Active Low-Carber Forums - View Single Post - Is a zero carb diet sustainable?

Quote:

Originally Posted by Liz53

Thanks, makes sense. I'm also going to copy and paste an earlier question that you may not have seen in this volley - I wonder if you have knowledge/opinions:

Has anyone read any convincing studies or observations on when the body converts "excess" protein to glucose? Is it any time that the body ingests more protein than it needs for immediate repair? Or is it dependent on the body (or the brain, most likely) needing a bit of glucose at the moment and protein is available? If both carbs and protein were available, would it be more likely to engage in direct carb burning or gluconeogenesis? Can/will the body convert protein to fat for storage or is gluconeogenesis the only mechanism for using that excess protein?

Closest thing I've seen is this;

http://www.ketotic.org/2012/08/if-y...rn.html#⁵

But it doesn't quite address our issue; we need something specific, where levels of gluconeogenesis on a very low carb diet in response to various fat vs protein ratios are measured.

It doesn't seem to be very hard to find an expert or guru who'll take either position--extra protein will be made into glucose, or only the amount you need will be synthesized, any other extra protein simply oxidized for energy. I've seen Dr. Michael Eades take this second stance a number of times.

This bit;

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It was therefore proposed by Cahill, Felig, and Marliss and their associates (7, 12, 13, 20) that the reduced glucose production rate in starvation was due to the reduced availability of gluconeogenic substrates; hence, gluconeogenic precursor supply was rate-limiting for glucose production rate.

Which probably comes closest to the point, now that I look at it again.

Think I'm switching sides here, at least when in the highly-ketogenic state that parallels fasting.

They counter this here;

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In contrast, the findings of several kinetic studies performed in human and dog do not support this proposal (1, 30, 34, 38). These studies in postabsorptive subjects employed either the isotope dilution or hepatic vein catheterization techniques and failed to show any significant change in glucose production rate in response to infusions of substantial quantities of alanine, lactate, and glycerol even when there was a fivefold increase in the hepatic uptake of the infused substrate

But here, they're just plain wrong. In starvation, most of the glucose production comes from gluconeogenesis. During a shorter term fast (postabsorptive) most of the glucose produced will come from the break down of glycogen. In the first case, gluconeogenesis may actually be rate-limiting for glucose production, in the second, it's not--so increased substrate wouldn't necessarily increase glucose appearance rate.

Quote:

Our data so far indicate that under almost any physiological situation, an increase in gluconeogenic precursor supply alone will not drive glucose production to a higher level, suggesting that factors directly regulating the activity of the rate-limiting enzyme(s) of glucose production normally are the sole determinants of the rate of production; hence, there will be no increase in glucose production if the increase in gluconeogenic precursor supply occurred in the absence of stimulation of the gluconeogenic system.

They seem to make the mistake of assuming that glucose appearance is a good proxy for gluconeogenesis, when it just plain isn't. Which I find kind of disappointing--since I love that they're at least trying to address this issue in some sort of organized way.