Effect of Noradrenaline on Glycerol Turnover and Lipolysis in the Whole Body and Subcutaneous Adipose Tissue in Humans in Vivo

1994 ◽  
Vol 86 (2) ◽  
pp. 177-184 ◽  
Author(s):  
A. Kurpad ◽  
K. Khan ◽  
A. G. Calder ◽  
S. Coppack ◽  
K. Frayn ◽  
...  

1. The effect of infusion of noradrenaline (0.42 μmol min−1 kg−1) on the exchange of non-esterified fatty acids, glycerol and other metabolites across subcutaneous abdominal adipose tissue was investigated in five healthy subjects using an arteriovenous catheterization technique and measurement of adipose tissue blood flow using the 133Xe clearance technique. At the same time, the net rate of fat oxidation in the whole body was assessed by indirect calorimetry, and the turnover of glycerol in the whole body and in subcutaneous adipose tissue was estimated using [5-2H]glycerol, which was administered as a primed constant infusion for 1 h before (basal turnover) noradrenaline administration and continued during the 1 h of noradrenaline infusion. 2. The noradrenaline infusion increased the plasma noradrenaline concentration from a basal value of 0.9 ± 0.1 to 12.6 ± 1.2 nmol/(mean ± SEM) at 60 min. It also increased the arterialized concentration of glycerol by 50% (basal value 81 ± 11/μmol/l−1) and that of plasma non-esterified fatty acids three-fold (basal value 357 ± 86 μmol/l). 3. Noradrenaline increased the net release of glycerol by adipose tissue three-fold and that of non-esterified fatty acids three- to four-fold. Although the ratio of non-esterified fatty acid to glycerol release by adipose tissue increased in all subjects from a mean value of 2.7 in the basal period to 3.6 and 3.9 at 50 and 60 min of the noradrenaline infusion, respectively (P < 0.02), at no time point did the ratio differ significantly from 3.0 4. Noradrenaline increased the estimated rate of appearance of glycerol in the whole body from a basal value of 1.5 ± 0.3 to 2.6 ± 0.3 μmol min−1 kg−1 body weight, and the net rate of triacylglycerol oxidation from 1.2 ± 0.1 to 1.7 ± 0.13 μmol min−1 kg−1. The enrichment of glycerol in venous blood draining adipose tissue was two-fold lower than that predicted from the net addition of glycerol to the blood in the basal period (P < 0.02). 5. This study provides a direct demonstration of a ‘hormone’ stimulating lipolysis in human adipose tissue in viva The effect of noradrenaline in significantly increasing the ratio of non-esterified fatty acid to glycerol release by adipose tissue may be partly explained by accumulation in adipose tissue of diacylglycerol, which is associated with release of non-esterified fatty acids but not glycerol. Finally, since the low enrichment of glycerol in venous blood draining adipose tissue cannot be entirely explained by the net addition of glycerol in adipose tissue, there must be exchange between enriched glycerol in blood and unenriched glycerol in adipose tissue. This raises questions about the accuracy of glycerol turnover studies, which are typically carried out over 1 h.

1976 ◽  
Vol 51 (1) ◽  
pp. 107-110 ◽  
Author(s):  
N. E. Miller ◽  
O. D. Mjøs ◽  
M. F. Oliver

1. The mechanism whereby p-chlorophenoxyisobutyrate (CPIB) lowers plasma non-esterified fatty acid concentrations has been studied in dogs by measuring the associated changes in adipose tissue metabolism. 2. CPIB lowered arterial concentrations of non-esterified fatty acids during isoprenaline infusion by a mean value of 41%. 3. This was accompanied by a proportionate decrease (45%) in the release of non-esterified fatty acids from subcutaneous adipose tissue in situ, and by a lesser reduction (22%) in that of glycerol. 4. Adipose tissue blood flow was unchanged by CPIB. 5. These findings indicate that the lowering effect of CPIB on non-esterified fatty acid concentrations derives principally from decreased mobilization rather than from increased tissue uptake of the fatty acids, and that this reflects both inhibited lipolysis and enhanced re-esterification of the fatty acids in adipose tissue.


Diabetes ◽  
2005 ◽  
Vol 54 (5) ◽  
pp. 1297-1303 ◽  
Author(s):  
F. Karpe ◽  
B. A. Fielding ◽  
S. W. Coppack ◽  
V. J. Lawrence ◽  
I. A. Macdonald ◽  
...  

2003 ◽  
Vol 285 (6) ◽  
pp. E1282-E1288 ◽  
Author(s):  
Michael D. Jensen ◽  
Michael G. Sarr ◽  
Daniel A. Dumesic ◽  
Peter A. Southorn ◽  
James A. Levine

Two protocols were performed to study meal fatty acid metabolism. In protocol 1, 14 patients scheduled for elective intra-abdominal surgery (11 undergoing bariatric surgery for severe obesity) consumed a meal containing [3H]triolein in the evening before surgery. This allowed us to measure adipose tissue lipid specific activity (SA) in mesenteric and omental, deep and superficial abdominal subcutaneous adipose tissue. Intra-abdominal adipose tissue lipid SA was greater than subcutaneous lipid SA. There were no significant differences between mesenteric and omental or between deep and superficial abdominal subcutaneous adipose tissue. In protocol 2, meal fatty acid oxidation and uptake into subcutaneous and omental adipose tissue ([3H]triolein) were measured in six normal, healthy volunteers. Meal fatty acid oxidation (3H2O generation) plus that remaining in plasma (∼1%) plus uptake into upper body subcutaneous, lower body subcutaneous, and visceral fat allowed us to account for 98 ± 6% of meal fatty acids 24 h after meal ingestion. We conclude that omental fat is a good surrogate for visceral fat and that abdominal subcutaneous fat depots are comparable with regard to meal fatty acid metabolic studies. Using [3H]triolein, we were able to account for virtually 100% of meal fatty acids 24 h after meal ingestion. These results support the meal fatty acid tracer model as a way to study the metabolic fate of dietary fat.


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.


2010 ◽  
Vol 53 (1) ◽  
pp. 73-84 ◽  
Author(s):  
M. Furman ◽  
Š. Malovrh ◽  
A. Levart ◽  
M. Kovač

Abstract. The fatty acid composition of meat and subcutaneous adipose tissue of the indigenous Slovenian pig breed (Krškopolje, KP), which is raised extensively, was compared with that of commercial fatteners (CP) from intensive farms. Commercial fatteners were divided into three groups according to lean meat percentage: meaty, normal and fatty. The m. longissimus dorsi of Krškopolje pigs contained less C18:0 fatty acids than that of commercial fatteners and less C16:0 than that of the fatty group. The proportions of long chain fatty acids C20:4 n-6, C20:5 n-3 and C22:5 n-3 in the Krškopolje pigs and fatty groups were also significantly different. The highest proportion of essential C18:2 n-6 and C18:3 n-3 fatty acids were found in the meaty and normal groups. Intramuscular fat content of the m. longissimus dorsi did not differ between the Krškopolje pigs, and the fatty and normal groups. The Krškopolje pigs had the lowest proportion of saturated fatty acids (SFAs), while both the Krškopolje pigs and the fatty group have a lower proportion of polysaturated fatty acids (PUFAs) than the meaty group. The fatty group had a lower polyunsaturated : saturated fatty acid ratio than the meaty and normal groups. In the subcutaneous adipose tissue, Krškopolje pigs had the highest proportion of C18:1 n-9 and differed from the normal group in C18:0 content, from the fatty group in C16:1 n-7 and from the meaty and fatty groups in C18:2 n-6. Furthermore, the Krškopolje pigs had the highest monounsaturated fatty acids (MUFAs), and lower PUFAs and n-6 PUFAs proportions than the fatty group. The meaty group had a higher n-6 : n-3 PUFA ratio than the Krškopolje pigs.


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.


1994 ◽  
Vol 266 (3) ◽  
pp. E308-E317 ◽  
Author(s):  
K. N. Frayn ◽  
S. Shadid ◽  
R. Hamlani ◽  
S. M. Humphreys ◽  
M. L. Clark ◽  
...  

There is net outward flow of fatty acids from adipose tissue in the fasted state but net inward flow and storage in the postprandial state. We investigated how this is regulated. Arteriovenous differences were measured across a subcutaneous adipose depot in six normal subjects before and for 5 h after a meal containing 80 g fat and 80 g carbohydrate. In five further experiments, insulin was infused at 40 mU.m-2.min-1 from 30 min after the meal, clamping the plasma glucose. Net transcapillary fatty acid flow changed from negative (outward flow from tissue to capillaries) in the postabsorptive state to consistently positive (net inward flow, implying fat storage) after the meal despite continued net efflux of fatty acids into venous blood. In the "clamped" experiments (with additional insulin), net fatty acid efflux in the venous blood was suppressed and positive transcapillary flux (storage) was more marked. Regulation of fatty acid flow appeared to depend on coordinated changes in hormone-sensitive lipase (HSL) and lipoprotein lipase (LPL) action and fatty acid esterification. Additional insulin caused no further suppression of HSL or activation of LPL but markedly stimulated fatty acid retention (presumed to represent esterification). In the absence of additional insulin, a high proportion of the fatty acids liberated by LPL are released into the venous plasma in both postabsorptive and postprandial states. We hypothesize that this "loss" of fatty acids is necessary to give precise control to the pathway of fat storage.


Sign in / Sign up

Export Citation Format

Share Document