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