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


    ABSTRACT
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 DISCLOSURES
 REFERENCES
 
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 {approx}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).


    METHODS
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 DISCLOSURES
 REFERENCES
 
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).


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Table 1. Clinical and biological features of subjects

 

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 {approx}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.



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Fig. 1. Clinical protocol. T, time.

 

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 {delta}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 {delta}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 {delta}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.


    RESULTS
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 DISCLOSURES
 REFERENCES
 
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 2. Basal insulin, insulin at clamp plateau, and glucose utilization at end of clamp in IS and IR subjects

 

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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

 

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. 2. Plasma acetate turnover (means ± SE) in the insulin-sensitive (IS; {diamondsuit}) and insulin-resistant (IR; {blacksquare}) groups (in µmol · kg-1 · min-1) at basal state during the clamp.

 


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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). *{Delta} = %increase of oxidation vs. basal conditions, with no significant difference between basal and clamp state for IS and IR groups.

 


    DISCUSSION
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 DISCLOSURES
 REFERENCES
 
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).


    DISCLOSURES
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 DISCLOSURES
 REFERENCES
 
This work was supported by La Délégation de la Recherche Clinique du Centre Hospitalier Universitaire de Nantes.


    ACKNOWLEDGMENTS
 
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.


    FOOTNOTES
 

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. Back


    REFERENCES
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 DISCLOSURES
 REFERENCES
 

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