What I have a problem with is a comment left at Jimmy's site that comes across as biased against and dismissive of the scientists who elucidated glyceroneogenesis:
"I actually had a look again at one of the so called ‘studies’ explaining this Glyceroneogenesis process in this post:
This study is basically flawed, even a layman like me can see things such as the fact that the test subjects were not keto-adapted and I believe that a total different set of rules apply for people who are not keto-adapted. There are some other flaws too, and I think at the end the basic biochemistry that Gary mentioned to in GCBC will carry more weight (take up a bigger part of a pie-chart of total processes) at the end."I'm not sure what study this person is referring to since I didn't reference any study (i.e. primary research) concerning glyceroneogenesis, only two review papers, but the quotation marks around the word studies, as well as the term so called, indicates to me that this person believes that the glyceroneogenesis research to date is either worthless, corrupted, laughable, or some combination of the three. I agree that keto-adaptation may affect the rate of glyceroneogenesis, but the fact that these researchers haven't examined that particular condition yet doesn't make their research "flawed". These scientists are not trying to prove or disprove any low carbohydrate diet theory; they are trying to understand basic biochemistry. And yes, glyceroneogenesis, although not well known, is a very important component of basic biochemistry because the ability to re-esterify fatty acids is critical to human metabolism.
I find it more than a bit ironic that an individual who appears to be an ardent fan of Taubes' Good Calories, Bad Calories would criticize the work of researchers who behave similarly to the "real" scientists lauded in the book. In this article, Richard Hanson, Ph.D., one of the discoverers of the glyceroneogenic pathway, tells us how his and his colleagues' desire to answer an intriguing question, brought about by a scientific observation, led them on the journey to uncover glyceroneogenesis:
"By 1967 it had been well established that both pyruvate carboxylase and PEPCK-C were involved in hepatic and renal gluconeogenesis. So it was a real surprise that year when John Ballard and I found pyruvate carboxylase in adipose tissue, a tissue that did not make glucose. We proposed that pyruvate carboxylase played an anaplerotic role (i.e. it replenished citric acid cycle anions) during lipogenesis in adipose tissue, because citrate efflux from the mitochondria depletes intermediates of the citric acid cycle. This is similar to the function of the enzyme in the liver during gluconeogenesis. We came to the totally incorrect conclusion that there were both mitochondrial and cytosolic forms of the pyruvate carboxylase in adipose tissue. It turned out that it is easy to break mitochondria during their isolation from adipose tissue and thus release the enzyme. In the same year, John and I, together with Gilbert Leveille, reported that adipose tissue also contained PEPCK-C. What was this gluconeogenic enzyme doing in a tissue that does not make glucose?"And the rest is scientific history. Something tells me Gary would approve.