The drug used was a caffeine salt but in the body it is metabolized to caffeine and sodium benzoate, so the effects are pretty much like those of caffeine. The concentration used (6microM - 60microM) corresponds to in vivo human dose of 30mg-300mg.
http://www.ncbi.nlm.nih.gov/pubmed/7456349
"...Sodium caffeine-benzoate at concentrations 6 x 10(-6) M and 6 x 10(-5) M increased the rate of free oxidation of succinic acid in myocardial mitochondria suggesting possibility of uncoupling of respiration and oxidative phosphorylation. The drug stimulates the free flow of electrons in respiratory chain. These phenomena might be responsible for an increase in metabolism and body temperature in patients after the treatment with this drug."
Another study, in vitro.
http://www.ncbi.nlm.nih.gov/pubmed/22710994
"...In HepG2 cells, caffeine induced a depolarisation of the inner mitochondrial membrane, a feature of mitochondrial thermogenesis, both directly and after 24 h incubation. Increased concentrations of uncoupling protein-2 (UCP-2) also indicated a thermogenic activity of caffeine. Energy generating pathways, such as mitochondrial respiration, fatty acid oxidation and anaerobic lactate production, were attenuated by caffeine treatment. Nevertheless, HepG2 cells demonstrated a higher energy charge potential after exposure to caffeine that might result from energy restoration through attenuation of energy consuming pathways, as typically found in hibernating animals. In 3T3-L1 cells, in contrast, caffeine increased fatty acid uptake, but did not affect lipid accumulation. We provide evidence that caffeine stimulates thermogenesis but concomitantly causes energy restoration that may compensate enhanced energy expenditure."
http://www.ncbi.nlm.nih.gov/pubmed/7456349
"...Sodium caffeine-benzoate at concentrations 6 x 10(-6) M and 6 x 10(-5) M increased the rate of free oxidation of succinic acid in myocardial mitochondria suggesting possibility of uncoupling of respiration and oxidative phosphorylation. The drug stimulates the free flow of electrons in respiratory chain. These phenomena might be responsible for an increase in metabolism and body temperature in patients after the treatment with this drug."
Another study, in vitro.
http://www.ncbi.nlm.nih.gov/pubmed/22710994
"...In HepG2 cells, caffeine induced a depolarisation of the inner mitochondrial membrane, a feature of mitochondrial thermogenesis, both directly and after 24 h incubation. Increased concentrations of uncoupling protein-2 (UCP-2) also indicated a thermogenic activity of caffeine. Energy generating pathways, such as mitochondrial respiration, fatty acid oxidation and anaerobic lactate production, were attenuated by caffeine treatment. Nevertheless, HepG2 cells demonstrated a higher energy charge potential after exposure to caffeine that might result from energy restoration through attenuation of energy consuming pathways, as typically found in hibernating animals. In 3T3-L1 cells, in contrast, caffeine increased fatty acid uptake, but did not affect lipid accumulation. We provide evidence that caffeine stimulates thermogenesis but concomitantly causes energy restoration that may compensate enhanced energy expenditure."
