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Original Studies |
Department of Endocrinology, Erasmus Hospital and Laboratory of Experimental Medicine, University of Brussels B-1070, Brussels, Belgium
Address all correspondence and requests for reprints to: Dr. Françoise Féry, Laboratory of Experimental Medicine, University of Brussels, 808 Route de Lennik, B-1070 Brussels, Belgium.
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Abstract |
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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A total of 45 studies were performed in 39 healthy nonobese male
volunteers (Table 1
), according to 3
different protocols described below. The purpose, nature, and potential
risks of the studies were explained to the subjects, and their written
informed consent was obtained before participation. The protocols were
reviewed and approved by the Ethics Committee of the Faculty of
Medicine of the University of Brussels.
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Study 2. To test whether the oxidation of [1-14C]-glucose is representative of the oxidation of all glucose carbons, 9 ONF healthy volunteers were tested according to the same protocol as for study 1, with two differences: [U-14C]-glucose, instead of [1-14C]-glucose, was used to label the oral load; and the tritiated glucose infusion was omitted.
Study 3. This study was designed to determine the fractional
recovery in expired air of the metabolic 14CO2
generated in experiments of studies 1 and 2 and to test whether
recovery was altered by previous fasting. To this end, 6 healthy
volunteers underwent a 5-h OGTT after both 14 h and 4 days of
total fasting. The recovery of 14CO2 was
evaluated in each test using an iv infusion of
[14C]-bicarbonate delivered at a variable rate mimicking
that of CHO oxidation measured by indirect calorimetry in the ONF
state. Thus, for the 10 30-min periods of the OGTTs, the rates of
infusion represented successively 8, 13, 15, 17, 13, 11, 9, 5, 4, and
4% of the total amount of [14C]-bicarbonate given (see
Fig. 4). The 14C-bicarbonate (Amersham, Little Chalfont,
Buckinghamshire, UK)) was diluted sterily in sodium bicarbonate (0.8
mol/L), and aliquots were kept in sealed ampoules until use. On the day
of the test, the content of an ampoule of the
[14C]-bicarbonate stock solution was diluted in saline
for iv infusion with a peristaltic pump. This mode of preparation
ensured a perfect stability of the [14C]-bicarbonate
content of the final solution (pH 8.4), with less than 1% of the
radioactivity being lost during the course of the infusion. The amount
of cold bicarbonate administered during the whole study amounted to 0.8
mmol. Serial sampling of arterialized venous blood and expired air, as
well as measurements of gaseous exchanges for indirect calorimetry,
were performed as in studies 1 and 2. Arterial blood was obtained by
puncture of the radial artery at the beginning and at the end of the
OGTT for blood gas and pH determinations.
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Blood samples were collected in heparinized tubes immediately centrifuged at 4 C, and the plasma was stored at -20 C until assayed. Plasma glucose concentration was determined using a glucose-oxidase method (Test Combination Glucose; Boehringer Mannheim Diagnostica, Mannheim, Germany). Plasma [3H]-glucose and [14C]-glucose concentrations were determined using methods that were recently described in detail (1). In brief, plasma was deproteinized, purified by ion exchange, evaporated to remove 3H2O, reconstituted with 1 mL water, and counted by dual-channel spectrometry. To determine specifically the amount of 14C present in the first carbon of glucose, other aliquots of the plasma samples were processed with a fermentation method using Leuconostoc Mesenteroides, as described before (1). The concentrations of plasma insulin (4) were determined by RIA, those of free fatty acids (FFAs) were assayed with an enzymic method (NEFA Quick; Boehringer Mannheim Yamanuchi, Tokyo, Japan), and those of ß-hydroxybutyrate (ßOHB) (5) and lactate (6) were determined on a neutralized perchloric acid filtrate of plasma using standard enzymic methods. Total urinary nitrogen was measured with the method of Kjeldahl using a Kjeltec 1 Apparatus (Tecator, Höganäs, Sweden). To measure 14CO2 specific activity in expired air, 3 mL of a solution of hyamine hydroxyde (Packard, Groningen, The Netherlands) in methanol (0.33 mol/L) was placed in 10-mL counting vials, and expired air from the rubber bags was pumped slowly through the solution until neutralization in the presence of phenolphtalein occurred. The vials were then counted after addition of scintillation fluid. For each experiment, the hyamine hydroxyde solution was titrated with HCl before use. All determinations were made in duplicate.
Calculations
The contribution to the plasma glucose concentration made by the ingested glucose was estimated by dividing the plasma concentration of [1-14C]-glucose by the 14C specific activity of the glucose drink. With the use of this calculated glucose concentration of exogenous origin and the measured [3H]-glucose counts, the rates of peripheral appearance and disappearance of oral glucose were calculated for each time period between two consecutive samples using the non-steady-state equations of Steele (7). For these calculations, it was assumed that the fractional volume of distribution of glucose represents 13% of body weight (8).
CHO and lipid oxidation rates were calculated from the CO2 production (VCO2), O2 consumption (VO2), and urinary nitrogen output (9). In the case of starved subjects, the VO2 and the VCO2 values used for calculation were corrected (9) for ketonuria, and the changes in ketone body pool were observed during the OGTT, assuming a functional volume of distribution of ketone bodies of 0.2 L/kg BW. Net CHO balance over the 0–5 h OGTT period was obtained by subtracting cumulated CHO oxidation from the total uptake of oral glucose. The latter, which includes uptake by splanchnic and peripheral tissues, was obtained by subtracting from the oral glucose load the amount of oral glucose remaining in extracellular fluid at 5 h. This calculation assumes that, at that time, oral glucose was totally absorbed by the gut (10). Expired 14CO2 in disintegretions (dpm)/min at the different time points was obtained by multiplying the CO2 specific activity of expired air (dpm/mmol) by the corresponding VCO2 (mmol/min). To calculate the 0–5 h oral glucose oxidation in studies 1 and 2, cumulated respiratory 14CO2 production (dpm/5 h) was divided by the specific activity of the glucose drink (dpm/g) after correction for the recovery factor estimated from study 3.
Statistics
All values are presented as the mean ± SEM. The comparison between groups considered the mean concentrations and fluxes for the basal period and mean concentrations and cumulated fluxes for the 0–5 h postprandial period. All comparisons were made using a paired or unpaired t test, as needed. Relationships between variables were analyzed by simple correlations. P less than 0.05 was considered significant.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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and 2 compare the time course of metabolic
changes occurring during the OGTT in the 14-h- and 110-h-fasted
subjects included in study 1. Before glucose ingestion, starvation was
associated with a significant lowering of glycemia (57 ± 3
vs. 89 ± 3 mg/dL; P < 0.001),
insulinemia (3.0 ± 0.4 vs. 6.0 ± 1.0 µU/mL;
P < 0.01), and CHO oxidation (3.3 ± 2.8
vs. 27.8 ± 4.7 g/5 h; P < 0.001) and
with an increase in plasma FFA levels (0.88 ± 0.06 vs.
0.49 ± 0.06 mmol/L; P < 0.001) and lipid
oxidation rates (35.7 ± 2.4 vs. 25.8 ± 3.4 g/5
h; P < 0.05). After glucose ingestion, mean 0–5 h
total glucose concentration was higher (P < 0.005) in
starved subjects (145 ± 7 mg/dL), as compared with ONF subjects
(115 ± 4 mg/dL). The contributions of exogenous to total glucose
concentration were, respectively, 79 ± 2 and 68 ± 2%
(P < 0.005). Mean insulin concentration was slightly
(but not significantly) increased (56 ± 9 vs. 43
± 8 µU/mL; P > 0.05), whereas FFA levels (0.49
± 0.04 vs. 0.28 ± 0.04 mmol/L; P <
0.005) and lipid oxidation rates (31.9 ± 2.3 vs.
19.3 ± 2.9 g/5 h; P < 0.005) were higher after
fasting. A marked drop in ßOHB levels was observed after oral glucose
in the starved individuals. Mean postprandial hyperlactatemic response
(0.88 ± 0.04 vs. 1.09 ± 0.07 mmol/L;
P < 0.025) was reduced and delayed after fasting.
Lactate concentrations at 5 h were not significantly different
from baseline in any group.
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. It should be pointed out that in this figure, which
intends mainly to document the time course of these metabolic events,
glucose disposal corresponds to the uptake of oral glucose from
systemic circulation only, because the rate of appearance (and
therefore, the rate of disposal) of oral glucose was calculated from
the dilution by oral glucose of the peripherally infused tritiated
tracer. In addition, in this figure, the oral glucose oxidation data
are uncorrected for incomplete recovery of metabolic
14CO2 in expired air because the correcting
factor has only been established for the entire 0–5 h period (see
below). Despite these limitations, it is clear that under both
experimental conditions, the changes in oral glucose disposal and CHO
oxidation are biphasic and tend to parallel glycemic levels, whereas
the rate of oxidation of oral glucose follows a slowly ascending curve.
More importantly, Fig. 2 shows that total CHO oxidation markedly
exceeds oral glucose oxidation in the ONF subjects, whereas only minor
differences between these curves exist after fasting. The possibility
that the latter observation could be caused by an effect of the
nutritional status on 14CO2 recovery has been
tested in study 3 with [14C]-bicarbonate infusions (see
Fig. 4). Although fasting was associated with a marked initial increase
in ßOHB levels (5.08 ± 0.77 vs. 0.34 ± 0.24
mmol/L) and a significant decrease in arterial blood pH (7.27 ±
0.01 vs. 7.39 ± 0.01; P < 0.001) and
plasma bicarbonate concentration (15.1 ± 0.8 vs.
24.5 ± 0.8 mmol/L; P < 0.001), appearance of
14CO2 in expired air followed the same pattern
under both experimental conditions, and total recovery was identical
(71.2 ± 3.0 vs. 70.9 ± 3.6%; P
> 0.05). This observation warrants the use of a single recovery factor
of 0.71 to correct the 14CO2 data obtained
after an oral load of 14C-labeled glucose, whether the
subjects were fasted or not.
The possibility that the rate of oxidation of the first glucose carbon
might not be representative of that of the other carbons was excluded
under our experimental conditions, as tested in study 2 (Fig. 3), which demonstrates that the kinetics
of 14CO2 appearance in expired air is virtually
identical whether oral glucose was labeled with [1-14C]-
or [U-14C]-glucose. Therefore, the results pertaining to
the ONF subjects of studies 1 (n = 8) and 2 (n = 9) were
combined for further analysis in Table 2.
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includes basal CHO and lipid oxidation rates and the 0–5 h
integrated values of oral glucose uptake, oral glucose oxidation
corrected for incomplete recovery of 14CO2
(factor 0.71), total CHO oxidation and net CHO balance in the ONF
(n = 17), and 4-day-fasted (n = 9) subjects during the OGTT.
Although the two groups ingested similar amounts of glucose (74.2
± 0.8 vs. 74.6 ± 0.8 g; P >
0.05), uptake of oral glucose was reduced in the fasted subjects
(64.8 ± 1.6 vs. 70.3 ± 1.1 g/5 h;
P < 0.01) because of the existence of a larger amount
of oral glucose remaining in the extracellular fluid at 5 h and
some slight glycosuria. In addition, fasting inhibited both oral
glucose oxidation (10.9 ± 0.7 vs. 20.0 ± 0.7
g/5h, P < 0.001) and total CHO oxidation, with the
latter effect being quantitatively the most important (12.5 ± 3.0
vs. 45.1 ± 1.9 g/5 h; P < 0.001).
Consequently, net CHO balance during the OGTT was doubled by prior
fasting (52.3 ± 2.6 vs. 25.2 ± 2.1 g/5 h;
P < 0.001). In ONF subjects, oral glucose oxidation
was approximately 55% lower than total CHO oxidation. This difference,
interpreted as corresponding to glycogen oxidation (see
Discussion) amounted to 25.1 ± 1.8 g/5 h. No such
difference existed in the 4-day-fasted group, so that glycogen
oxidation (1.6 ± 2.6 g/5 h) was not significantly different from
zero.
The possible relationships between basal CHO oxidation and the various
parameters of CHO metabolism during OGTT were analyzed for the whole
group of 33 subjects included in studies 1 and 2. As shown (see Fig. 5), the oxidation of oral glucose, total CHOs, and glycogen were all
strongly (P < 0.001) and positively correlated with
basal CHO oxidation (with respective r values of 0.80; 0.88, and 0.83),
whereas net CHO balance was negatively correlated with basal CHO
oxidation (r = -0.85; P < 0.001). Correlation
coefficients between the same parameters of postprandial CHO metabolism
and basal fat oxidation amounted, respectively, to -0.55, -0.55,
-0.50, and 0.48 (all P values < 0.01).
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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). These
observations confirm previous reports (1). The fact that the glucose
curve reaches higher levels despite normal or elevated insulin levels
is in agreement with the notion that fasting is associated with insulin
resistance (1). In this study, the assessment of the changes in CHO fluxes after glucose ingestion is based on 3 independent measurements (including uptake of oral glucose, oxidation of oral glucose, and total CHO oxidation), the other parameters being obtained by calculation. Before interpreting these data, it is necessary to discuss some methodological problems related to the measurement of glucose oxidation using [14C]-glucose and to clarify the significance of the difference between glucose oxidation and total CHO oxidation measured by indirect calorimetry.
Significance of oxidative and nonoxidative glucose disposal measured isotopically
Because the [14C]-glucose was mixed with the
ingested glucose, the ratio between 14CO2
production and the specific activity of the oral load measures oral
glucose oxidation. As shown in Fig. 2, there is a slow continuous rise
in respiratory 14CO2 appearance during the
5 h of the OGTT, in the face of a biphasic pattern of oral glucose
uptake. This delay in 14CO2 production is
related to trapping of 14CO2 in the bicarbonate
pool and its fixation in other metabolic pools of the body (11). These
processes lead to an underestimation of oral glucose oxidation unless
breath 14CO2 production is corrected for
incomplete recovery. The recovery factor obtained under our
experimental conditions (study 3; Fig. 4)
averaged 0.71 ± 0.02, a figure somewhat lower than that usually
obtained using constant [14C]-bicarbonate infusion (12).
This factor is necessarily approximate. One of the reasons is that the
fates of 14CO2 of intracellular and
extracellular origins are not identical, as shown by the differences in
the kinetics of breath 14CO2 appearance between
experiments with [14C]-glucose and
[14C]-bicarbonate. Although some studies have shown that
14CO2 retention is influenced by fasting (12, 13) and acid-base balance (14), this was not the case in the present
experiments (Fig. 4). Therefore, any inaccuracy in the recovery factor
should have the same impact on the calculation of oral glucose
oxidation in ONF and starved individuals and should not invalidate the
comparison between the two groups.
It has been suggested that the site of labeling of glucose carbon might
influence estimations of glucose oxidation because of a differential
contribution of each carbon of glucose to CO2 (11, 13).
Thus, it could theoretically be anticipated that the
14CO2 generation would be lower with
[1-14C]-glucose than with [U-14C]-glucose,
because C1 of glucose will form C3 of pyruvate
and C2 of acetyl-CoA with greater possibilities of isotopic
exchange in the tricarboxylic acid cycle than for other glucose carbons
such as C3 or C4. Indeed, the latter carbons
will form C1 of pyruvate, a carbon readily converted to
CO2 in the pyruvate-dehydrogenase reaction. The results
depicted in Fig. 4, comparing 14CO2 production
from [1-14C]- and [U-14C]-glucose, indicate
that under our experimental conditions, a differential rate of carbon
oxidation was not observed, and C1 was therefore considered
as representative of all glucose carbons.
The nonoxidative disposal of oral glucose (uptake of oral glucose
- oral glucose oxidation corrected for incomplete recovery of
14CO2) corresponds to the sum of glycogen
synthesis, de novo lipogenesis, and formation of the amount
of lactate that has not undergone oxidation within the time limits of
the experiments. De novo lipogenesis should be minimal
because the nonprotein RQ never exceeded 1.0 during the OGTTs. Because
lactate concentrations at 5 h were not significantly elevated
above baseline (Fig. 1), it is likely that during the OGTT, most of the
excess lactate formed, having escaped oxidation, has entered
gluconeogenesis, with subsequent glycogen formation in the liver by the
indirect pathway. We therefore considered (Table 2 and Fig. 5) that nonoxidative oral glucose
disposal represents essentially the sum of glycogen formation by both
the direct and indirect pathways. It should be realized that some of
the labeled glucose initially deposited as labeled glycogen might have
been subsequently mobilized and oxidized, so that oral glucose storage
at 5 h represents the amount of glycogen of dietary origin still
present as glycogen in liver and muscle at 5 h.
Significance of total CHO oxidation measured from respiratory gas exchange
In the basal state, CHO oxidation, calculated using the equations of indirect calorimetry (9), includes two components: 1) oxidation of the portion of extracellular glucose that derives from hepatic glycogenolysis but not gluconeogenesis (indeed, oxidation of glucose derived from glycerol is computed as fat oxidation, oxidation of glucose derived from proteins is computed as protein oxidation, and gluconeogenesis from lactate is not taken into account by respiratory calorimetry because it does not involve any gaseous exchange); and 2) oxidation of glycogen without passage through extracellular glucose. Therefore it should be considered that basal CHO oxidation corresponds entirely to glycogen oxidation from hepatic and muscular sources.
After glucose ingestion, CHO oxidation includes oxidation of dietary
glucose and that of intracellular glycogen. Glycogen oxidation during
the OGTT was therefore calculated as the difference between CHO
oxidation and oral glucose oxidation (3). This calculation is likely to
be somewhat inaccurate because of the necessarily approximate
corrections that have to be applied to both glucose oxidation measured
isotopically and to CHO oxidation measured by indirect calorimetry when
the latter is performed under conditions of ketosis. The reliability of
our estimates of glycogen oxidation during the OGTT is nevertheless
supported by the observation that figures close to zero are obtained in
the starved subjects in whom basal CHO oxidation (and therefore,
glycogen oxidation) is already totally suppressed in the basal state
(Table 2).
Influence of fasting on postprandial CHO metabolism
The main observation resulting from these studies is that net
glycogen storage during the 5 h of an OGTT is enhanced by previous
fasting in proportion to the duration of food deprivation. Table 2
shows that in ONF subjects, from the approximately 70 g of oral
glucose taken up, approximately 50 g are converted to glycogen,
but only approximately 25 g remain stored at 5 h because
glycogen breakdown and oxidation persist at a significant rate (
25
g/5 h). This observation implies the existence of an important cycling
between glucose-1-phosphate and glycogen under conditions of net CHO
storage. Several studies have shown that simultaneous synthesis and
degradation of glycogen can occur both in vitro in liver and
skeletal muscle (15, 16) and in vivo in liver of various
species (17, 18), including man (19).
In 4-day-fasted (as compared with 14-h-fasted) subjects (Table 2), the
uptake of oral glucose is slightly reduced (by less than 8%), but net
CHO storage is more than doubled (52 g/5 h). Conversion of oral
glucose to glycogen is significantly enhanced, but this effect is
quantitatively very small (54 vs. 50 g/5 h;
P < 0.05). The main cause of the increased glycogen
retention is that, at difference with ONF subjects, starved individuals
do not oxidize their hepatic or muscular glycogen stores at a
significant rate, nor in the basal state, nor during the OGTT (Table 2). Therefore, there is no glycogen cycling, and net CHO balance is
approximately equal to the amount of oral glucose stored. These data
are in line with in vivo studies performed in rats and
humans, using 13C-nuclear magnetic resonance methodology,
showing that glycogen turnover in liver is more rapid in the fed state
than after short-term fasting (17, 19). Interestingly, it has been
shown that the improved efficiency of protein retention after
starvation is related to a similar process, i.e. a decreased
rate of protein turnover (20).
A first mechanism that could enhance postprandial glycogen synthesis
and net CHO storage after prior starvation is the increased duration
and amplitude of the postglucose hyperglycemic response (the so-called:
starvation diabetes), which is known to be an important stimulus of
glycogen deposition (21). Other metabolic features of fasting that
could play a more essential role include increased fat oxidation and
depletion of glycogen stores. Elevated rates of fat oxidation after
fasting were observed in the basal state and were maintained almost
unabated during the course of the OGTT (Fig. 2), despite marked changes
in FFA levels, suggesting that intracellular fat oxidation remained
markedly stimulated during the early refeeding period. According to the
glucose-fatty acid cycle hypothesis, increased fat oxidation could
account for the decrease in oral glucose oxidation (22) and, therefore,
for the enhancement of oral glucose storage (23); but, as mentioned
before, this effect is quantitatively very small. It could also account
for the marked reduction in glycogen oxidation. This hypothesis is in
keeping with observations made by Wolfe et al. (24) who
showed, in humans, that during hyperinsulinemic clamp (when rates of
glucose uptake are maintained constant), a fat infusion has virtually
no inhibitory action on isotopically measured plasma glucose
oxidation but markedly inhibits glycogen oxidation. Another plausible
explanation of our data is the fasting induced reduction in glycogen
stores. Indeed, glycogen depletion is known to stimulate glycogen
synthesis in muscle (25) and liver (26) and could thus account for the
increase in oral glucose storage and, consequently, for its reduced
oxidation. On the other hand, low glycogen stores are likely to be
associated with low glycogen oxidation rates (27), both in the basal
state and during the OGTT, leading to the suppression of the glycogen
cycling that is observed in the ONF subjects. As a matter of fact, a
relationship between the levels of glycogen stores and the rapidity of
glycogen turnover has been documented in rat, dog, and human livers
(17, 18, 19). Although it is likely that both factors (increased fat
oxidation and glycogen depletion) participate in the regulation of
postprandial CHO metabolism after fasting, our data suggest that
glycogen depletion may play the predominant role. Indeed, parameters of
postprandial CHO metabolism correlate much more strongly with basal CHO
oxidation (assumed to reflect the level of glycogen stores) (Fig. 5)
than with basal or postprandial lipid oxidation.
In conclusion, prior fasting stimulates whole-body glycogen retention after glucose refeeding. Mechanisms include a modest stimulation of oral glucose storage and a marked inhibition of glycogen oxidation, leading to the suppression of the glycogen turnover that normally exists in ONF subjects during the absorptive period. Because the amplitude of these modifications is inversely related to basal CHO oxidation, it is suggested that the degree of initial glycogen depletion after fasting is a major determinant of net CHO storage, a phenomenon with obvious physiological relevance. The elevated rate of fat oxidation and the exaggerated postprandial hyperglycemic response associated with fasting could also favor CHO retention.
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Acknowledgments |
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Footnotes |
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Received February 2, 1998.
Revised April 3, 1998.
Accepted May 5, 1998.
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References |
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