In the article, Post-Starvation Gene Expression of Skeletal Muscle Uncoupling Protein 2 and Uncoupling Protein 3 in Response to Dietary Fat Levels and Fatty Acid Composition, published in the February 01, 1999 issue of Diabetes, Abdul G. Abdul presents studies that examine post-starvation gene transcription of muscle UCP2 and UCP3 during re feeding on diets varying in fat levels and fat types (Abdul). These studies "raise the possibility that high-fat induced upregulation of muscle UCP2 and UCP3 may be more closely linked to the development of insulin resistance rather than to changes in circulating FFAs" (Abdul). The studies also provide additional data that are at variance with a role for skeletal muscle UCP2 and UCP3 in dietary regulation of thermogenesis, "but remain consistent with the hypothesis that these UCP homologs may function as regulators of lipids as fuel substrate" (Abdul). .

             UCP2 and UCP3 are two recently cloned genes with high sequence homology to the "gene for uncoupling protein (UCP)-I, which regulates thermogenesis in brown adipose tissue" (Abdul). The recent association, in obese and diabetic humans, between polymorphisms in UCP3 with marked reduction in basal lipid oxidation and not with differences in resting metabolic rate would also be consistent with this proposal of a physiological role for UCP3 in regulating lipids as fuel substrate rather than in regulating thermogenesis (Abdul).

             In the August 01, 2004 issue of Emerging Infectious Diseases, Ben Adler gives his perspective in an article titled Genomic-scale analysis of bacterial gene and protein expression in the host (Adler). Adler begins, "The developing complementary technologies of DNA microarrays and proteomics are allowing the response of bacterial pathogens to different environments to be probed at the whole genome level" (Adler). While using these technologies to analyze pathogens within a host is its initial stages, present studies suggest that these technologies will be valuable tools for understanding how the pathogen reacts to the in vivo microenvironment (Adler).