Thermogenic response to epinephrine in the forearm and abdominal subcutaneous adipose tissue

1992 ◽  
Vol 263 (5) ◽  
pp. E850-E855 ◽  
Author(s):  
L. Simonsen ◽  
J. Bulow ◽  
J. Madsen ◽  
N. J. Christensen

Whole body energy expenditure, thermogenic and metabolic changes in the forearm, and intercellular glucose concentrations in subcutaneous adipose tissue on the abdomen determined by microdialysis were measured during epinephrine infusion in healthy subjects. After a control period, epinephrine was infused at rates of 0.2 and 0.4 nmol.kg-1 x min-1. Whole body resting energy expenditure was 4.36 +/- 0.56 (SD) kJ/min. Energy expenditure increased to 5.14 +/- 0.74 and 5.46 +/- 0.79 kJ/min, respectively (P < 0.001), during the epinephrine infusions. Respiratory exchange ratio was 0.80 +/- 0.04 in the resting state and did not change. Local forearm oxygen uptake was 3.9 +/- 1.3 mumol.100 g-1 x min-1 in the basal period. During epinephrine infusion, it increased to 5.8 +/- 2.1 (P < 0.03) and 7.5 +/- 2.3 mumol.100 g-1 x min-1 (P < 0.001). Local forearm glucose uptake was 0.160 +/- 0.105 mumol.100 g-1 x min-1 and increased to 0.586 +/- 0.445 and 0.760 +/- 0.534 mumol.100 g-1 x min-1 (P < 0.025). The intercellular glucose concentration in the subcutaneous adipose tissue on the abdomen was equal to the arterial concentration in the basal period but did not increase as much during infusion of epinephrine, indicating glucose uptake in adipose tissue in this condition. If it is assumed that forearm skeletal muscle is representative for the average skeletal muscle, it can be calculated that on average 40% of the enhanced whole body oxygen uptake induced by infusion of epinephrine is taking place in skeletal muscle. It is proposed that adipose tissue may contribute to epinephrine-induced thermogenesis.

2000 ◽  
Vol 279 (2) ◽  
pp. E376-E385 ◽  
Author(s):  
Bente Stallknecht ◽  
Jens J. Larsen ◽  
Kari J. Mikines ◽  
Lene Simonsen ◽  
Jens Bülow ◽  
...  

Training increases insulin sensitivity of both whole body and muscle in humans. To investigate whether training also increases insulin sensitivity of adipose tissue, we performed a three-step hyperinsulinemic, euglycemic clamp in eight endurance-trained (T) and eight sedentary (S) young men [insulin infusion rates: 10,000 ( step I), 20,000 ( step II), and 150,000 ( step III) μU · min−1 · m−2]. Glucose and glycerol concentrations were measured in arterial blood and also by microdialysis in interstitial fluid in periumbilical, subcutaneous adipose tissue and in quadriceps femoris muscle (glucose only). Adipose tissue blood flow was measured by 133Xe washout. In the basal state, adipose tissue blood flow tended to be higher in T compared with S subjects, and in both groups blood flow was constant during the clamp. The change from basal in arterial-interstitial glucose concentration difference was increased in T during the clamp but not in S subjects in both adipose tissue and muscle [adipose tissue: step I ( n = 8), 0.48 ± 0.18 mM (T), 0.23 ± 0.11 mM (S); step II ( n = 8), 0.19 ± 0.09 (T), −0.09 ± 0.24 (S); step III( n = 5), 0.47 ± 0.24 (T), 0.06 ± 0.28 (S); (T: P < 0.001, S: P > 0.05); muscle: step I ( n = 4), 1.40 ± 0.46 (T), 0.31 ± 0.21 (S); step II ( n = 4), 1.14 ± 0.54 (T), −0.08 ± 0.14 (S); step III( n = 4), 1.23 ± 0.34 (T), 0.24 ± 0.09 (S); (T: P < 0.01, S: P > 0.05)]. Interstitial glycerol concentration decreased faster in T than in S subjects [half-time: T, 44 ± 9 min ( n = 7); S, 102 ± 23 min ( n = 5); P < 0.05]. In conclusion, training enhances insulin sensitivity of glucose uptake in subcutaneous adipose tissue and in skeletal muscle. Furthermore, interstitial glycerol data suggest that training also increases insulin sensitivity of lipolysis in subcutaneous adipose tissue. Insulin per se does not influence subcutaneous adipose tissue blood flow.


2000 ◽  
Vol 278 (6) ◽  
pp. E1144-E1152 ◽  
Author(s):  
Jeffrey F. Horowitz ◽  
Samuel Klein

We measured whole body and regional lipolytic and adipose tissue blood flow (ATBF) sensitivity to epinephrine in 8 lean [body mass index (BMI): 21 ± 1 kg/m2] and 10 upper body obese (UBO) women (BMI: 38 ± 1 kg/m2; waist circumference >100 cm). All subjects underwent a four-stage epinephrine infusion (0.00125, 0.005, 0.0125, and 0.025 μg ⋅ kg fat-free mass−1 ⋅ min−1) plus pancreatic hormonal clamp. Whole body free fatty acid (FFA) and glycerol rates of appearance (Ra) in plasma were determined by stable isotope tracer methodology. Abdominal and femoral subcutaneous adipose tissue lipolytic activity was determined by microdialysis and 133Xe clearance methods. Basal whole body FFA Ra and glycerol Ra were both greater ( P < 0.05) in obese (449 ± 31 and 220 ± 12 μmol/min, respectively) compared with lean subjects (323 ± 44 and 167 ± 21 μmol/min, respectively). Epinephrine infusion significantly increased FFA Ra and glycerol Ra in lean (71 ± 21 and 122 ± 52%, respectively; P < 0.05) but not obese subjects (7 ± 6 and 39 ± 10%, respectively; P = not significant). In addition, lipolytic and ATBF sensitivity to epinephrine was blunted in abdominal but not femoral subcutaneous adipose tissue of obese compared with lean subjects. We conclude that whole body lipolytic sensitivity to epinephrine is blunted in women with UBO because of decreased sensitivity in upper body but not lower body subcutaneous adipose tissue.


2007 ◽  
Vol 102 (5) ◽  
pp. 1767-1772 ◽  
Author(s):  
Michael J. Ormsbee ◽  
John P. Thyfault ◽  
Emily A. Johnson ◽  
Raymond M. Kraus ◽  
Myung Dong Choi ◽  
...  

The purpose of this study was to investigate the effect of acute resistance exercise (RE) on lipolysis within adipose tissue and subsequent substrate oxidation to better understand how RE may contribute to improvements in body composition. Lipolysis and blood flow were measured in abdominal subcutaneous adipose tissue via microdialysis before, during, and for 5 h following whole body RE as well as on a nonexercise control day (C) in eight young (24 ± 0.7 yr), active (>3 RE session/wk for at least 2 yr) male participants. Fat oxidation was measured immediately before and after RE via indirect calorimetry for 45 min. Dialysate glycerol concentration (an index of lipolysis) was higher during (RE: 200.4 ± 38.6 vs. C: 112.4 ± 13.1 μmol/l, 78% difference; P = 0.02) and immediately following RE (RE: 184 ± 41 vs. C: 105 + 14.6 μmol/l, 75% difference; P = 0.03) compared with the same time period on the C day. Energy expenditure was elevated in the 45 min after RE compared with the same time period on the C day (RE: 104.4 ± 6.0 vs. C: 94.5 ± 4.0 kcal/h, 10.5% difference; P = 0.03). Respiratory exchange ratio was lower (RE: 0.71 ± 0.004 vs. C: 0.85 ± .03, 16.5% difference; P = 0.004) and fat oxidation was higher (RE: 10.2 ± 0.8 vs. C: 5.0 ± 1.0 g/h, 105% difference; P = 0.004) following RE compared with the same time period on the C day. Therefore, the mechanism behind RE contributing to improved body composition is in part due to enhanced abdominal subcutaneous adipose tissue lipolysis and improved whole body fat oxidation and energy expenditure in response to RE.


2021 ◽  
Author(s):  
Han-Chow E. Koh ◽  
Stephan van Vliet ◽  
Terri A. Pietka ◽  
Gretchen A. Meyer ◽  
Babak Razani ◽  
...  

We used stable isotope-labeled glucose and palmitate tracer infusions, a hyperinsulinemic-euglycemic clamp, positron-emission tomography of muscles and adipose tissue after [<sup>18</sup>F]fluorodeoxyglucose and [<sup>15</sup>O]water injections, and subcutaneous adipose tissue (SAT) biopsy to test the hypotheses that: i) increased glucose uptake in SAT is responsible for high insulin-stimulated whole-body glucose uptake in people with obesity who are insulin-sensitive, and ii) putative SAT factors thought to cause insulin resistance are present in people with obesity who are insulin-resistant but not in those who are insulin-sensitive. We found high insulin-stimulated whole-body glucose uptake in insulin-sensitive participants with obesity was not due to channeling of glucose into SAT, but was due to high insulin-stimulated muscle glucose uptake. Furthermore, insulin-stimulated muscle glucose uptake was not different between insulin-sensitive obese and lean participants even though adipocytes were larger, SAT perfusion and oxygenation were lower, and markers of SAT inflammation, fatty acid appearance in plasma in relation to fat-free mass, and plasma fatty acid concentration were higher in the insulin-sensitive obese than lean participants. In addition, we observed only marginal or no differences in adipocyte size, SAT perfusion and oxygenation, and markers of SAT inflammation between insulin-resistant and insulin-sensitive obese participants. Plasma fatty acid concentration was also not different between insulin-sensitive and insulin-resistant obese participants even though SAT was resistant to the inhibitory effect of insulin on lipolysis in the insulin-resistant obese group. These data suggest several putative SAT factors that are commonly implicated in causing insulin resistance are normal consequences of SAT expansion unrelated to insulin resistance.


2021 ◽  
Author(s):  
Han-Chow E. Koh ◽  
Stephan van Vliet ◽  
Terri A. Pietka ◽  
Gretchen A. Meyer ◽  
Babak Razani ◽  
...  

We used stable isotope-labeled glucose and palmitate tracer infusions, a hyperinsulinemic-euglycemic clamp, positron-emission tomography of muscles and adipose tissue after [<sup>18</sup>F]fluorodeoxyglucose and [<sup>15</sup>O]water injections, and subcutaneous adipose tissue (SAT) biopsy to test the hypotheses that: i) increased glucose uptake in SAT is responsible for high insulin-stimulated whole-body glucose uptake in people with obesity who are insulin-sensitive, and ii) putative SAT factors thought to cause insulin resistance are present in people with obesity who are insulin-resistant but not in those who are insulin-sensitive. We found high insulin-stimulated whole-body glucose uptake in insulin-sensitive participants with obesity was not due to channeling of glucose into SAT, but was due to high insulin-stimulated muscle glucose uptake. Furthermore, insulin-stimulated muscle glucose uptake was not different between insulin-sensitive obese and lean participants even though adipocytes were larger, SAT perfusion and oxygenation were lower, and markers of SAT inflammation, fatty acid appearance in plasma in relation to fat-free mass, and plasma fatty acid concentration were higher in the insulin-sensitive obese than lean participants. In addition, we observed only marginal or no differences in adipocyte size, SAT perfusion and oxygenation, and markers of SAT inflammation between insulin-resistant and insulin-sensitive obese participants. Plasma fatty acid concentration was also not different between insulin-sensitive and insulin-resistant obese participants even though SAT was resistant to the inhibitory effect of insulin on lipolysis in the insulin-resistant obese group. These data suggest several putative SAT factors that are commonly implicated in causing insulin resistance are normal consequences of SAT expansion unrelated to insulin resistance.


1990 ◽  
Vol 70 (1) ◽  
pp. 199-206 ◽  
Author(s):  
O. ADEOLA ◽  
B. W. McBRIDE ◽  
R. O. BALL ◽  
L. G. YOUNG

Subcutaneous adipose tissue and intercostal and sartorius muscles from five barrows and five gilts at 20 kg liveweight were used to study lipogenesis, lipolysis, Na+, K+-ATPase-dependent respiration and protein synthesis. Lipogenesis rate measured by 14C-acetate incorporation into lipid was similar between barrows and gilts; and 100 μg insulin per mL enhanced (P < 0.1) subcutaneous adipose tissue lipogenesis by 74%. Lipolysis rate quantitated by glycerol release was similar between barrows and gilts (3546 and 4160 nmol g−1 2 h−1). Adenosine deaminase and norepinephrine together enhanced adipose tissue lipolytic response by 102%. Fractional and absolute rates of protein synthesis were similar between barrows and gilts (3.24 and 3.69% d−1; 6.01 and 6.06 mg g−1 d−1); and between intercostal and sartorius muscles. Barrows had lower Na+, K+-ATPase-dependent respiration than gilts and the maintenance of Na+ and K+ transmembrane ionic gradient in the muscle preparations accounted for 23–26% of total respiration. Key words: Pigs, adipose tissue, skeletal muscle, metabolism


2009 ◽  
Vol 297 (5) ◽  
pp. E999-E1003 ◽  
Author(s):  
Birgit Gustafson ◽  
Silvia Gogg ◽  
Shahram Hedjazifar ◽  
Lachmi Jenndahl ◽  
Ann Hammarstedt ◽  
...  

Obesity is associated mainly with adipose cell enlargement in adult man (hypertrophic obesity), whereas the formation of new fat cells (hyperplastic obesity) predominates in the prepubertal age. Adipose cell size, independent of body mass index, is negatively correlated with whole body insulin sensitivity. Here, we review recent findings linking hypertrophic obesity with inflammation and a dysregulated adipose tissue, including local cellular insulin resistance with reduced IRS-1 and GLUT4 protein content. In addition, the number of preadipocytes in the abdominal subcutaneous adipose tissue capable of undergoing differentiation to adipose cells is reduced in hypertrophic obesity. This is likely to promote ectopic lipid accumulation, a well-known finding in these individuals and one that promotes insulin resistance and cardiometabolic risk. We also review recent results showing that TNFα, but not MCP-1, resistin, or IL-6, completely prevents normal adipogenesis in preadipocytes, activates Wnt signaling, and induces a macrophage-like phenotype in the preadipocytes. In fact, activated preadipocytes, rather than macrophages, may completely account for the increased release of chemokines and cytokines by the adipose tissue in obesity. Understanding the molecular mechanisms for the impaired preadipocyte differentiation in the subcutaneous adipose tissue in hypertrophic obesity is a priority since it may lead to new ways of treating obesity and its associated metabolic complications.


Diabetes ◽  
2005 ◽  
Vol 54 (6) ◽  
pp. 1635-1639 ◽  
Author(s):  
J. K. Nielsen ◽  
C. B. Djurhuus ◽  
C. H. Gravholt ◽  
A. C. Carus ◽  
J. Granild-Jensen ◽  
...  

1995 ◽  
Vol 269 (6) ◽  
pp. E1059-E1066 ◽  
Author(s):  
B. Stallknecht ◽  
L. Simonsen ◽  
J. Bulow ◽  
J. Vinten ◽  
H. Galbo

Trained humans (Tr) have a higher fat oxidation during submaximal physical work than sedentary humans (Sed). To investigate whether this reflects a higher adipose tissue lipolytic sensitivity to catecholamines, we infused epinephrine (0.3 nmol.kg-1.min-1) for 65 min in six athletes and six sedentary young men. Glycerol was measured in arterial blood, and intercellular glycerol concentrations in abdominal subcutaneous adipose tissue were measured by microdialysis. Adipose tissue blood flow was measured by 133Xe-washout technique. From these measurements adipose tissue lipolysis was calculated. During epinephrine infusion intercellular glycerol concentrations were lower, but adipose tissue blood flow was higher in trained compared with sedentary subjects (P < 0.05). Glycerol output from subcutaneous tissue (Tr: 604 +/- 322 nmol.100 g-1.min-1; Sed: 689 +/- 203; mean +/- SD) as well as arterial glycerol concentrations (Tr: 129 +/- 36 microM; Sed: 119 +/- 56) did not differ between groups. It is concluded that in intact subcutaneous adipose tissue epinephrine-stimulated blood flow is enhanced, whereas lipolytic sensitivity to epinephrine is the same in trained compared with untrained subjects.


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