“…Indeed, initial studies that applied the power of transcriptomics and genetics further stressed male-female differential use of lipids and carbohydrates and pinpointed some of the molecular pathways involved. The transcriptomic profiling and biochemical analyses in rodents indicated that about 10% of the transcriptionally active genes in the liver have a sex-dependent expression; transcripts for the synthesis of triglycerides, cholesterol, and very-low-density lipoprotein (VLDL) particles were more expressed in females while genes for FA oxidation, gluconeogenesis, and glycogen synthesis were predominant in males, further stressing the tendency of females to privilege lipid synthesis and males to create large glycogen stores ( Hagve and Christophersen, 1986 , Ivey and Gaesser, 1987 , Kushlan et al., 1981 , Lorbek et al., 2013 , Mauvais-Jarvis, 2015 , Price and Sanders, 2017 , Tarnopolsky and Ruby, 2001 ). Experiments done with mutants of PPARα (the master regulator of FA oxidation) showed that in PPARα −/− mice the pharmacological inhibition of FA oxidation leads to lipid accumulation and death for hypoglycemia mainly in males, while only 25% of females undergoing the same treatment die because of their major ability to oxidize FAs even in the absence of the PPARα receptor ( Djouadi et al., 1998 ).…”