Basically, diazoxide is a compound that has been used to treat hypoglycemia and reduces insulin secretion. Two groups of 12 obese hyperinsulinemic adults were treated with diazoxide or placebo for 8 weeks while each consuming the same Optifast diet. Compared with the placebo group, DZ subjects had greater weight loss (9.5 ± 0.69% vs. 4.6 ± 0.61%, P < 0.001), greater decrease in body fat (P < 0.01), greater increase in fat-free mass to body fat ratio (P < 0.01), and greater attenuation of acute insulin response to glucose (P < 0.01). This is pretty phenomenal and difficult to fathom -- almost twice the weight loss. It was also reported that there was no significant change in resting energy expenditure (REE, RMR, BMR), and substrate use, as derived from indirect calorimetry, did not reveal any significant change in carbohydrate or fat metabolism in either group. IOW, there was no stimulation of fatty acid oxidation accompanying the proposed decreased lipogenesis (presumably they're referring to esterification not de novo lipogenesis) and/or increased lipolysis (as evidenced by increases in FFA/NEFA levels).
Now, some may accuse me of rationalizing, but for all the claims I may disagree with, I have yet to see any of the "experts" -- even Taubes and Eades and the MA crowd -- imply that fatty acids can magically be "flushed" from the body without being "burnt" off (beta oxidation). The only way out is for the LCFA to be broken down ultimately to CO2. Therefore, there HAS to be an explanation here because insulin is not a magic molecule capable of creating or destroying matter. If the diazoxide (DZ) didn't lead to increased fatty acid oxidation, and REE was unchanged, then likely futile cycling and uncoupling were not involved either -- these would cause increases in both FA oxidation and REE as they "blow off" or "waste" fatty acids.
So ... where did the fatty acid mass go?
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