Angiotensin II and its type 1 receptor (AT1R) are both expressed in the adipose tissue and involved in the genesis of atherosclerosis as well as hypertension. However, the influence of the AT1R gene A1166C polymorphism on atherosclerosis risk factors and on the development of early atherosclerosis is not clear. We evaluated 416 healthy young women to investigate the effects of this genotype on atherosclerosis risk factors and on carotid intima-media thickness as a validated marker of early atherosclerosis. After adjusting for confounding factors including body mass index, homeostasis model assessment of insulin resistance and plasma high-density lipoprotein (HDL)-cholesterol levels, plasma adiponectin concentrations were significantly lower in carriers of the C allele compared with non-carriers. Moreover, multiple logistic regression analysis showed that the C allele was the strongest and most independent determinant of lower plasma adiponectin concentrations. It is noted that the participants with the lowest quartile of plasma adiponectin concentrations had thicker levels of carotid intima-media thickness, lower plasma HDL-cholesterol and lipoprotein lipase levels, as well as higher trunk fat mass compared with the highest quartile. In addition, a weak but significant positive correlation was observed between percentages of fat in the diet and plasma adiponectin concentrations in non-carriers of the C allele. In conclusion, AT1R A1166C was associated with plasma adiponectin concentrations and influenced the correlations between dietary fat intake and plasma concentrations of adiponectin. These findings may help to identify vulnerable populations that are susceptible to the development of atherosclerosis and require early dietary recommendations for young women.