Nutrient Metabolism—Research Communication

Nutrient Metabolism—Research Communication
Bioavailability of Phloretin and
Phloridzin in Rats
(Manuscript received 3 July 2001. Initial review completed 16
August 2001. Revision accepted 26 September 2001.)
Vanessa Crespy, 1 Olivier Aprikian, Christine Morand,
Catherine Besson, Claudine Manach, Christian Demigné
and Christian Rémésy
Laboratoire des Maladies Métaboliques et des Micronutriments,
I.N.R.A. de Clermont-Ferrand/Theix, 63122 Saint Genès
Champanelle, France
ABSTRACT Phloretin is a flavonoid found exclusively in
apples and in apple-derived products where it is present as
the glucosidic form, namely, phloridzin (phloretin 2-O-glucose).
In the present study, we compared the changes in
plasma and urine concentrations of these two compounds
in rats fed a single meal containing 0.25% phloridzin or
0.157% phloretin (corresponding to the ingestion of 22 mg
of phloretin equivalents). In plasma, phloretin was recovered
mainly as the conjugated forms (glucuronided and/or
sulfated) but some unconjugated phloretin was also detected.
By contrast, no trace of intact phloridzin was
detected in plasma of rats fed a phloridzin meal. These
compounds presented different kinetics of absorption;
phloretin appeared more rapidly in plasma when rats were
fed the aglycone than when fed the glucoside. However,
whatever compound was administered, no significant difference
in the plasma concentrations of total phloretin
were observed 10 h after food intake. At 24 h after the
beginning of the meal, the plasma concentrations of phloretin
were almost back to the baseline, indicating that this
compound was excreted rapidly in urine. The total urinary
excretion rate of phloretin was not affected by the forms
administered, and was estimated to be 8.5 mol/24 h in rats
fed phloretin or phloridzin. Thus, 10.4% of the ingested
dose was recovered in urine after 24 h. J. Nutr. 132:
3227–3230, 2002.
KEY WORDS: ● flavonoids ● phloridzin ● metabolism ● rats
Flavonoids are widely distributed in edible plants (1). They
are classified in different groups as follows: anthocyanidins,
flavones, flavanones, flavonols, isoflavones and some minor
flavonoids such as dihydrochalcones (2). The principal members
of this last-mentioned category are phloretin and its
glucoside, phloridzin (phloretin-2-glucose). These compounds
are found exclusively in apples, which are frequently
consumed by humans. Phloridzin is present primarily in the
1 To whom correspondence should be addressed.
E-mail: crespy@clermont.inra.fr.
0022-3166/02 $3.00 © 2002 American Society for Nutritional Sciences.
3227
peel of apples (80–420 mg/kg Reineta) but also in the pulp
(16–20 mg/kg Reineta) (3); its concentration is highly dependent
on the variety of apple (3). The most frequently described
biological effect of phloridzin is its competitive inhibition of
intestinal glucose uptake via sodium D-glucose cotransporter 1
(SGLT1) 2 (4). This property has led to the classification of
phloridzin as an antidiabetic agent (5–8). Therefore, it is of
interest to study the bioavailability of these dihydroxychalcons
(phloretin and phloridzin) to fully appreciate their real physiologic
effect. However, until recently, only a few studies have
described the metabolism of these two compounds (9,10).
Malathi and Crane (9) reported the presence of -glucosidase
activity in the brush border of the hamster small intestine,
which hydrolyzes phloridzin to phloretin and glucose.
This enzyme, identified as lactase-phloridzin hydrolase (LPH),
is also present in other species (11,12). When phloretin was
administered to rats by gavage (200 mg/kg), this compound
was hydrolyzed by the cecal microflora into phloretic acid and
phloroglucinol, which were then detected in urine (10). Phloretin
also was found in urine, suggesting that this compound
may be absorbed before its degradation by the microflora.
Nevertheless, no data are available on the characterization of
the circulating forms of phloretin. Thus, the aim of the present
study was to investigate the bioavailability of phloretin and its
glucoside in rats.
MATERIALS AND METHODS
Chemicals. Phloridzin, -glucuronidase/sulfatase (Helix pomatia)
were purchased from Sigma (L’Isle D’Abeau, Chesnes, France).
Phloretin was purchased from Extrasynthese (Genay, France).
Animals and diets. Male Wistar rats (n 48; Institute Nationale
de la Recherche Agronomique) weighing 160 g were housed
individually in metabolic cages fitted with urine/feces separators, in
temperature-controlled rooms (22°C), with a dark period from 0800
to 1600 h and free access to food throughout that period. Rats were
fed a control diet with the following composition: 75.5% wheat
starch, 15% casein, 3.5% mineral mixture [AIN 93M formula (13)],
1% vitamin mixture [AIN 76A formula (14)] and 5% corn oil. Rats
consumed this control diet for 14 d, and were then randomly divided
into three groups. Each group received 20 g of a single different
experimental meal as follows: 1) the control diet, 2) the control diet
supplemented with 0.25% phloridzin or 3) the control diet supplemented
with 0.157% phloretin. The two supplemented meals contained
31.4 mg of phloretin equivalents. For each group of rats, food
intake was controlled. Whatever the supplementation (phloretin or
phloridzin), rats consumed 14 0.5 g of food, corresponding to an
ingestion of 22 mg of phloretin equivalents (88 mg/kg body). Rats
were maintained and handled according to the recommendations of
the Institutional Ethic Committee of INRA, in accordance with the
decree N° 87–848.
Sampling procedure. At 4, 10 and 24 h after the beginning of the
experimental meal, six rats of each group were sampled. They were
anesthetized with sodium pentobarbital (40 mg/kg body). Blood was
withdrawn from the abdominal aorta into heparinized tubes. Plasma
samples were acidified with 10 mmol/L acetic acid. Urine was col-
2 Abbreviations used: GLUT, glucose transporter protein; LPH, lactase-phloridzin
hydrolase; SGLT1, sodium D-glucose cotransporter 1.
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lected for 24 h after the beginning of the meal. All of the biological
samples were stored at 20°C until analysis.
HPLC analysis. Plasma samples were acidified (to pH 4.9) with
0.1 volume of 0.58 mol/L acetic acid and incubated at 37°C for2h
(plasma) or for 30 min (urine) with or without -glucuronidase/
sulfatase (100 U/L). Plasma proteins were precipitated by the addition
of 500 L of methanol/200 mmol/L HCl and the extract was
centrifuged for 50 min at 14000 g. After this extraction step, 20 L
of supernatant was injected and analyzed by HPLC. The concentrations
of conjugated derivatives were estimated as the difference
between the concentrations of phloretin measured before and after
the enzymatic treatment. For the analysis of phloretin in plasma,
plasma standards containing 0, 0.25, 0.5, 1, 5 and 10 mol/L added
phloretin were prepared. The standards were treated exactly as the
samples (hydrolysis and extraction). Day-to day-variation and withinday
variation for phloretin from all matrices were 10%. The recovery
of phloretin from all matrices reached 97%. The limit of detection
for phloretin was 25 nmol/L.
The HPLC analysis was performed using isocratic conditions (1.5
mL/min) with a 150 4.6 mm Hypersil BDS C18–5 m (Life
Sciences International, Cergy, France). The mobile phase consisted
of 30 mmol/L NaH 2PO 4 buffer, pH 3, containing 25% acetonitrile.
The detection was performed using a multielectrode coulometric
detection (4-electrodes CoulArray, Eurosep, France) with potentials
set at 375, 500, 600 and 700 mV.
To visualize the conjugated forms of phloretin and to detect the
presence of phloridzin, the chromatographic conditions were as follows
(flow rate 1 mL/min): 0–2 min, solvent A 85%/solvent B15%;
2–22 min, solvent A 85%/solvent B15% 3 solvent A 63%/solvent B
37%; 22–28 min, solvent A 63%/solvent B 37%; 28–32 min, solvent
A 63%/solvent B 37% 3 solvent A 85%/solvent B15%; solvent A
contained water and 30mmol/L NaH 2PO 4 buffer, pH 3, and solvent
B, acetonitrile.
Glucose measurements. The glucose concentration in urine,
sampled from bladder, was determined by an enzymatic procedure as
described by Bergmeyer et al. (15).
Data analysis. Values are means SEM. Significance of differences
between means was determined by ANOVA and the Student-
Newman-Keuls multiple comparison test (Instat; GraphPad, San Diego,
CA). Differences were considered significant at P 0.05.
RESULTS
When rats were fed a meal containing phloridzin, this
compound was not recovered in plasma that was not subjected
to enzymatic hydrolysis. However, unconjugated phloretin was
detected in the plasma of rats fed phloridzin as in those fed
phloretin (9.0 3.0 and 6.9 0.9 mol/L, respectively) (Fig.
1A). After hydrolysis by -glucuronidase/sulfatase, the phloretin
peak markedly increased (Fig. 1B), suggesting that the
major circulating forms were glucuronidated and/or sulfated
derivatives of phloretin. We did not detect any methoxylated
forms of phloretin in plasma. These data indicate that the
nature of the circulating metabolites was independent of the
administrated form of phloretin (aglycone vs. glucoside).
At 4 h after the beginning of the meal containing phloretin,
22.8 2.8 mol/L of phloretin was measured in hydrolyzed
plasmas (Fig. 2A). Of this total amount, expressed as
phloretin equivalents, 5% was represented by unconjugated
phloretin and 95% by conjugated forms. When measured 4 h
after the meal, the plasma concentration of phloretin in rats
fed phloridzin was markedly lower (50%; P 0.05) (Fig. 2B)
than that found in plasma of rats fed phloretin. Thus, phloretin
appeared more rapidly in plasma when it was administered
to rats in the aglycone rather than in the glucosidic form (Fig.
2). Whatever the supplementation (phloretin or phloridzin),
the ratio between unconjugated aglycone and total forms was
of the same magnitude (5%).
When rats were sampled 10 h after the meal, the plasma
concentrations of total phloretin were not significantly differ-
CRESPY ET AL.
FIGURE 1 Representative chromatograms of plasma from rats
fed phloretin or phloridzin before ( panel A) or after ( panel B) enzymatic
hydrolysis by -glucuronidase/sulfatase. The detection was performed
using multielectrode coulometric detection (4-electrodes CoulArray,
Eurosep, France) with potentials set at 375, 500, 600 and 700 mV.
ent between rats fed the two diets, i.e., they were 66.9 19.4
mol/L for those fed the phloridzin meal and 54.2 8.0
mol/L for those fed the phloretin meal. Whatever compound
was administered (phloretin or phloridzin), the level of unconjugated
aglycone recovered in plasma represented 10% of
the total.
At 24 h after food intake, the total plasma concentrations
in phloretin dramatically decreased to 4.8 2.1 and 7.7 4.0
mol/L after phloridzin and phloretin intake, respectively
(Fig. 2). In both cases, 14% of the total was constituted by the
aglycone forms.
The urinary excretion of phloretin was measured over a
24-h period after the ingestion of each experimental meal.
Excretion rates did not differ between rats fed the phloretin
meal (8.5 0.9 mol/24 h) and those fed the phloridzin meal
(8.2 1.7 mol/24 h). These urinary excretions corresponded
to 10.4% of the ingested dose.
Because phloridzin increases glucosuria in diabetic rats (6),
we checked whether the consumption of phloretin (22 mg)
affected glucosuria. The measurements were made in urine
sampled from the bladder 10 h after food intake when the total
plasma concentration of phloretin was high. Glucosuria was
73.4 13 mol/L in the phloretin group and 74.0 14
mol/L in the phloridzin group, not different from that of
control rats (38.8 4 mol/L; P 0.05).
DISCUSSION
The present study clearly demonstrates that whatever form
was administered (phloretin or phloridzin), their bioavailability
was similar, as reflected by the absence of significant dif-
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FIGURE 2 Plasma concentrations of total (unconjugated and
conjugated forms) phloretin over 24 h in rats fed 0.157% phloretin
(panel A) or 0.25% phloridzin (panel B). Values are means SEM, n 6.
*P 0.05; (A) vs. (B).
ferences in the 24-h urinary excretions. However, the plasma
kinetics of phloretin and phloridzin differed because phloretin
appeared more rapidly in plasma when rats were fed phloretin
vs. phloridzin. The high level of phloretin measured in plasma
4 h after the beginning of the meal supplemented with phloretin
suggests that its absorption occurred chiefly in the small
intestine. In a previous study, using an in situ intestinal perfusion
model, we showed that these two compounds were
absorbed in the small intestine and that phloretin was absorbed
more efficiently than its glucoside (16).
In the plasma of rats fed a phloridzin meal, no trace of this
glucoside was detected, indicating that it must be hydrolyzed,
probably by LPH, before its absorption and metabolism. The
analysis of plasma from rats fed a meal supplemented with
phloridzin or phloretin showed that 85–95% of the circulating
forms are conjugated metabolites of phloretin (glucuronides
and/or sulfates) and that the remainder was present as the
unconjugated form. This last result is quite surprising because
when flavonoid aglycones are administered in a meal, all of the
circulating forms are generally conjugated derivatives (17–20).
The few studies reporting the presence of unconjugated aglycone
in rat plasma used gavage as the mode of administration
(21,22). Such a procedure delivers a large amount of compound
in short time, leading to a direct diffusion of the
compound administered through the intestinal wall; thus, this
does not reflect a phenomenon that could occur under physiologic
conditions. Our present data suggest that when dihydrochalcones
were administered in a meal, a part of the compound
added to the diet could be metabolized by conjugative
enzymes, and thus could be recovered intact in plasma. Moreover
we did not detect any methoxylated forms of phloretin in
plasma, confirming the importance of the presence of the
BIOAVAILABILITY OF PHLORETIN AND PHLORIDZIN IN RATS 3229
catechol group in the methoxylation process, as previously
reported (23,24).
It has been shown in vivo that some flavonoid glucosides,
especially quercetin-3-O-glucose, are absorbed more rapidly
than their corresponding aglycones (25,26). Different hypotheses
have been proposed to explain the rapid absorption of the
glucosides. Hollman et al. (25) suggested that the active
SGLT1 could be involved in the transport of flavonol glucosides.
Phloridzin blocks SGLT1 (4) but is not absorbed into
enterocytes by this transporter (27). Similarly, Day et al. (28)
proposed that if in vivo LPH is responsible for the hydrolysis
of flavonoid glucosides, the proximity of the released aglycone
to the membrane may facilitate the passive diffusion of the
flavonoid into the enterocytes. The present study showed that
when rats were fed control diets containing phloridzin or
phloretin, phloretin was absorbed more rapidly than its glucoside.
This is not consistent with the hypothesis of Day et al.
(28). During the first hours after ingestion, this hydrolysis step
by LPH seems to represent a bottleneck for absorption. Nevertheless,
the hydrolysis did not seem to constitute a limiting
step because 10 h after the beginning of the experimental
meal, the plasma concentrations of phloretin did not differ in
rats fed the phloridzin or phloretin meals.
At 24 h after the beginning of food intake, the plasma
concentration of phloretin metabolites returned to a low level.
By contrast, it has been reported that flavonoids such as
quercetin or naringenin are still present at high concentrations
in rat plasma 24 h after administration (19,29). This phenomenon
could be due to the fact that the elimination of quercetin
may be balanced by some digestive absorption, which still
occurred during the postabsorptive period, and by some from
enterohepatic cycling. This phenomenon allows an increase in
the half-lives of these compounds. Because the conjugated
forms of phloretin were quickly eliminated via the urinary
route and enterohepatic cycling activity was insufficient to
maintain the plasma concentration during the postabsorptive
period, its half-life was decreased. We noted an enhancement
in the proportion of unconjugated phloretin measured in the
plasma between 4 (5%) and 24 h (14%). This rise could be due
to the easier elimination of the conjugated metabolites of
phloretin than of the aglycone itself.
When phloretin was administered as the aglycone or as the
glucoside, 10.4% of the ingested dose was recovered in urine.
Both ingested compounds were excreted to the same extent in
urine. Nevertheless, phloretin was excreted more efficiently in
this biological fluid, as in a previous study (4% of the ingested
dose) (10). This excretion difference could be explained by
the dose and the mode of administration (200 vs. 88 mg/kg in
our study and gavage vs. meal).
The biological properties of phloridzin, which have been
investigated extensively, include its ability to block the absorption
of glucose by SGLT1. Moreover, phloretin inhibits
the facilitated glucose transporter protein GLUT2, located on
the basolateral side of the enterocytes (30). By this mechanism,
phloretin could also limit the intestinal absorption of
glucose. These properties have been demonstrated in in vivo
studies using diabetic rats. Their plasma glucose concentration
was normalized by treatment with phloridzin (7,8), notably by
an increase of glucosuria, which limited hyperglycemia (6).
The identification of unconjugated phloretin in plasma could
be of physiologic interest. Because phloretin interacts with
GLUT2, which is also present in kidney (31), it is conceivable
that this aglycone could increase glucose urinary excretion by
limiting its reabsorption.
In conclusion, the present study shows that phloretin, administered
as the aglycone or as the glucoside, is absorbed
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3230
rapidly in the intestine and essentially not recovered in plasma
at 24 h, suggesting an efficient elimination in urine. However,
it must be kept in mind that the dose of phloretin added to the
experimental meals was relatively high (22 mg). It is conceivable
that the bioavailability of phloretin could be modified by
lower doses and especially by consuming apples. It will be
interesting to evaluate the matrix effect of the fruit on phloretin
bioavailability.
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