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This study was conducted to explore the effect of graded levels of pyrroloquinoline quinone disodium (PQQ·Na2) on the performance and intestinal development of weaned pigs. A total of 216 pigs weaned at 28 d were assigned in a randomized complete block design to 6 diets containing 0, 1.5, 3.0, 4.5, 6.0, or 7.5 mg/kg PQQ·Na2 for 28 d. Performance, diarrhea incidence, intestinal morphology, redox status, cytokines, and the expression of tight junction proteins were determined. Pigs had increased ADG (linear, P < 0.01), G:F (quadratic, P < 0.01), and lower diarrhea incidence (P < 0.01) with the increase of PQQ·Na2 supplementation. Villus height increased (quadratic, P < 0.01) in all segments of the small intestine, and crypt depth in the duodenum and jejunum was decreased (linear, P < 0.05) in pigs with the increase of PQQ·Na2 supplementation. Pigs fed PQQ·Na2-supplemented diets had higher (P < 0.05) activities of antioxidant enzymes including total superoxide dismutase in duodenum, jejunum, and ileum; glutathione peroxidase (GSH-Px) in jejunum and ileum; catalase (CAT) in duodenum and ileum; and lower (P < 0.05) malondialdehyde concentrations in the intestinal mucosa of all segments. In the intestinal mucosa, cytokines including interleukin (IL)-1β, IL-2, and interferon-γ were significantly decreased (P < 0.05) in pigs fed PQQ·Na2-supplemented diets. The protein expression of zonula occluden protein-1 (ZO-1) and occludin in the jejunum was significantly increased (P < 0.05) in pigs fed diets containing PQQ·Na2. In conclusion, these results have indicated that dietary PQQ·Na2 supplementation improves growth performance and gut health in weaned pigs. Moreover, pigs fed diet with as low as 1.5-mg/kg PQQ·Na2 have better performance compared with pigs fed no PQQ·Na2-supplemented diet; pigs fed diet with 4.5-mg/kg PQQ·Na2 have highest G:F among treatments during the whole period.
When pyrroloquinoline quinone (PQQ) is added to an amino acid-based, but otherwise nutritionally
complete basal diet, it improves growth-related variables in young mice. We examined PQQ and mitochondrial
function based on observations that PQQ deficiency results in elevated plasma glucose concentrations in young
mice, and PQQ addition stimulates mitochondrial complex 1 activity in vitro. PQQ-deficient weanling mice had a 20–
30% reduction in the relative amount of mitochondria in liver; lower respiratory control ratios, and lower respiratory
quotients than PQQ-supplemented mice (2 mg PQQ/kg diet). In mice from dams fed a conventional laboratory diet,
but switched at weaning to the basal diet, plasma glucose, Ala, Gly, and Ser concentrations were elevated at 4 wk
(PQQ� vs. PQQ1), but not at 8 wk. The relative mitochondrial content (ratio of mtDNA to nuclear DNA) also tended
(P , 0.18) to be lower (PQQ� vs. PQQ1) at 4 wk, but not at 8 wk. PQQ also counters the mitochondrial complex 1
inhibitor, diphenylene iodonium (DPI). Mice were gavaged with 0, 0.4, or 4 mg PQQ/g body weight (BW) daily for 14 d.
At each PQQ level, DPI was injected (i.p.) at 0, 0.4, 0.8, or 1.6 mg DPI/g BW. The PQQ-deficient mice exposed to 0.4
or 4.0 mg DPI/g lost weight and had lower plasma glucose levels than PQQ-supplemented mice (P , 0.05). In
addition, fibroblasts took up 3H-PQQ added to cell cultures, and cultured hepatocytes maintained mitochondrial PQQ
concentrations similar to those observed in vivo. Collectively, these results indicate that dietary PQQ can influence
mitochondrial amount and function, particularly in perinatal and weanling mice.
Addendum LB 80, ASBMB/DBC-ACS Joint Meetearlier support the presence of PQQ in biological fluids, ing
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ing, San Diego, CA. [Abstract]
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