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Original Studies |
Oxford Lipid Metabolism Group, Nuffield Department of Clinical Medicine, Radcliffe Infirmary, Oxford, United Kingdom OX2 6HE; the Department of Physiology and Pharmacology, Medical School, Queen’s Medical Center (I.A.M.), Nottingham, United Kingdom NG7 2UH; and the Unit of Metabolic Medicine, Imperial College School of Medicine at St. Mary’s (P.A.B.), London, United Kingdom W2 1PG
Address all correspondence and requests for reprints to: Dr. Keith N. Frayn, Oxford Lipid Metabolism Group, Radcliffe Infirmary, Oxford, OX2 6HE United Kingdom. E-mail: keith.frayn{at}oxlip.ox.ac.uk
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Abstract |
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Lipolysis in the sc adipose tissue of the anterior abdominal wall was studied by measurement of arterio-venous differences, and lipolysis in the whole body was studied by constant infusion of [1,2,3-2H5]glycerol for measurement of the systemic glycerol appearance rate. Hypercortisolemia led to significantly increased arterialized plasma nonesterified fatty acid (NEFA; P < 0.01) and blood glycerol concentrations (P < 0.05), with an increase in systemic glycerol appearance (P < 0.05). However, in sc abdominal adipose tissue, hypercortisolemia decreased veno-arterialized differences for NEFA (P < 0.05) and reduced NEFA efflux (P < 0.05). This reduction was attributable to decreased intracellular lipolysis (P < 0.05), reflecting decreased hormone-sensitive lipase action in this adipose depot. Hypercortisolemia caused a reduction in arterialized plasma TAG concentrations (P < 0.05), but without a significant change in the local extraction of TAG (presumed to reflect the action of adipose tissue lipoprotein lipase). There was no significant difference in plasma insulin concentrations between the control and hypercortisolemia study. Site-specific regulation of the enzymes of intracellular lipolysis (hormone-sensitive lipase) and intravascular lipolysis (lipoprotein lipase) may explain the ability of acute cortisol treatment to increase systemic glycerol and NEFA appearance rates while chronically promoting net central fat deposition.
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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In adipose tissue, lipolysis is regulated by two enzymes, hormone-sensitive lipase (HSL; EC 3.1.1.3) and lipoprotein lipase (LPL; EC 3.1.1.34). The activities of these enzymes are reciprocally linked. After an overnight fast, adipose tissue LPL activity is low, whereas HSL activity is high (7). HSL regulates intraadipocyte TAG hydrolysis, whereas LPL regulates intravascular lipoprotein-TAG hydrolysis. In the fasting state both enzymes may contribute glycerol and nonesterified fatty acid (NEFA) to the circulation (8), and these contributions are not distinguished by measurement of systemic glycerol or NEFA turnover.
In vitro, cortisol increases LPL (9) and HSL (10) activity in adipose tissue. It has been thought that hyperglycemia caused by hypercortisolemia leads to hyperinsulinemia, which inhibits HSL activity and potentiates LPL activity (11). This has been used to explain the increased fat mass observed in chronic hypercortisolemia. The main aim of this study was to examine the effects of hypercortisolemia on NEFA efflux and the rates of action of HSL and LPL in adipose tissue in vivo, and to compare these with its effects on systemic lipolysis estimated by glycerol appearance.
The control studies reported here were part of a larger group of control studies of the effects of blockade of cortisol secretion, the results of which were reported previously (12).
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Six healthy subjects (five men and one woman) volunteered for the study; their ages ranged from 22.5–50.4 yr (median, 26.0 yr), and their body mass indexes ranged from 20.3–26.9 kg/m2 (median, 24.0 kg/m2). The study was approved by the Central Oxford Research ethics committee, and all subjects gave their informed consent before the study. All subjects were asked to refrain from smoking and unaccustomed exercise for a period of 24 h before the study. None of the volunteers was taking any medication, and a detailed history was taken to exclude any recent illness or family history of metabolic disease.
Protocol
Subjects arrived at the laboratory at 1800 h after a typical day. A low fat meal [total energy content, 2524 kJ (597 Cal); total protein content, 53.5 g; total carbohydrate content, 52.9 g; total fat content, 20.8 g] was provided at approximately 1800 h on each occasion.
After the meal a 10-cm 22-gauge catheter (Secalon Hydrocath, Viggo-Spectramed, Swindon, UK) was threaded anterogradely into the superficial inferior epigastric vein draining the sc abdominal adipose tissue, as described previously (13). This catheter was filled with saline and sealed for the night. A 20-gauge cannula was placed into a forearm vein, and the distal part of the forearm was wrapped in a warm blanket to obtain partially arterialized blood. Hourly blood samples were obtained from 2200 h for overnight hormone analysis using a low volume long line. At 1100 h, the lights were switched off, and the subjects were allowed to sleep until 0630 h the following day. On one occasion hydrocortisone sodium succinate was infused iv between 0300–1400 h to achieve supraphysiological plasma cortisol concentrations (1500–1700 nmol/L). All subjects were studied twice, and the order of the study was random.
Between 0700–0800 h, infusion of deuterated glycerol ([1,2,3-2H5]-glycerol, Cambridge Isotope Laboratories, Woburn, MA) was begun with a priming dose of 0.5 µmol/kg followed by constant infusion at 3 µmol/kg·h, as described by Beylot et al. (14). The infusion was continued until the study concluded at 1400 h. Isotopically labeled glycerol infusion was only carried out in five of the six subjects.
Arterialized venous blood was obtained through a 20-gauge cannula placed retrogradely in the dorsal venous arch of the hand at 0700 h. This hand was warmed in a hot box, which was maintained at 65 C (15). All cannulas were kept patent by slow saline (0.9% NaCl) infusion at a rate of 30 mL/h. Adipose tissue blood flow (ATBF) was measured by the 133Xe clearance technique (16). Briefly, 3 megabecquerels 133Xe (CIS UK, High Wycombe, UK) dissolved in 0.9% saline were injected paraumbilically into the adipose tissue at 0715 h. A CsI crystal detector (Oakfield Instruments, Eynsham, UK) was used to measure the residual radioactivity in the adipose tissue (17).
From 0800 h, both arterialized and adipose tissue venous blood samples were obtained simultaneously every hour until 1400 h. ATBF was measured immediately after the blood samples were obtained. The ambient temperature was maintained at 23 ± 1 C. The subjects rested in a supine position for the duration of the study and were allowed to drink water ad libitum.
Analytical methods
During the night a blood sample was drawn into a heparinized syringe every hour. The sample was rapidly centrifuged at 4 C, and the plasma was separated and stored at -20 C for cortisol and insulin analyses.
At 0800 h, both arterialized and adipose venous blood samples were drawn into heparinized syringes (Monovette, Sarstedt, Leicester, UK). A portion (100 µL) was immediately deproteinized in 7% (wt/vol) perchloric acid, and the supernatant was stored for measurements of glycerol and lactate and 3-hydroxybutyrate. The remainder of the blood was rapidly centrifuged at 4 C. Plasma glucose concentrations were measured before freezing. One milliliter of the arterialized plasma was mixed with 20 µL catecholamine preservative, the sample was stored at -70 C, and an additional 0.5 mL was stored at -20 C for hormone analysis. The remaining arterialized and adipose venous plasma was frozen at -20 C for NEFA and TAG analysis and for measurement of glycerol isotopic enrichment in the arterialized samples. An arterialized sample was also obtained for hematocrit and blood gas analysis to ensure adequate arterialization.
Enzymatic methods were adapted to a Monarch centrifugal analyzer (Instrumentation Laboratory, Warrington, UK) for NEFA (Wako NEFA C kit, Alpha Laboratories, Eastleigh, UK), TAG (18), and metabolite analysis (19). Cortisol was measured in the arterialized plasma using a solid phase RIA (DPC, Gwynedd, UK). Insulin (Pharmacia, Milton Keynes, UK) and glucagon (DPC) were measured using double antibody RIAs. Plasma catecholamines were measured by high performance liquid chromatography with electrochemical detection (20).
The isotopic enrichment of plasma glycerol was determined by preparation of the Tris-(t-butyl-dimethylsilyl) derivative and analyzed on a Varian 3400 gas chromatograph/Finnegan Incos XL mass spectrometer (Finnegan Mat, Hemel Hempstead, UK). The samples were injected onto a BPX5 column (25 m x 0.35 mm od; 0.25-µm film; SGE, Milton Keynes, UK), and the temperature was programmed from 120–320 C (25 C/min to 200 C, 10 C/min to 240 C). The m-57 ions, m/z 377 (DO) and m/z 382 (D5), were monitored on the mass spectrometer, and the area under the ion peaks was calculated to obtain new values of atoms percent excess (APE). Background enrichment was measured in a sample taken at 0700 h, before administration of the isotope. Calibration enrichment curve samples [0–5 mol percent excess (MPE)] were run with each sample.
Calculations
The raw APEs of the plasma glycerol enrichments were converted to MPEs by application of the calibration enrichment curve slopes, obtained by regression analysis of the plot of theoretical MPE against observed APE. Systemic glycerol appearance rates were calculated using steady state equations (14, 21).
The ATBF was calculated, as described by Larsen (16), from the product of the slope of decay and the partition coefficient. The partition coefficient for human adipose tissue was assumed to have a value of 10 g/mL (22).
For calculation of substrate fluxes in adipose tissue, NEFA and TAG concentrations in plasma (P) were converted to those in the whole blood (B) using the hematocrit (H): B = P x (1 - H).
Arterio-venous differences (a-v) or veno-arterial differences (v-a) were calculated for whole blood concentrations in micromoles per L. The rate of NEFA efflux (nanomoles per 100 g/min) was calculated as ATBF x (v-a)NEFA. The rate of extraction of TAG (nanomoles per 100 g/min), which reflects the rate of action of LPL in adipose tissue (23), was calculated as ATBF x (a-v)TAG.
Intracellular lipolysis, assumed to reflect the rate of action of HSL, was calculated in terms of the transcapillary flux of glycerol (i.e. the difference between total glycerol efflux and that assumed to arise from LPL action) (23): HSL rate of action (nmol/100 g·min) = ATBF x [(v-a)glycerol - (a-v)TAG].
These calculations have been discussed previously (23, 24) and were based on the following assumptions: 1) no significant oxidation of fatty acids in adipose tissue, 2) complete hydrolysis of TAG into fatty acids and glycerol (25), and 3) no significant glycerol reutilization in adipose tissue (26).
Statistical analysis
Data in the text and figures are expressed as the mean ± SEM. Repeated measures ANOVA with SPSS (SPSS UK, Chertsey, UK) was used to assess changes in the concentrations of substrates and metabolites, and analysis of covariance was used to test a systematic change with time. Areas under the curve (AUCs) were calculated for hormone concentrations and substrate fluxes and compared using the paired t test, as recommended by Matthews et al. (27). Trends with time were tested by analysis of covariance using the general linear model (SPSS), computing a pooled regression line with time as the independent variable and testing the difference of its slope from zero.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The plasma cortisol concentrations between 2000–0300 h were
similar during the control and hypercortisolemia studies, as measured
by AUC (631 ± 133 vs. 479 ± 65
nmol·L-1·h; P = 0.29). Hydrocortisone
infusion caused a significant increase in the mean plasma cortisol
concentration between 0300–1400 h compared with that in the control
study, as measured by AUC (14,920 ± 943 vs. 3,404
± 265 nmol·L-1·h; P < 0.0001; Fig. 1A
).
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The mean arterialized plasma NEFA concentrations were
significantly higher during the hypercortisolemia study than during the
control study (725 ± 65 vs. 527 ± 60 µmol/L;
P < 0.01, by ANOVA). Adipose venous plasma NEFA
concentrations were significantly higher than the arterialized plasma
NEFA concentrations during both studies (P < 0.01, by
ANOVA), indicating net release of NEFA from the sc adipose tissue. The
veno-arterial plasma NEFA concentration differences were significantly
lower during the hypercortisolemia study than during the control study
(P < 0.05, by ANOVA; Fig. 2A).
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).
Arterialized plasma TAG concentrations decreased significantly with
time during both studies (P < 0.001, by ANOVA). In
addition, hypercortisolemia caused a significantly greater reduction in
the arterialized plasma TAG concentration with time compared with that
in the control study (P < 0.05, by ANOVA). There was
small, but consistent, TAG extraction by adipose tissue. However, the
veno-arterial plasma TAG concentration differences were similar during
hypercortisolemia and control studies (P = 0.58, by
ANOVA; Fig. 2C).
ATBF and reesterification of NEFA
Hypercortisolemia had no significant effect on ATBF
(P = 0.91, by ANOVA) or the ratio of NEFA to glycerol
release (P = 0.90, by ANOVA; Table 1).
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Although hypercortisolemia had no significant effect on TAG
extraction (LPL rate of action) in sc adipose tissue compared with that
in the control study as measured by the AUC (30.9 ± 9.0
vs. 51.6 ± 9.95 µmol/100 g; P =
0.21; Fig. 3B), intracellular lipolysis
(rate of action of HSL) was significantly lower during the
hypercortisolemia study compared with that during the control study as
measured by AUC (98.1 ± 30.6 vs. 194.7 ± 46.8
µmol/100 g; P < 0.05; Fig. 3A). This was associated
with decreased NEFA efflux from adipose tissue during hypercortisolemia
compared with that during the control study as measured by AUC
(230 ± 38 vs. 500 ± 102 µmol/100 g;
P < 0.05; Fig. 3C).
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Systemic glycerol appearance rates, measured isotopically in five
subjects, increased with time (P < 0.01, by analysis
of covariance), reflecting increasing whole body lipolysis with
continued fasting (Fig. 4). Glycerol
appearance rates were significantly higher during hypercortisolemia
than in the control study (P < 0.05, by ANOVA; Fig. 4).
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Arterialized plasma glucose concentrations did not change with
time, and mean values were significantly higher during the
hypercortisolemia study compared with those during the control study
(5.85 ± 0.12 vs. 4.76 ± 0.08 mmol/L;
P < 0.001, by ANOVA). Arterialized blood lactate
concentrations were also constant with time and were not significantly
different between the studies (540 ± 35 vs. 630
± 90 µmol/L; P = 0.34, by ANOVA). Blood
3-hydroxybutyrate concentrations were significantly greater and
increased more rapidly in the hypercortisolemia study than in the
control study (P < 0.05, P < 0.05, by
ANOVA; Fig. 2D).
Plasma insulin, glucagon, and catecholamine concentrations
Hypercortisolemia had no significant effect on the plasma insulin
concentration compared with that in the control study as measured by
AUC (69.9 ± 12.9 vs. 61.39 ± 7.9
mU·L-1·h; P = 0.47; Fig. 1B). Arterialized
plasma concentrations of glucagon, epinephrine, and norepinephrine did
not change with time, and there were no significant differences in
their concentrations between the hypercortisolemia and control studies
as measured by AUC [603 ± 46 vs. 719 ± 75
ng/L·h (P = 0.29); 0.619 ± 0.113 vs.
0.745 ± 0.098 nmol·L-1·h (P = 0.45);
4.99 ± 0.81 vs. 4.81 ± 0.52
nmol·L-1·h (P = 0.83), respectively].
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Our finding that acute hypercortisolemia caused a reduction in the efflux of fatty acids from a central adipose depot would be consistent with the morphological findings in chronic hypercortisolemia of truncal fat mass preservation or increase (5, 6). The HSL mass in adipose tissue increases significantly in the presence of glucocorticoids in vitro (10). However, in our study, acute hypercortisolemia led to a significant reduction in the rate of action of HSL. The HSL mass in adipose tissue may not reflect its activity, as translocation of the HSL molecule to the lipid surface is essential for its action (28). Adipocytes have well defined intracellular glucocorticoid receptors (29). These receptors can modulate the sensitivity to glucocorticoids by decreasing their own numbers (30). In addition, they can alter the glucocorticoid response (31). Thus, the chronic effects of glucocorticoids can be markedly different from the acute effects. However, in our study the findings of acute hypercortisolemia correlate well with the morphological findings of chronic hypercortisolemia.
The mechanism for the reduction in HSL action is not clear. Hypercortisolemia causes hyperglycemia which may lead to increased plasma insulin concentrations (11, 32); inhibition of insulin secretion by somatostatin leads to increased fatty acid turnover (4). Elevated plasma insulin concentrations increase the rate of action of adipose tissue LPL and reduce the rate of action of HSL, resulting in net TAG accumulation in adipose tissue (23). In the present study acute hypercortisolemia increased plasma glucose concentrations, but had no significant effect on plasma insulin concentrations. It could be that a nondetectable increase in plasma insulin was sufficient to suppress lipolysis in this depot, as adipose tissue lipolysis is exquisitely sensitive to insulin concentrations in the physiological range (33). However, the fact that blood 3-hydroxybutyrate concentrations were significantly higher during hypercortisolemia compared with those during the control study, as found also by Johnston et al. (11), argues against this. Ketogenesis in hepatocytes is also extremely sensitive to insulin (34); thus, a small rise in the plasma insulin concentration would have been expected to depress 3-hydroxybutyrate concentrations. The hyperglycemia observed in our study is not thought to affect lipolysis (35, 36). The reduction in the HSL rate of action might also be explained by feedback inhibition through higher arterial NEFA concentrations (37, 38).
As intracellular lipolysis was suppressed by hypercortisolemia, the increased arterial NEFA concentrations must have had another origin. Cortisol is known to increase the mass of adipose tissue LPL (9, 39, 40), and the increased LPL activity might have led to increased intravascular lipoprotein TAG hydrolysis. This may account for the increasing reduction in plasma TAG concentration, compared with the control value, that we observed during acute hypercortisolemia. Because induction of enzyme synthesis is involved, the time course of this effect is probably comparable to the time course of the present study. In the fasting state, there is almost quantitative spillover of fatty acids into the venous plasma during intravascular hydrolysis of TAG (8, 41). Thus, acute hypercortisolemia may result in decreasing arterial TAG concentrations, increased systemic glycerol production (from intravascular TAG hydrolysis), and elevated arterial NEFA concentrations. The last two could only be transient, because at steady state, plasma TAG removal (and thus glycerol and NEFA liberation) must equal plasma TAG appearance. Therefore, it seems necessary in addition to postulate site-specific activation of HSL in peripheral depots during cortisol infusion to explain the increased plasma NEFA concentrations and systemic glycerol production. Although we did not observe increased TAG extraction (LPL action) in the sc abdominal adipose depot, the effects of cortisol on LPL activity are probably site specific (42) and possibly have different time courses in different adipose depots.
Our study, therefore, supports the hypothesis that hypercortisolemia causes site-specific alterations in lipolytic enzyme activities. Although systemic glycerol production and plasma NEFA concentrations are increased, an inhibition of lipolysis is observed in a central adipose depot. Although there are probably differences between the metabolic effects of acute and chronic glucocorticoid excess, the observations reported here parallel the adipose tissue redistribution observed in chronic hypercortisolemia.
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Acknowledgments |
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Footnotes |
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Received January 23, 1997.
Revised July 22, 1997.
Accepted October 14, 1997.
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References |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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) and during cortisol infusion (•). B, Plasma
insulin concentrations during the control (
) and hypercortisolemia (• and 
) studies
are shown. 
