible that a low-carb diet shifts cellular machinery towards efficient fat metab, decreasing carb metab efficiency, thus increasing insulin resistance. I'm not sure if HOMA takes this into account. Ideally, insulin resistance should be tested after all three groups are returned to a reference diet at the end of trials. An improved cholestrol profile and Hb1Ac may not relate to improved fBG and IR due to additional factors. For example, loCarb will likely give lower HbA1c. But loCarb is higher in lipophilic toxins (ie PCBs, dixions, etc). TCDD, a potent dioxin, increases mito ROS. Cellular ROS is likely to increase insulin resistance. Lipophilic toxins are highest in animal, fish, dairy & egg fats. [TCDD decreases ATP levels and increases reactive oxygen production through changes in mitochondrial F(0)F(1)-ATP synthase and ubiquinone.] Mitochondria generate ATP and participate in signal transduction and cellular pathology and/or cell death. TCDD (2,3,7,8-tetrachlorodibenzo- p-dioxin) decreases hepatic ATP levels and generates mitochondrial oxidative DNA damage, which is exacerbated by increasing mitochondrial glutathione redox state and by inner membrane hyperpolarization. This study identifies mitochondrial targets of TCDD that initiate and sustain reactive oxygen production and decreased ATP levels. One week after treating mice with TCDD, liver ubiquinone (Q) levels were significantly decreased, while rates of succinoxidase and Q-cytochrome c oxidoreductase activities were increased. However, the expected increase in Q reduction state following TCDD treatment did not occur; instead, Q was more oxidized. These results could be explained by an ATP synthase defect, a premise supported by the unusual finding that TCDD lowers ATP/O ratios without concomitant changes in respiratory control ratios. Such results suggest either a futile cycle in ATP synthesis, or hydrolysis of newly synthesized ATP prior to release. The TCDD-mediated decrease in Q, concomitant with an increase in respiration, increases complex 3 redox cycling. This acts in concert with glutathione to increase membrane potential and reactive oxygen production. The proposed defect in ATP synthase explains both the greater respiratory rates and the lower tissue ATP levels. PMID: 17109908 |
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