During metabolic acidosis, the kidneys produce NH4+ to buffer acids through metabolism of glutamine derived from liver and muscle. We have shown that expression of the glutamine transporter, SNAT3, increases in kidney during metabolic acidosis (MA). In addition, K+ depletion and high dietary protein results in enhanced renal H+ excretion. In this study, we examined the role of SNAT3 and PEPCK during a normal (0.36%) or K+ deficient (0.02%) diet; or a normal (20%) or high protein (50%) diet for 7 days. MA was induced in the control and low K+ groups by giving 0.28M NH4Cl in the drinking water for the final 48hrs. Food and water intake, urine, and arterial blood gases (ABG) were assessed. Urinary ammonia excretion was increased during MA and ingestion of the high protein diet, but not in the low K+ group. Similarly, SNAT3 mRNA expression in kidney was elevated in control and low K+ acidotic groups and the high protein group, however not in K+-depleted animals. Further, PEPCK abundance was increased during MA but not in the low K+ and high protein groups. In summary, expression of SNAT3 and PEPCK parallels urinary ammonia excretion during MA but dissociates under high protein intake. In contrast, 7 days of dietary K+-depletion did not affect urinary ammonia excretion, or SNAT3 and PEPCK expression.