Effects of Citrus aurantium (Bitter Orange) Fruit Extracts ...

2.1. Effects of

C. aurantium

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on Glycogen Catabolism, Glycolysis, Oxygen Uptake

C. aurantium

on glycogen catabolism and glycolysis. When perfused with substrate-free medium the livers from fed rats survive at the expense of the oxidation of endogenous fatty acids (major route) and glycolysis from endogenous glycogen (minor route). Under these conditions the livers release glucose, lactate and pyruvate as a result of glycogen catabolism [

C. aurantium

extract at the concentration of 400 mg/L. It also illustrates a typical experimental protocol, which was used for all other extract concentrations. After a pre-perfusion period of 10 min, the

C. aurantium

extract was infused during 20 min. This was followed by additional 10 min of extract-free perfusion. Four parameters were measured: glucose release, lactate and pyruvate production and oxygen consumption. As noted in

C. aurantium

infusion. After the onset of the infusion, however, oxygen uptake increased and remained so during the entire infusion period. Glucose release and lactate production were also increased with peak values 200 and 100% above the basal values, respectively. Pyruvate production was not changed. After removing the extract from the perfusion fluid, the stimulations of glucose release and lactate production returned to their basal levels. The recovery of oxygen consumption, however, was incomplete.

The first experiments were planned in order to test the possible effects ofon glycogen catabolism and glycolysis. When perfused with substrate-free medium the livers from fed rats survive at the expense of the oxidation of endogenous fatty acids (major route) and glycolysis from endogenous glycogen (minor route). Under these conditions the livers release glucose, lactate and pyruvate as a result of glycogen catabolism [ 29 ]. Figure 2 illustrates the responses of perfused livers to the infusion of aextract at the concentration of 400 mg/L. It also illustrates a typical experimental protocol, which was used for all other extract concentrations. After a pre-perfusion period of 10 min, theextract was infused during 20 min. This was followed by additional 10 min of extract-free perfusion. Four parameters were measured: glucose release, lactate and pyruvate production and oxygen consumption. As noted in Figure 2 , all parameters were stable before the initiation ofinfusion. After the onset of the infusion, however, oxygen uptake increased and remained so during the entire infusion period. Glucose release and lactate production were also increased with peak values 200 and 100% above the basal values, respectively. Pyruvate production was not changed. After removing the extract from the perfusion fluid, the stimulations of glucose release and lactate production returned to their basal levels. The recovery of oxygen consumption, however, was incomplete.

Figure 2. Time courses of the changes caused by the

C. aurantium

extract (400 mg/L) on glycogen catabolism and endogenous fatty acids-driven oxygen uptake. Livers from fed rats were perfused as described in the Experimental Section.

C. aurantium

(400 mg/L) was infused during 20 min, as indicated by the horizontal bar. The ef'uent perfusate was sampled in 2-min intervals and analyzed for glucose, lactate, and pyruvate. Oxygen consumption was followed polarographically. Each datum point represents the means of three liver perfusion experiments. Bars are standard errors of the mean.

Figure 2. Time courses of the changes caused by the

C. aurantium

extract (400 mg/L) on glycogen catabolism and endogenous fatty acids-driven oxygen uptake. Livers from fed rats were perfused as described in the Experimental Section.

C. aurantium

(400 mg/L) was infused during 20 min, as indicated by the horizontal bar. The ef'uent perfusate was sampled in 2-min intervals and analyzed for glucose, lactate, and pyruvate. Oxygen consumption was followed polarographically. Each datum point represents the means of three liver perfusion experiments. Bars are standard errors of the mean.

C. aurantium

extract in order to investigate the concentration dependence of the effects. The mean results are shown in

C. aurantium

extract concentration. As revealed by

C. aurantium

extract increased almost linearly both glycogenolysis and glycolysis in the range up to 400 mg/L (196 μM synephrine). Oxygen uptake, however, was already maximal at the concentration of 25 mg/L (12.3 μM synephrine) with no significant modifications in the range up to 400 mg/L.

C. aurantium

extract on the lactate to pyruvate ratio, which is an indicator of the cytosolic NADH/NAD+ ratio [

C. aurantium

extract, stimulations of glycogenolysis, glycolysis and oxygen uptake, were also reported for the adrenergic agonists epinephrine [

Experiments like those illustrated in the Figure 2 were repeated with 25, 50, and 100 mg/L ofextract in order to investigate the concentration dependence of the effects. The mean results are shown in Figure 3 A and represent the final values of each parameter at the end of the drug infusion period (25'30 min perfusion time in Figure 2 ). Oxygen consumption, glycogenolysis (glucose plus ½[pyruvate + lactate]) and glycolysis (pyruvate plus lactate) were represented against theextract concentration. As revealed by Figure 3 A, theextract increased almost linearly both glycogenolysis and glycolysis in the range up to 400 mg/L (196 μM synephrine). Oxygen uptake, however, was already maximal at the concentration of 25 mg/L (12.3 μM synephrine) with no significant modifications in the range up to 400 mg/L. Figure 3 B shows the changes caused by theextract on the lactate to pyruvate ratio, which is an indicator of the cytosolic NADH/NADratio [ 30 ]. It is apparent that the extract produced a considerable increase in the lactate to pyruvate ratio (200% at the concentration of 400 mg/L). It is noteworthy to mention that all these effects of theextract, stimulations of glycogenolysis, glycolysis and oxygen uptake, were also reported for the adrenergic agonists epinephrine [ 23 24 ], norepinephrine [ 25 26 ] and phenylephrine [ 26 ]. These effects are different from those of glucagon which, while stimulating glycogenolysis and oxygen uptake, strongly inhibits glycolysis [ 23 ].

Figure 3. Concentration dependences of the effects of the

C. aurantium

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extract on glycogen catabolism and endogenous fatty acids-driven oxygen uptake. Data were obtained from experiments of the kind illustrated by

post hoc

Student-Newman-Keuls testing (+

p

< 0.05, **

p

< 0.01).

Concentration dependences of the effects of theextract on glycogen catabolism and endogenous fatty acids-driven oxygen uptake. Data were obtained from experiments of the kind illustrated by Figure 2 . Glycogenolysis and glycolysis are expressed as glucosyl units and were calculated as glucose production +½(lactate production + pyruvate production) and lactate production + pyruvate production, respectively. Each datum point represents the mean of three liver perfusion experiments. Bars are standard errors of the mean. Asterisks and crosses indicate statistical signi'cance in comparison with the control condition as revealed by variance analysis withStudent-Newman-Keuls testing (< 0.05,< 0.01).

Figure 3. Concentration dependences of the effects of the

C. aurantium

extract on glycogen catabolism and endogenous fatty acids-driven oxygen uptake. Data were obtained from experiments of the kind illustrated by

post hoc

Student-Newman-Keuls testing (+

p

< 0.05, **

p

< 0.01).

Concentration dependences of the effects of theextract on glycogen catabolism and endogenous fatty acids-driven oxygen uptake. Data were obtained from experiments of the kind illustrated by Figure 2 . Glycogenolysis and glycolysis are expressed as glucosyl units and were calculated as glucose production +½(lactate production + pyruvate production) and lactate production + pyruvate production, respectively. Each datum point represents the mean of three liver perfusion experiments. Bars are standard errors of the mean. Asterisks and crosses indicate statistical signi'cance in comparison with the control condition as revealed by variance analysis withStudent-Newman-Keuls testing (< 0.05,< 0.01).

C. aurantium

extract in the presence of cyanide showed only a discrete increase in oxygen uptake. This is strongly indicative for a predominantly mitochondrial origin of the

C. aurantium

effects on oxygen consumption.

To verify if oxygen uptake stimulation comes from the mitochondria, the microsomal electron transport chain or from both, experiments were done with cyanide, which at the concentration of 2 mM completely blocks the mitochondrial respiratory chain [ 29 ]. The results are shown in Figure 4 . As expected cyanide greatly inhibited oxygen uptake. The infusion of theextract in the presence of cyanide showed only a discrete increase in oxygen uptake. This is strongly indicative for a predominantly mitochondrial origin of theeffects on oxygen consumption.

Figure 4. Effects of the

C. aurantium

extract on oxygen uptake in the presence of cyanide. Livers from fed rats were perfused as described in the Experimental Section. The infusion of cyanide was started after stabilization of oxygen uptake. The times at which infusion of cyanide and

C. aurantium

extracts (400 mg/L) were started are indicated. Oxygen consumption was followed polarographically. Each datum point represents the means of three liver perfusion experiments. Bars are standard errors of the mean.

Figure 4. Effects of the

C. aurantium

extract on oxygen uptake in the presence of cyanide. Livers from fed rats were perfused as described in the Experimental Section. The infusion of cyanide was started after stabilization of oxygen uptake. The times at which infusion of cyanide and

C. aurantium

extracts (400 mg/L) were started are indicated. Oxygen consumption was followed polarographically. Each datum point represents the means of three liver perfusion experiments. Bars are standard errors of the mean.

p

-synephrine in isolated lipocytes [

Stimulation of oxygen uptake in the liver from fed rats perfused with substrate-free medium represents mainly an increased oxidation of endogenous fatty acids [ 29 ]. The source includes already existent free fatty acids as well as fatty acids arising from lipolysis [ 31 ]. The latter is stimulated by adrenergic agents, as indeed demonstrated for-synephrine in isolated lipocytes [ 32 ]. This is a typically catabolic process, but it is not necessarily thermogenic in nature. In fact, it has been shown that stimulation of oxygen uptake by the adrenergic agonist epinephrine is accompanied by a significant increase in the mitochondrial ATP content without significant changes in the cytosolic content [ 23 ]. This overall increase in the cellular ATP content is, in principle, not indicative of a merely thermogenic activity of adrenergic agents in the liver.

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