Dear Rachael, can you give me the full reference on the Peronnet & Massciotte, 1991 paper? If you have a PDF version, can you send it to my e-mail address: [email protected].
There are means of measuring or estimating rates of substrate oxidation, using isotopic tracers and/or respirometry. The calculations work across taxa, but the measurements themselves require some effort.
See the seminal paper by Frayn (1983) and a recent application of the technique by Houser et al (2012). McCue developed a similar methodology using isotopic tracers captured in exhaled breath (2010).
Article Calculation of substrate oxidation rates in vivo from gaseous exchange
It is difficult to account with precision the ratio of carbohydrates and fat utilization. Probably, as mentioned by Cory Champagne, isotopic tracers + respirometry will help. With isolated mitochondria I have found that the usual usage of substrates: sucinate+rotenone; glutamate+malate; pyruvate+malate is not informative, particularly when comparing mitochondria from different organs. Usage of succinate + rotenine is particularly stupid. Unfortunately, to this day I did not published in full my data on physiological mixtures of substrates, except for brain and spinal cord mitochondria (see my ResearchGate account). Though, in my book "Practical Mitochcomdriology. Pitfalls and Problems in Studies of Mitochondria" I presented polarographic evidence of sharp increase in the efficiency of oxidative phosphorylation with heart mitochondria simultaneosly oxidizing palmitoyl-carnitine and a substrate originated from carbohydrates (pyruvate, succinate) or aminoacid (glutamate). Simultaneosly, there is a several-fold increase in production of ROS. This means, that under situations of increased oxidation of fatty acids (metabolic syndrome) the primary danger is not in development of atherosclerosis, but in increased Oxidatiove Stress. Thus mitochondria in each organ have particular mixture of substrates. Bouever, this problem is very poorly studied.