Its physiologic role in modulating energy metabolism. In contrast to the modest phenotypes seen in CTRP2 Tg mice, overexpressing the related CTRP family members�CCTRP1, CTRP3, and CTRP9�Cin mice using a similar transgenic approach has resulted in significant improvements in the metabolic profiles of these animals compared to WT littermate controls. When fed an HFD, CTRP1 Tg mice have lower body weights due to increased energy expenditure, leading to greater systemic insulin sensitivity. CTRP1 Tg mice also have higher basal AMPK activation in the skeletal muscle, leading to enhanced fat oxidation. While no differences in body weight, energy expenditure, and glucose tolerance are Ganoderic-acid-G observed between CTRP3 Tg and WT mice, the transgenic animals are strikingly resistant to the development of fatty liver in response to high-fat feeding. Overexpressing CTRP3 in mice suppresses the expression of genes involved in triglyceride synthesis, leading to decreased triglyceride accumulation in the liver of the Tg animals. Of the CTRP Tg mouse models described to date, the most dramatic and striking phenotypes are observed in mice overexpressing CTRP9. CTRP9 Tg mice are lean and resistant to weight gain when fed an HFD. All the metabolic dysfunctions associated with high-fat feeding are prevented in CTRP9 Tg mice. These remarkable metabolic phenotypes are due to a combination of reduced caloric intake and increased energy metabolism. The present study and recent findings using transgenic mouse models suggest that each CTRP has a unique role in regulating glucose and/or lipid metabolism in vivo, consistent with their high degree of conservation throughout vertebrate evolution. Nevertheless, descriptive observations support the hypothesis that tubal implantation is likely caused by embryo retention within the Kaempferide Fallopian tube due to impaired tubal transport and alterations in the tubal microenvironment allowing early implantation to occur. Transport of the embryo through the Fallopian tube is controlled by a combination of smooth muscle contractility and ciliary beating. The factors that regulate and maintain the normal tubal microenvironment are largely unknown. Epidemiological studies have shown that cigarette smoking is a major risk factor for tubal ectopic pregnancy. Animal and human studies have demonstrated effects on oviductal/Fallopian tube function resulting from smoke exposure. Despite these findings, the exact mechanism by which cigarette smoking leads to ectopic pregnancy remains uncertain. We recently reported that cotinine increases the expression of prokineticin PROKR1 in the Fallopian tube, a regulator of smooth muscle contractility and a gene thought to be important for intrauterine implantation. We proposed that cigarette smoking attenuates tubal PROKR1 expression resulting in changes in Fallopian tube function, providing a possible explanation for the link between smoking and tubal ectopic pregnancy. In this study, we take this finding forward by investigating how smoking alters global gene expression and function of tubal epithelial cells. Our in vitro array studies indicate that cotinine exposure appears to affect expression of genes involved in epithelial cell turnover.