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Altering pyrroloquinoline quinone nutritional status modulates mitochondrial, lipid, and energy metabolism in rats.

Bauerly K, Harris C, Chowanadisai W, Graham J, Havel PJ, Tchaparian E, Satre M, Karliner JS, Rucker RB - PLoS ONE (2011)

Bottom Line: Although no striking differences in serum glucose, insulin, and free fatty acid levels were observed, energy expenditure was lower in PQQ- vs.Moreover, PQQ administration (i.p. at 4.5 mg/kg BW for 3 days) resulted in a greater than 2-fold decrease in plasma triglycerides during a 6-hour fast than saline administration in a rat model of type 2 diabetes.Collectively, these data demonstrate that PQQ deficiency impacts a number of parameters related to normal mitochondrial function.

View Article: PubMed Central - PubMed

Affiliation: Nutrition, University of California Davis, Davis, California, United States of America.

ABSTRACT
We have reported that pyrroloquinoline quinone (PQQ) improves reproduction, neonatal development, and mitochondrial function in animals by mechanisms that involve mitochondrial related cell signaling pathways. To extend these observations, the influence of PQQ on energy and lipid relationships and apparent protection against ischemia reperfusion injury are described herein. Sprague-Dawley rats were fed a nutritionally complete diet with PQQ added at either 0 (PQQ-) or 2 mg PQQ/Kg diet (PQQ+). Measurements included: 1) serum glucose and insulin, 2) total energy expenditure per metabolic body size (Wt(3/4)), 3) respiratory quotients (in the fed and fasted states), 4) changes in plasma lipids, 5) the relative mitochondrial amount in liver and heart, and 6) indices related to cardiac ischemia. For the latter, rats (PQQ- or PQQ+) were subjected to left anterior descending occlusions followed by 2 h of reperfusion to determine PQQ's influence on infarct size and myocardial tissue levels of malondialdehyde, an indicator of lipid peroxidation. Although no striking differences in serum glucose, insulin, and free fatty acid levels were observed, energy expenditure was lower in PQQ- vs. PQQ+ rats and energy expenditure (fed state) was correlated with the hepatic mitochondrial content. Elevations in plasma di- and triacylglyceride and β-hydroxybutryic acid concentrations were also observed in PQQ- rats vs. PQQ+ rats. Moreover, PQQ administration (i.p. at 4.5 mg/kg BW for 3 days) resulted in a greater than 2-fold decrease in plasma triglycerides during a 6-hour fast than saline administration in a rat model of type 2 diabetes. Cardiac injury resulting from ischemia/reperfusion was more pronounced in PQQ- rats than in PQQ+ rats. Collectively, these data demonstrate that PQQ deficiency impacts a number of parameters related to normal mitochondrial function.

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Related in: MedlinePlus

Oral glucose tolerance in response to a glucose load in diabetic UCD-T2DM Rats following the administration of PQQ (i.p.) at 4.5 mg PQQ/Kg BW for 3 days or saline.The area under the respective curves was reduced by 7 percent when rats given saline were compared to rats administered PQQ (p∼0.09).
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pone-0021779-g005: Oral glucose tolerance in response to a glucose load in diabetic UCD-T2DM Rats following the administration of PQQ (i.p.) at 4.5 mg PQQ/Kg BW for 3 days or saline.The area under the respective curves was reduced by 7 percent when rats given saline were compared to rats administered PQQ (p∼0.09).

Mentions: As an additional validation of these findings, the availability of the UC Davis type-2 diabetic model rat (UCD-T2DM) [22] allowed the testing of whether PQQ can influence glucose tolerance in animals with existing diabetes. The data in Figure 5 indicate that modest changes in oral glucose tolerance may occur in response to PQQ administration. The area under the respective curves was reduced by 7 percent when rats given saline was compared to rats administered PQQ for 3 days at 4.5 mg/ kg BW (p∼0.09). PQQ was also administered to UCD-T2DM rats, which were then subjected to a 6 h fast. No differences were observed (PQQ vs. saline) in plasma glucose or NEFA concentrations over the test period. For example, at 0, 3, and 6 h, the values for plasma free fatty acids were 0.43±0.02, 0.76±0.08, and 0.6±0.06 mg/dL for rats administered saline; in contrast, to 0.39±0.02, 0.69±0.07 and 0.58±0.06 mg/dL for rats administered PQQ. With regard to plasma triacylglyceride levels, values for control rats fell from 310 mg/dL ±49 to 236 mg/dL ±37 (i.e., Δ 74 mg triglyceride/dL) over the period of the 6 h fast following saline administration. In contrast, PQQ administration resulted in a greater than a 2-fold decrease to 141 mg/dL ±28 (p<0.05) or a Δ169 mg change in triglyceride/dL.


Altering pyrroloquinoline quinone nutritional status modulates mitochondrial, lipid, and energy metabolism in rats.

Bauerly K, Harris C, Chowanadisai W, Graham J, Havel PJ, Tchaparian E, Satre M, Karliner JS, Rucker RB - PLoS ONE (2011)

Oral glucose tolerance in response to a glucose load in diabetic UCD-T2DM Rats following the administration of PQQ (i.p.) at 4.5 mg PQQ/Kg BW for 3 days or saline.The area under the respective curves was reduced by 7 percent when rats given saline were compared to rats administered PQQ (p∼0.09).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3140972&req=5

pone-0021779-g005: Oral glucose tolerance in response to a glucose load in diabetic UCD-T2DM Rats following the administration of PQQ (i.p.) at 4.5 mg PQQ/Kg BW for 3 days or saline.The area under the respective curves was reduced by 7 percent when rats given saline were compared to rats administered PQQ (p∼0.09).
Mentions: As an additional validation of these findings, the availability of the UC Davis type-2 diabetic model rat (UCD-T2DM) [22] allowed the testing of whether PQQ can influence glucose tolerance in animals with existing diabetes. The data in Figure 5 indicate that modest changes in oral glucose tolerance may occur in response to PQQ administration. The area under the respective curves was reduced by 7 percent when rats given saline was compared to rats administered PQQ for 3 days at 4.5 mg/ kg BW (p∼0.09). PQQ was also administered to UCD-T2DM rats, which were then subjected to a 6 h fast. No differences were observed (PQQ vs. saline) in plasma glucose or NEFA concentrations over the test period. For example, at 0, 3, and 6 h, the values for plasma free fatty acids were 0.43±0.02, 0.76±0.08, and 0.6±0.06 mg/dL for rats administered saline; in contrast, to 0.39±0.02, 0.69±0.07 and 0.58±0.06 mg/dL for rats administered PQQ. With regard to plasma triacylglyceride levels, values for control rats fell from 310 mg/dL ±49 to 236 mg/dL ±37 (i.e., Δ 74 mg triglyceride/dL) over the period of the 6 h fast following saline administration. In contrast, PQQ administration resulted in a greater than a 2-fold decrease to 141 mg/dL ±28 (p<0.05) or a Δ169 mg change in triglyceride/dL.

Bottom Line: Although no striking differences in serum glucose, insulin, and free fatty acid levels were observed, energy expenditure was lower in PQQ- vs.Moreover, PQQ administration (i.p. at 4.5 mg/kg BW for 3 days) resulted in a greater than 2-fold decrease in plasma triglycerides during a 6-hour fast than saline administration in a rat model of type 2 diabetes.Collectively, these data demonstrate that PQQ deficiency impacts a number of parameters related to normal mitochondrial function.

View Article: PubMed Central - PubMed

Affiliation: Nutrition, University of California Davis, Davis, California, United States of America.

ABSTRACT
We have reported that pyrroloquinoline quinone (PQQ) improves reproduction, neonatal development, and mitochondrial function in animals by mechanisms that involve mitochondrial related cell signaling pathways. To extend these observations, the influence of PQQ on energy and lipid relationships and apparent protection against ischemia reperfusion injury are described herein. Sprague-Dawley rats were fed a nutritionally complete diet with PQQ added at either 0 (PQQ-) or 2 mg PQQ/Kg diet (PQQ+). Measurements included: 1) serum glucose and insulin, 2) total energy expenditure per metabolic body size (Wt(3/4)), 3) respiratory quotients (in the fed and fasted states), 4) changes in plasma lipids, 5) the relative mitochondrial amount in liver and heart, and 6) indices related to cardiac ischemia. For the latter, rats (PQQ- or PQQ+) were subjected to left anterior descending occlusions followed by 2 h of reperfusion to determine PQQ's influence on infarct size and myocardial tissue levels of malondialdehyde, an indicator of lipid peroxidation. Although no striking differences in serum glucose, insulin, and free fatty acid levels were observed, energy expenditure was lower in PQQ- vs. PQQ+ rats and energy expenditure (fed state) was correlated with the hepatic mitochondrial content. Elevations in plasma di- and triacylglyceride and β-hydroxybutryic acid concentrations were also observed in PQQ- rats vs. PQQ+ rats. Moreover, PQQ administration (i.p. at 4.5 mg/kg BW for 3 days) resulted in a greater than 2-fold decrease in plasma triglycerides during a 6-hour fast than saline administration in a rat model of type 2 diabetes. Cardiac injury resulting from ischemia/reperfusion was more pronounced in PQQ- rats than in PQQ+ rats. Collectively, these data demonstrate that PQQ deficiency impacts a number of parameters related to normal mitochondrial function.

Show MeSH
Related in: MedlinePlus