Pyrroloquinoline quinone nutritional status and parameters important to mitochondrial function

Abstract

Pyrroloquinoline quinone (PQQ) deficiency influences the mitochondrial content of heart and liver (Stites T et al., J Nutr., 2006) and impacts the metabolism of lysine and other amino acids oxidized via mitochondrial and peroxisomal pathways (Bauerly K et al., Biochim Biophys Acta, 2006). Because of mitochondria’s central role in metabolism, we investigated the effect of PQQ deficiency on mitochondriogenesis. Herein are data for serum glucose and fatty acids (FA) in rats fed amino-acid based diets with (2 mg PQQ/Kg diet) or devoid of PQQ for 3–5 weeks in post-weanling rats (fed and/or fasted states). Serum glucose, free fatty acids (FFA), RQ, triglycerides (TG), sphingomyelin (SM), total energy expenditure (EE) per metabolic body size (Wt3/4), relative mitochondrial amount, and expression of serine palmitoyl transferase (SPT) were estimated. Mitochondria content decreased 20% in PQQ deficient rats. Although no differences in serum glucose and FFA levels were observed (PQQ+ vs. PQQ−, fed or fasted), EE was significantly lower in PQQ deficiency. In the fed state, EE was positively correlated with mitochondrial amount and less in PQQ deficiency. Composition of FFA, TG, and SM were altered with PQQ deficiency, suggesting disturbances in long-chain FA metabolic pathways; serum TG were elevated while serum SM tended to be lower with corresponding decreases in liver SPT activity and mRNA levels in deficient rats. These data are consistent with our previous observations regarding PQQ status, mitochondrial function and associated activities. Funded in part by Mitsubishi, Inc., CA Vitamin Settlement Fund, and NDC.