Insulin effects on acetate metabolism
H. Piloquet,*
V. Ferchaud-Roucher,*
F. Duengler,
Y. Zair,
P. Maugere, and
M. Krempf
Centre de Recherche en Nutrition Humaine, Institut National de la
Santé et de la Recherche Médicale U539, 44093 Nantes,
France
Submitted 30 January 2003
; accepted in final form 19 May 2003
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ABSTRACT
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Acetate metabolism was studied in patients with insulin resistance. To
evaluate the interaction between glucose and acetate metabolism, we measured
acetate and glucose turnover with a hyperinsulinemic euglycemic clamp (hot
clamp) in obese and diabetic patients with insulin resistance (n = 8)
and in a control group with normal insulin sensitivity (n = 6). At
baseline, acetate turnover and plasma concentrations were similar between the
two groups (group means: 4.3 ± 0.4 µmol ·
kg-1 · min-1 and 128.2
± 11.1 µmol/l). Acetate concentrations decreased in both groups with
hyperinsulinemia but were significantly lower in the insulin-resistant group
(20% vs. 12%, P < 0.05). After the hot clamp treatment, acetate
turnover increased for the two groups and was higher in the group with normal
insulin sensitivity: 8.1 ± 0.7 vs. 5.5 ± 0.5 µmol ·
kg-1 · min-1 (P
< 0.001). No change related to insulin action was observed in either group
in the percentage of acetate oxidation. This was
70% of overall
utilization at baseline and during the clamp. No correlation between glucose
and acetate utilization was observed. Our results support the hypothesis that,
like glucose metabolism, acetate metabolism is sensitive to insulin.
stable isotopes; turnover; insulin resistance; hot clamp
PLASMA ACETATE IS DERIVED from an exogenous production by
colonic fermentation of nondigestible carbohydrates and an endogenous source
from amino acid, fatty acid, and glucose metabolism. In ruminant mammals,
exogenous contribution is the major component, whereas in nonruminants such as
rats or humans, the endogenous source is more important. Several studies
(11,
14,
15) have investigated acetate
kinetics in healthy human volunteers and in diabetic patients. Plasma acetate
concentrations are increased in type 2 diabetic patients
(3,
16,
18). It was suggested that
blood glucose or insulin can control acetate metabolism
(2,
7,
13). The relationship between
acetate and glucose concentration in the blood remains unclear, but a key
enzyme [acetyl-coenzyme A (CoA) synthetase (ACAS)] of acetate metabolism is
regulated by insulin in in vitro models
(17). The purpose of this
study was to evaluate the effects of insulin on acetate metabolism in humans
and its relationship to glucose metabolism. By using a hyperinsulinemic
euglycemic clamp technique (hot clamp), we have measured acetate and glucose
turnover in two groups of patients: control (normal insulin sensitivity; IS
group) and insulin resistant (obese and diabetic patients; IR group).
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METHODS
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Subjects
Six healthy human volunteers of normal weight [body mass index (BMI): 25.5
± 1.4 kg/m2] (Table
1), five abdominally fat obese patients (BMI 35.0 ± 0.7
kg/m2 and height/hip ratio >1), and three type 2 diabetic
patients (Hb A1c >7%, BMI 35.0 ± 3.0 kg/m2)
participated in this protocol. These patients represented a wide range of
insulin sensitivity. Their clinical and biochemical parameters are shown in
Table 1. These 14 subjects (7
females and 7 males, 47.9 ± 8.3 yr old) were divided into two groups
according to their insulin sensitivity. The IS group consisted of six
volunteers (subjects 1-6) with normal insulin sensitivity.
Eight insulin-resistant volunteers (subjects 7-14) formed
the IR group. The subjects were considered to be insulin resistant when the
glucose consumption required for maintaining baseline blood glucose during a
euglycemic clamp was <7.5 mg · kg-1 ·
min-1
(6). The subjects had no acute
pathology and were not under any medication. The experimental protocol was
approved by the Ethics Committee of the University Hospital of Nantes
(France).
Experimental Design
To avoid exogenous acetate production, a low-fiber diet (<5 g/day) was
consumed by the volunteers for 3 days before the protocol began. The study was
conducted after a 12-h overnight fast. On the morning of the experiment, two
short polyethylene catheters (20 gauge; Vigon, Paris, France) were inserted
into the antecubital vein for tracer infusion and on the wrist of the second
arm to sample venous blood.
A primed constant infusion technique with the use of
[l-13C]acetate and [6,6-2H2]glucose (99%
enrichment; Cambridge Isotope Laboratories, Andover, MA) was performed. The
primes were 19.25 and 18.3 µmol/kg, respectively. The rate of the acetate
infusion was 0.5 µmol · kg-1 ·
min-1 for 6 h and the rate of the glucose infusion was
9.75 µmol · kg-1 ·
h-1 for 3 h. After 3 h of infusion, a hot clamp was
started to obtain insulin concentration at
100 µU/l
(6). During the clamp, the
glucose tracer rate was adjusted to the glucose infusion rate (ml/h) to
maintain the glycemia between 4.9 and 5.5 mmol/l. Arterialized blood samples
were collected at -180, -60, -45, -30, -20, -10, 0, 60, 120, 150, 160, 170,
and 180 min (Fig. 1).
Respiratory gas exchanges were measured with the use of indirect calorimetry
(Deltatrac, Helsinki, Finland) throughout the study. Expired breath gases were
sampled before and after each blood sample.
Sampling Procedures and Gas Chromatograph-Mass Spectrometer
Analysis
Acetate analysis. Measurement of plasma acetate enrichment was
performed as previous described
(14). Briefly, an internal
standard (24 µl of [2H3]acetate, 2.35 mmol/l) was
added to 500 µl of plasma sample to measure plasma acetate concentration.
Plasma samples were deproteinized with 10 mg of sulfosalicylic acid (Sigma,
St. Quentin Fallavier, France) and centrifuged at 2,200 g for 30 min.
The supernatants were transferred into a glass tube and acidified by the
addition of 30 µl of HCl (10 mol/l) (Fluka, Bushs, Switzerland). Acetate
and standards were extracted from plasma into 3 ml of diethyl ether (Fluka) by
being vortexed for 15 min. The samples were centrifuged for 15 min at 1,200
g, and 8 µl of tert-butyldimethylsilyl imidazole (Fluka)
were added to the separated organic phase. The
tert-butyldimethylsilyl derivatives were heated at 60°C for 30
min and then cooled and evaporated to 500 µl.
Two microliters of acetate were injected into a split/splitless injector
(splitless mode) into a gas chromatograph (GC; model 5890A, Hewlett-Packard,
Palo Alto, CA) with the use of a 30 m x 0.25 mm capillary column (model
DB1, J/W Scientific, Folsom, CA) and connected with a quadrupole mass
spectrometer (MS; model 5971A, Hewlett-Packard). The injector temperature and
the transfer line between GC and MS were 250°C and 290°C,
respectively. The temperature program started at 50°C and ramped to
85°Cat5°C/min, then up to 250°C at 50°C/min, followed by 1 min
at 250°C. Electron impact ionization was operated with an electron energy
rate of 70 eV. Selected ion monitoring mode of
M-[C-(CH3)3], corresponding to ions at
mass-to-charge ratios (m/z) 117, 118, and 120, was used to measure
acetate enrichment and concentration. Calibration curve for isotopic
enrichments was prepared in the range of 0% to 20% for
[l-13C]acetate. Concentration calibration levels were obtained from
baseline to 390 µmol/l of acetate.
Glucose analysis. Fifty microliters of plasma samples were
deproteinized with 300 µl of acetone, vortexed, and centrifuged at 2,200
g for 15 min. The supernatants were dried under nitrogen vacuum
(10). The samples were
derivatized with a mixture of 50 µl of acetic anhydride and 50 µl of
pyridine (Sigma), at 80°C for 1 h, evaporated, and diluted in 1 ml of
ethyl acetate (19).
One microliter of a penta-acetate derivative was injected in the GC-MS
system described above. The temperature program started at 80°C and ramped
to 250°C at 30°C/min, followed by 3 min at 250°C. Electron impact
ionization and selected ion monitoring mode were used on ions with
m/z 98 and 100. Calibration curve was obtained from known isotopic
enrichment solutions prepared in ethyl acetate ranging from 0% to 10%
enrichment for [6,6-2H2]glucose.
CO2 analysis. CO2
production (
CO2) was
determined by indirect calorimetry and isotopic enrichment of expired
CO2 was measured by GC-IRMS (Breathmat Plus, ThermoFinnigan,
Bremen, Germany) with the use of a packed steel column (3 m Hayes Sep-D). A
laboratory CO2 standard calibration against the international P
Belemnite (PDB) carbonate was used as a reference. The data were obtained in
13C (in %thou).
Calculation Methods
Acetate. The rate of total appearance of acetate (Ra)
was calculated according to the equations for steady state as follows
where i was the infusion rate (in µmol ·
kg-1 · min-1),
Et and Ep were, respectively, the
isotopic enrichment of the tracer ([l-13C]acetate), and the plasma
at plateau given as mole percent excess (MPE).
Extracellular pool (µmol/kg) was C · Vd,
where Vd is the distribution volume of acetate (0.2 l/kg)
(12).
Glucose. Before the hot clamp treatment was started, the
[6,6-2H2]glucose infusion was constant for 3 h.
Therefore, the glucose Ra was calculated according to the equation
used for acetate.
During the hot clamp treatment, the glucose Ra was calculated
with the Steele equation for nonsteady state, as follows
where F was the infusion flow of the tracer (in mg ·
kg-1 · min-1), p
was the pool fraction (0.65), V was the distribution volume of glucose (0.2
l/kg), G was the plasma concentration of glucose at time t (in g/l),
and Ep was the plasma isotopic enrichment of glucose at
time t. For the constant isotopic enrichment in time, the equation
used was
Oxidation of acetate. Enrichment of CO2 was expressed
in
13C (in %thou). The values were transposed in atom
percent (AP)
R was the 13C/12C ratio of international PDB standard (R
= 0.0112372), and
13C was the 13C enrichment of
the samples. The isotopic enrichment of expired CO2 was calculated
[in AP excess (APE)] as
APs and AP0 were the AP of the sample and at time
0, respectively. The oxidation (Oxi) was expressed in µmol ·
kg-1 · min-1 and was
where ECO2 was the isotopic enrichment of expired
CO2 in APE,
CO2 was the expired rate
of CO2 (µmol/min), C was the recovery coefficient
(0.78) for [l-13C]acetate in the postabsorptive state
(20), and M was the
weight of the volunteer.
The percent oxidized (%Ox) was determined as
where Rd was the rate of disappearance of acetate. The percentage
of
CO2 from oxidation of
acetate (%
CO2) was
The acetate energy contribution (Cea, in %) was calculated with the
equation as below
where Ea was the energy derived from acetate (1 mol of oxidized
acetate = 879 kJ) (5), and
Et was the total energy (in kJ/min).
Statistical Analysis
Data are reported as means ± SE unless otherwise stated. Correlation
studies were realized among acetate rate, glucose rate, and insulin
sensitivity. Statistical analysis was performed with the use of Instat
Statistical software (Graph-Pad, San Diego, SA). Student's t-test was
used to compare clinical and kinetic data of the subjects. Correlation
analyses were performed with the use of Spearman's coefficient analysis. A
two-tailed probability level of 0.05 was accepted as statistically
significant.
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RESULTS
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At the end of the clamp study, all the IS subjects had a glucose
consumption >7.5 mg · kg-1 ·
min-1 and was 9.6 ± 1.1 for the IS group vs. 4.9
± 0.5 mg · kg-1 ·
min-1 for the IR group (P < 0.01)
(Table 2). In the IR group, BMI
and the height/hip ratio were significantly higher for the IR group compared
with the IS group: 35.0 ± 1.1 versus 25.6 ± 1.2 kg/m2
(P < 0.01) and 1.0 ± 0.01 versus 0.9 ± 0.02
(P < 0.01). Glycemia and Hb A1c were also higher in the
IR group compared with the IS group: 7.4 ± 1.2 mmol/l and 6.2 ±
0.4% vs. 5.4 ± 0.1 mmol/l and 5.4 ± 0.1%, respectively
(P = 0.11 and 0.17). In the IS group, only one subject (subject
5) was obese, but all subjects showed a normal glucose tolerance
(Table 1). In the IR group, all
subjects were obese, three were diabetic (subjects 11-13),
and one showed glucose intolerance (subject 10). During and at the
end of the protocol, mean glycemia and insulinemia were similar in the two
groups: 5.2 ± 0.05 mmol/l and 103.7 ± 19.4 pmol/l in the IS
group vs. 5.3 ± 0.08 mmol/l and 143 ± 11.3 pmol/l in the IR
group (Table 2). Free fatty
acid plasma concentrations were higher in the IR group (0.6 ± 0.04
mmol/l) than in the IS group (0.4 ± 0.05 mmol/l) at baseline but
decreased and became similar at the end of the clamp (IR: 0.07 ± 0.01
mmol/l, IS: 0.06 ± 0.01 mmol/l). No significant difference in baseline
acetate concentrations was found between the two groups
(Table 3).
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Table 3. Glucose turnover rates, acetate turnover rates, and plasma acetate
concentration at basal state and after the clamp in IS and IR groups
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In the basal state, the constant infusion of
[6,6-2H2]glucose led to similar glucose turnover in the
two groups: 8.8 ± 0.4 vs. 8.8 ± 0.2 mmol ·
kg-1 · min-1 (P =
0.6). During the hot clamp treatment, the glucose turnover rate increased and
was higher in the IS group: 45.1 ± 3.8 vs. 15.9 ± 2.2 µmol
· kg-1 · min-1
(P < 0.001) in the IR group
(Table 3).
The baseline acetate turnover rates were not significantly different among
both groups (Fig. 2). After the
clamp, mean acetate turnover of the two groups increased and was higher in the
IS group: 8.1 ± 0.7 vs. 5.5 ± 0.5 µmol ·
kg-1 · min-1 (P
< 0.001) (Table 3). No
significant correlation was found between acetate turnover or acetate
concentration and glucose rate of infusion. No significant correlations were
found between acetate turnover and glucose turnover or plasma free fatty acid
concentration. The oxidation of acetate increased significantly with
hyperinsulinemia in both groups and was higher in the IS group: 5.7 ±
0.7 µmol · kg-1 ·
min-1 for IS group vs. 4.4 ± 0.3 µmol ·
kg-1 · min-1 for IR group
(P < 0.001). In basal conditions, the percentage of oxidized
acetate calculated from acetate production was similar in both groups 67.7
± 3.4% (IS group) vs. 70.0 ± 5.4% (IR group). After the clamp,
it was 76.0 ± 4.3% vs. 76.9 ± 3.7%, respectively
(Fig. 3). The percentage of
expired CO2 from
CO2 and Cea
were also similar,
3%, in both groups under basal conditions and
increased significantly
(
CO2 70% for IS vs. 35%
for IR; Cea 80% for IS vs. 70% for IR) after insulin administration
(IS: P < 0.01, IR: P < 0.05).

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Fig. 3. Percentage of acetate oxidation (means ± SE) in basal state for IS
group (open bar) and for IR group (dark gray bar), during hot clamp for IS
group (light gray bar), and for IR group (solid bar). * =
%increase of oxidation vs. basal conditions, with no significant difference
between basal and clamp state for IS and IR groups.
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DISCUSSION
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In this study, the effect of insulin on acetate metabolism was analyzed.
Under basal conditions, acetate turnover rate and plasma acetate concentration
were similar in patients with normal or impaired insulin resistance. Acetate
concentrations decreased with hyperinsulinemia in both groups but tended to be
lower in the group with insulin resistance. The acetate turnover increased
with insulin infusion, suggesting a concomitant increase in acetate production
and utilization, but this effect was significantly lower in IR patients.
Akanji et al. (3)
investigated changes in acetate concentration induced by a hyperinsulinemic
euglycemic clamp in 13 nondiabetic individuals, including 7 obese patients,
and in 9 diabetic patients. Acetate concentrations decreased in both groups
during insulin administration. In the nondiabetic subjects, acetate
concentrations returned to baseline during the second hour of the clamp. It
was suggested that the lack of increase in acetate concentration of the
diabetic patients was not related to insulin resistance, but rather to a
difference in postreceptor glucose metabolism toward glycogenesis or
glycolysis (1,
3). In diabetic patients,
decreased glycolysis may explain the decreased production of acetyl-CoA and
therefore of acetate. Some studies
(2,
8,
18) have already found a
correlation between plasma acetate and glucose, thus supporting a conversion
between acetate and glucose via acetyl-CoA.
Insulin induced an increase in acetate turnover and a decrease in acetate
concentrations, but this effect was lower in patients with insulin resistance.
On the one hand, the results indicated a reduction in acetate production in
subjects with insulin resistance. On the other hand, insulin accelerated the
catabolism of acetate, which is dependent on glucose availability
(7). Consequently, decreased
glucose uptake associated with insulin resistance may result in a decrease in
acetate utilization. This permissive effect of glucose may have led to the
increase in acetate flux seen during the hyperinsulinemic clamp because
glucose turnover was increased, not only by the administration of insulin but
also by the exogenous glucose supply needed to maintain blood glucose
concentrations within the normal range. However, in our study, acetate
turnover was correlated neither to glucose flux nor to fasting blood glucose
concentrations, suggesting that acetate metabolism is sensitive to insulin
rather than to glucose.
Insulin increased the rate of acetate catabolism, as shown by the increase
in acetate metabolic clearance during the clamp. However, this effect was less
marked in patients with insulin resistance. Mechanisms that may explain this
decreased acetate catabolism associated with insulin resistance include
decreased activity of the enzyme ACAS, decreased glucose utilization, and
decreased acetate oxidation.
ACAS, which is involved in the conversion of acetate to acetyl-CoA, is
sensitive to insulin action
(13). The decrease in acetate
utilization that results from a decrease in ACAS activity is induced by
insulin resistance. This mechanism has been recently documented in rats
(17). A decrease in acetate
oxidation via acetyl-CoA may also explain the decrease in acetate utilization.
In both groups, 65-68% of the acetate underwent oxidation. These percentages
were similar to those found by our group in healthy volunteers
(11). Acetate oxidation was
more marked in subjects with normal sensitivity to insulin, both under basal
conditions and with insulin stimulation. However, the contribution of acetate
to energy expenditures was similar in the two groups under basal conditions,
3%, and increased twofold with insulin administration, indicating that
acetate oxidation was proportional to acetate utilization. Insulin probably
acts on the enzyme ACAS, which regulates acetate homeostasis and not
oxidation. Insulin decreases the oxidation of free fatty acids and total
lipids (9). Thus acetate
behaves differently compared with other fatty acids. Conversely, insulin
increases glucose oxidation and nonoxidative glucose utilization
(9). Furthermore, the
alteration in insulin effects associated with insulin resistance results in a
decrease in glucose utilization. Our hypothesis supports the sensitivity of
acetate to insulin action. Acetate metabolism is similar in this respect to
glucose metabolism. Insulin resistance seems to contribute to the alteration
in acetate metabolism associated with diabetes or obesity. Several authors
have suggested that short-chain triglyceride solutions, such as triacetin, may
be useful parenteral nutrients
(4). In case of insulin
resistance, acetate should be used cautiously to avoid possible adverse
effects as previously reported with acetate dialysis treatment
(21).
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DISCLOSURES
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This work was supported by La Délégation de la Recherche
Clinique du Centre Hospitalier Universitaire de Nantes.
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ACKNOWLEDGMENTS
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We are grateful to A. Wolfe for careful reading of the manuscript. We also
thank I. Falconi of the Pharmacie Hotel-Dieu (Nantes, France) for the
preparation of the stable isotope solutions, and V. Plattner
(Délégation de la Recherche Clinique-Nantes) for administrative
support.
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FOOTNOTES
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Address for reprint requests and other correspondence: M. Krempf, Clinique
d'Endocrinologie-Nutrition, Hôtel-Dieu, 44093 Nantes 01, France (E-mail:
mkrempf{at}sante.univ-nantes.fr).
The costs of publication of this article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section 1734
solely to indicate this fact.
* H. Piloquet and V. Ferchaud-Roucher contributed equally to this work. 
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Copyright © 2003 by the American Physiological Society.