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The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 8 2815-2819
Copyright © 1999 by The Endocrine Society

From the Clinical Research Centers

Norepinephrine Spillover in Forearm and Subcutaneous Adipose Tissue before and after Eating1

J. N. Patel, G. Eisenhofer, S. W. Coppack and J. M. Miles

Royal London Hospital Medical College, London E1 18B, United Kingdom; Clinical Neuroscience Branch, National Institutes of Health, Bethesda, Maryland 20892; and St. Luke’s Hospital, Kansas City, Missouri 64110

Address all correspondence and requests for reprints to: Dr. Jigisha Patel, M.R.C.P., National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive, MSC-1424, Building 10, Room 6N252, Bethesda, Maryland 20892-1424. E-mail: jnpatel{at}box-j.nih.gov


   Abstract
Top
 Abstract
Introduction
 Experimental Subjects
 Materials and Methods
 Results
 Discussion
 References
 
The sympathetic nervous system regulates lipolysis. There are regional differences in the sensitivity of lipolysis to adrenergic regulation. Little is known about regional sympathetic activity in response to eating in humans. We studied the effect of feeding on systemic and local sympathetic nervous system activity and lipolysis in lean healthy subjects (three women and five men; age, 27.0 ± 2.0; body mass index, 23.4 ± 1.2 kg/m-2) using isotope dilution methodology and arterio-venous sampling. Feeding increased arterial norepinephrine (NE) concentration (mean premeal, 0.96 ± 0.12 nmol/L·L; mean postmeal, 1.28 ± 0.14 nmol/L·L; P < 0.02) and total body NE spillover (mean premeal, 2.11 ± 0.30 nmol/min·L; mean postmeal, 2.76 ± 0.31 nmol/min·L; P < 0.02), whereas the arterial epinephrine concentration decreased (mean premeal, 289 ± 61 pmol/L; mean postmeal, 170 ± 5 pmol/L; P < 0.02). Palmitate concentration and total body systemic rate of appearance of palmitate declined postprandially (mean premeal, 117 ± 15 µmol/min; mean postmeal, 38 ± 4 µmol/min; P < 0.01). NE spillover increased by the same proportion in both forearm and adipose tissue [in forearm, mean premeal and postmeal, 1.02 ± 0.11 and 2.41 ± 0.44. nmol/100 mL·min, respectively (P < 0.02); in adipose tissue, mean premeal and postmeal, 0.41 ± 0.12 and 0.73 ± 0.17 nmol/100 g·min, respectively (P < 0.02)]. The results show that a meal caused differential changes in systemic sympatho-adrenal activity and an increase in sympathetic activity in adipose tissue postprandially, However, this increase in postprandial sympathetic activity was not enough to overcome the inhibition of lipolysis by insulin


   Introduction
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 Abstract
 Introduction
Experimental Subjects
 Materials and Methods
 Results
 Discussion
 References
 
THE SYMPATHETIC nervous system (SNS) regulates numerous metabolic processes. The adrenergic regulation of lipolysis is particularly complex, as it involves both catecholamines delivered to adipose tissue via the circulation (1, 2, 3) and norepinephrine (NE) that is released locally in adipose tissue from sympathetic neurons (4). Moreover, adrenergic regulation of lipolysis depends on the balance between the stimulatory effects mediated through ß-receptors and the inhibitory effects that are mediated through {alpha}2-receptors (4, 5). To make matters more complicated, in vivo studies in humans have demonstrated regional differences in the lipolytic activity of adipose tissue (6, 7, 8). However, such studies of regional adipose tissue metabolism are difficult to interpret in the absence of data on local sympathetic activity.

Little is known from human in vivo studies about changes in NE spillover in adipose tissue in response to such activities as eating, fasting, and exercise. This is principally because no convenient method for measuring exocytotic release of NE in adipose tissue has heretofore been available. NE is synthesized and stored in sympathetic nerve endings and is the neurotransmitter involved in SNS signal transmission. Although most of the NE released from sympathetic postganglionic neurons is cleared locally by neuronal and extra-neuronal reuptake, a portion of released NE spills over into the bloodstream. Measurements of the rates of spillover of NE to the systemic circulation provides a better reflection of the activity of the SNS than simple measurements of plasma NE concentration (9).

Total body NE spillover, however, reflects the release of NE from many tissues, including the adrenal medulla, and thus does not provide information on SNS activity within specific tissues. The combined use of isotope dilution and arterio-venous sampling allows the investigator to measure spillover from individual tissues (10). Radiolabeled NE has thereby been used to determine regional NE clearance and spillover in skeletal muscle (11), myocardium (12), kidney (11), lung (11), and mesenteric organs and liver (13). There are very little data on the sympathetic response to food in adipose tissue, but sympathetic activity in brown adipose tissue has been shown to decrease in response to food intake in rats (14).

We combined the isotope dilution method with the arterio-venous sampling technique to estimate NE spillover in sc abdominal adipose tissue in vivo in humans. We studied the effect of feeding on adipose tissue and forearm norepinephrine kinetics in a group of lean healthy subjects. Postprandial measurements were made during the time period that previous studies (15) suggested that metabolic responses to a mixed meal would be maximal. We postulated that there would be a heterogeneous regional sympathetic response to eating so that sympathetic activity in adipose tissue would decrease as lipolysis was inhibited postprandially, whereas that in the forearm would increase as part of the thermogenetic response to eating (16).


   Experimental Subjects
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 Abstract
 Introduction
 Experimental Subjects
Materials and Methods
 Results
 Discussion
 References
 
Eight healthy lean Caucasian subjects (Table 1Go) were recruited. The protocol was approved by the Mayo Clinic institutional review board, and written informed consent was obtained from all volunteers. The subjects were at a stable weight and taking no medication other than occasional acetaminophen.


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  		Table 1. Subject details

 

   Materials and Methods
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 Abstract
 Introduction
 Experimental Subjects
 Materials and Methods
Results
 Discussion
 References
 
At 1700 h on day 0 of the study, subjects reported to the Mayo General Clinical Research Center and on arrival were given a standard meal containing 15 Cal/kg lean body mass (LBM), with a 50% carbohydrate, 30% fat, and 20% protein caloric distribution. Body composition was determined by dual energy x-ray absorptiometry (Lunar Corp., Madison, WI). A blood sample was collected at that time to serve as a blank for the NE assay. At 2200 h, the subject was given a fat-free snack (5 Cal/kg LBM). At 0630 h the next morning sampling catheters were inserted under local anesthesia in a radial artery and in the superficial abdominal and deep forearm veins as previously described (17). We assumed that the deep forearm vein drained principally muscle, and the sc adipose tissue vein drained principally adipose tissue (15, 17). An infusion catheter was placed in a superficial midforearm vein contralateral to the sampling catheters. At 0800 h an infusion of levo-[ring-2,5,6-3H]NE at 0.8 µCi/min and an infusion of [9,10-3H]palmitate (both from New England Nuclear, Boston, MA) at 0.4 µCi/min were started and continued to the end of the study. At the same time, 150 µCi 133Xe (Malinkrodt, Northampton, UK) in approximately 0.5 mL normal saline were injected into the sc abdominal adipose tissue in the drainage of the abdominal vein being sampled, and tracings of 133Xe activity were obtained 15 min before the meal, immediately before the meal, and 100 and 120 min after the meal (18). Forearm blood flow, with the wrist occluded, was determined 30 and 10 min before and 60 and 100 min after the meal using mercury strain gauge plethysmography (Hokanson, Inc., Bellevue, WA) (19). At 0 min, the subject was given a mixed meal containing 15 Cal/kg LBM (50% carbohydrate, 30% fat, and 20% protein). Blood samples were taken from the three sampling sites at 30, 20, and 10 min and immediately before the meal and again at 60, 80, 100, and 120 min after the meal for measurement of NE, epinephrine, [3H]NE, and palmitate. Samples were also taken from the arterial site for measurement of insulin.

Analytical methods

Blood samples were taken, immediately transferred to precooled tubes containing ethylenediamine tetraacetate, and kept on ice until centrifuged at 4 C, which was performed within 30 min of the sample being drawn. Plasma was stored at -70 C.

Plasma insulin concentrations were determined by RIA as previously described (1). Plasma epinephrine concentrations, together with NE concentration and radioactivity, were determined as previously published (20).

Plasma palmitate concentrations and specific activity were determined by high performance liquid chromatography using [2H31]-palmitate as an internal standard (21),

Calculations

Systemic rates of appearance (Ra) of palmitate in the postabsorptive state were calculated using steady state equations (22, 23): Ra = tracer infusion rate/SAa, where SAa is the arterial specific activity. In the postprandial period nonsteady state equations were used (22, 23): Ra = {2F - [(C60 + C120)(Vd)(SAa120 - SAa60)}/(t120 - t60)]/(SAa60 - SAa120), where F is the isotope infusion rate in disintegrations per min (kilograms per min), Vd is the estimated volume of distribution for palmitate (90 mL/kg) (22), C is the arterial plasma concentration, t is the time in minutes, and subscripts 60 and 120 indicate values at 60 and 120 min.

Local rates of appearance of palmitate were calculated as previously described (23).

Total body NE spillover (TBS) was calculated according to the equation (10): TBS = I/SAa, where I is the infusion rate of [3H]NE in arterial plasma (disintegrations per min), and SAa is the specific activity of [3H]NE in arterial plasma (disintegrations per min/pg).

Regional spillover of NE in adipose tissue or the forearm (Rs) was calculated according to the equation: RS = [([3H]NEa - [3H]NEv)/[3H]NEa] x [3H]NEa + (NEv - NEa) x PF, where [3H]NEa and [3H]NEv are the arterial and venous plasma concentrations of [3H]NE (disintegrations per min/mL), NEa and NEv are the arterial and venous plasma concentrations of NE (picograms per mL), respectively, and PF is the plasma flow.

Adipose tissue and muscle densities were taken from the report by Durnin and Wormersley (24).

Data was log transformed, and paired t tests were used to examine differences between pre- and postprandial values.


   Results
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 Abstract
 Introduction
 Experimental Subjects
 Materials and Methods
 Results
Discussion
 References
 
As expected, the insulin concentration increased (P < 0.001) in response to the meal (Fig. 1Go, upper panel). After the meal, the palmitate concentration declined (Fig. 1Go, lower panel). Arterio-venous differences across adipose tissue (Fig. 1Go), systemic rates of appearance of palmitate, uptake by forearm tissue of palmitate, and release by sc adipose tissue of palmitate all declined (Table 2Go).



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  		Figure 1. Upper panel, Arterial concentration of insulin before and after a mixed meal eaten between 0–15 min. Lower panel, Arterial (black line, squares), sc abdominal venous (black line, diamonds), and deep forearm venous (black filled squares) concentrations of palmitate before and after a mixed meal eaten between 0–15 min.

 

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  		Table 2. Systemic and net local palmitate kinetics

 
Effect of meal on the systemic sympatho-adrenal medullary system

The effect of feeding on plasma catecholamine concentrations and NE kinetics is shown in Table 3Go. There was a significant postprandial increase in the arterial NE concentration, whereas the arterial epinephrine concentration decreased after the meal. (Fig. 2Go). Total body NE spillover increased postprandially (Fig. 3Go).


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  		Table 3. Catecholamine concentrations and norepinephrine kinetics

 


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  		Figure 2. Upper panel, Arterial NE concentrations before and after a mixed meal eaten between 0–15 min. *, Postmeal values significantly different from premeal values, P < 0.02. Lower panel, Arterial epinephrine concentrations before and after a mixed meal eaten between 0–15 min. *, Postmeal values significantly different from premeal values, P < 0.02.

 


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  		Figure 3. Upper panel, Total body NE spillover before and after eating a mixed meal. *, Postmeal values significantly different from premeal values, P < 0.02. Lower panel, Adipose tissue and forearm NE spillover before and after eating a mixed meal. *, Postmeal values significantly different from baseline, P < 0.02.

 
Effect of meal on local NE spillover

Forearm plasma flow did not change significantly (1.40 ± 0.30 vs. 1.78 ± 0.3 mL/100 mL·min), whereas adipose tissue plasma flow increased significantly from 1.27 ± 0.1 to 2.08 ± 0.3 mL/100 mg·min (P < 0.05) in response to the meal. Feeding increased NE spillover in both forearm and adipose tissue (Fig. 3Go).

Regional differences

Regional comparisons between forearm and adipose tissue were made after using the density of adipose tissue to convert spillover from units of weight to units of volume (24). NE spillover was higher in the forearm compared to adipose tissue in both the baseline and postprandial states. The absolute increase in forearm spillover (1.39 ± 0.47 pmol/100 mL·min) was greater (P < 0.05) than the absolute increase in adipose tissue spillover (0.32 ± 0.12 pmol/100 g·min), but the proportional changes in each tissue in response to the meal were not significantly different.


   Discussion
Top
 Abstract
 Introduction
 Experimental Subjects
 Materials and Methods
 Results
 Discussion
References
 
We have combined novel measurements of NE spillover from adipose tissue with measurements of total body and forearm NE spillover and plasma concentrations of epinephrine. The results show that ingestion of a meal causes differentiated changes in sympatho-adrenal medullary activity; systemic epinephrine concentrations declined, whereas both systemic and local NE spillover increased.

In previous studies of SNS activity in the postprandial state systemic, SNS activity has been shown to increase after a meal (25), and this may contribute to the increase in energy expenditure known as the thermic effect of food (26). Local NE spillover has also been shown to increase postprandially in forearm and renal tissues (27).

The current study measured the systemic, local forearm, and local sc adipose tissue catecholamine responses to eating a mixed meal. The postprandial period is known to be associated with an increase in energy expenditure (28), an increase in cardiac output, and a redistribution of the circulating volume (29). The time course of the postprandial changes in systemic and local fatty acid suggested that the response of the sympatho-adrenal system was measured around the time when such changes were maximal. In some tissues, catecholamines and insulin have antagonistic effects, and the response to food is the consequence of divergent effects of insulin and catecholamines.

Plasma insulin concentrations increased after the mixed meal, whereas the different indexes of sympatho-adrenal system activity showed a more heterogeneous response. Thus, eating caused plasma epinephrine to decrease, in line with a similar trend previously seen using mixed meals (29, 30). The change in epinephrine concentration presumably reflects a fall in adrenal gland output. In contrast, systemic NE concentrations and systemic NE spillover increased postprandially. This suggests that sympathetic nerve terminal activity increased. However, changes in NE spillover can reflect either or both changes in local removal or neuronal release of NE. The design of the present study did not allow these influences to be distinguished.

Previous local NE spillover studies suggest that spillover from forearm tissue increases postprandially (27). This was also seen in our data. Whether NE spillover in forearm principally mediates an effect of NE on vascular structures to induce a vasomotor response, an effect on skeletal muscle cells to induce a metabolic response, or both is a matter of speculation.

NE kinetics have not previously been measured in an adipose tissue depot after a meal. We expected sympathetic activity to adipose tissue to decrease after the meal, as lipolysis is suppressed postprandially; however, NE spillover to sc adipose tissue increased after the meal, suggesting increased SNS activity in this tissue. Although there is uncertainty about the target cells of the increased NE release in the forearm, the chief result of increased NE release in adipose tissue would presumably be increased lipolysis in fat cells. However the net release of palmitate from the sc adipose tissue declined. The inhibition of local palmitate release was practically complete in all subjects, thereby obscuring any possible interindividual differences in relative sensitivity of palmitate release to insulin levels or to local NE spillover. The results would imply that any prolipolytic effect of increased NE spillover within the adipose tissue was being overridden by the increased insulinemia postprandially. This is in agreement with recent work by Horowitz et al. (31), who showed that in the fasting state, insulin concentration, not local NE spillover, determines local NEFA release. Thus, whereas adipose tissue sympathetic activity might be an important modulator of lipolytic activity in other situations, it would appear that during meal absorption in normal lean subjects, an increase in the insulin concentration is sufficient to override any effect of NE and completely inhibit lipolysis in sc adipose tissue.

In this study we have examined the responses of the SNS to a mixed meal in a group of healthy lean subjects. As expected, there were increases in systemic NE concentrations and spillover as well as an increase in forearm NE spillover. We also found that epinephrine concentrations declined after this meal. We report for the first time that the meal also increased NE spillover in sc adipose tissue. However, this increased NE spillover did not prevent the complete suppression of adipose tissue lipolysis in the tissue bed. This observation affirms the primacy of insulin in lipolytic regulation during meal absorption in healthy individuals.


   Acknowledgments
 
We thank Dr. R. A. Rizza for providing insulin measurements, the staff of the Mayo General Clinical Research Center for excellent assistance, and Douglas Hooper of the NIH for technical expertise.


   Footnotes
 
1 This work was supported in part by NIH Grants DK-38092 and RR-00585, The Wellcome Trust, and the British Diabetic Association. Back

Received November 23, 1998.

Revised April 16, 1999.

Accepted April 21, 1999.


   References
Top
 Abstract
 Introduction
 Experimental Subjects
 Materials and Methods
 Results
 Discussion
 References
 

  1. Jensen MD, Haymond MW, Gerich JE, Cryer PE, Miles JM. 1987 Lipolysis during fasting: decreased suppression by insulin and increased stimulation by epinephrine. J Clin Invest. 79:207–213.
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