Foods containing large amounts of fats and sodium chloride (NaCl) are highly palatable (e.g. - potato chips), and their consumption is associated with obesity.  We therefore hypothesized that eating a diet with high fat and high NaCl content (HFHS) would increase weight gain over eating a diet with high fat, but low NaCl content (HFLS). Surprisingly, we found that nine week old male C57BL/6Jmice fed HFLS gain more weight than mice fed HFHS.  We determined that this increase was not due to increased food intake, reduced resting metabolism, or reduced physical activity.  We then tested the hypothesis that increased dietary NaCl reduces digestive efficiency.  Mice were fed chow (n=6), HFHS (n=7), or HFLS (n=8), and fat absorption by the intestine was determined by fecal acid steatocrit.  HFHS significantly increased the fat loss to feces versus HFLS (Chow: 0.5±0.2, HFHS: 2.4±0.2,HFLS: 1.5±0.1 %, P<0.05), confirming our hypothesis.  Further, dietary sodium is known to suppress circulating renin-angiotensin system activity.  We found that replacement of angiotensin II in HFHS-fed mice normalized fecal acid steatocrit (1.4±0.3 %, n=7, P<0.05 vs HFHS).  In contrast, blockade of angiotensin AT1receptors by losartan in HFLS-fed mice had no effect (1.5±0.1 %, n=5).  We conclude that dietary sodium suppresses weight gain with high fat diet feeding, and this is mediated through a suppression of the renin-angiotensin system – though not through the AT1 receptor. Mice with genetic deletion of the angiotensin AT2 receptor are currently under study to evaluate its role in digestive efficiency.