the literature, as almost all the reported studies combined varying proportions of male and female subjects within each experimental group. Nevertheless, these data demonstrate that there is a gender specific regulation and function of CTRP3 that needs to be explored in more detail. Further, all of these studies have examined the total amount of CTRP3 with no attention being given to the different splice variants or in the multimeric structures of the circulating CTRP3. This is worth noting as high molecular weight adiponectin is thought to be the active form (20, 32), and similarly the different splice variants and multimeric structure may also contribute to the function of CTRP3. Lastly, the associations between circulating CTRP3 levels (splice variants and multimeric structures) and hepatic steatosis in human subjects have not been explored even though animal experiments have shown a specific hepatic effect of both CTRP3A and CTRP3B (51).