Human Adipose Tissue Blood Flow Research Articles

Subcutaneous adipose tissue metabolism and pharmacology: a new investigative technique

According to the Fick principle, any metabolic or hormonal exchange through a given tissue depends on the product of blood flow by arteriovenous difference. Because adipose tissue plays dual storage and endocrine roles, regulation of adipose tissue blood flow (ATBF) is of pivotal importance. Monitoring ATBF in humans can be achieved through different methodologies, such as the (133)Xe washout technique, considered to be the "gold standard", as well as microdialysis and other methods that are not well validated as of yet. This report describes a new method, called "adipose tissue microinfusion" or "ATM", which simultaneously quantifies ATBF by combining the (133)Xe washout technique together with variations of ATBF induced by local infusion of vasoactive agents. The most appropriate site for ATM investigation is the subcutaneous adipose tissue of the anterior abdominal wall. This innovative method conveniently enables the direct comparison of the effects on ATBF of any vasoactive compound, drug, or hormone against a contralateral saline control. The ATM method improves the accuracy and feasibility of physiological and pharmacological studies on the regulation of ATBF in vivo in humans.

Influence of circulating NE and Epi on adipose tissue vascular resistance and lipolysis in humans.

The effects of circulating norepinephrine (NE) and epinephrine (Epi) on vascular resistance in subcutaneous adipose tissue and the calf as well as on plasma glycerol, an indicator of lipolysis, were studied in healthy volunteers. Adipose tissue blood flow was determined by the local clearance of 99mTcO-4 or 133Xe. The two isotopes gave similar results. Calf blood flow was determined by venous occlusion plethysmography. Intravenous infusion of NE caused increases in systolic and diastolic blood pressures, adipose tissue and calf vascular resistances, and plasma glycerol and a decrease in plasma insulin and heart rate, all of which were significant when arterial plasma NE was elevated from 1.17 +/- 0.14 to 8.38 +/- 0.30 nM (n = 16). Epi reduced diastolic and mean arterial pressures and adipose tissue and calf vascular resistances and increased plasma glycerol without affecting systolic blood pressure or plasma insulin. An increase of arterial plasma Epi from 0.20 +/- 0.03 to 1.15 +/- 0.05 nM (n = 6) was sufficient to induce vasodilatation in adipose tissue and lipolysis. Human adipose tissue differs from canine adipose tissue inasmuch as Epi causes vasodilatation in humans (present results) but vasoconstriction in the dog (previous results), presumably due to a predominance of vascular beta 2-adrenoceptors in human and beta 1-adrenoceptors in canine adipose tissue. Furthermore, Epi is a considerably more potent lipolytic hormone than NE in humans but not in the dog. Our results indicate that both NE and Epi may influence human adipose tissue blood flow and lipolysis as circulating hormones.

Blood flow in human adipose tissue after infusion of (Gln4)-neurotensin.

(Gln4)-neurotensin, 18 pmolXkg-1Xmin-1, was infused i.v. during 20 min in 10 healthy male volunteers. Adipose tissue blood flow was continuously monitored by measuring the disappearance rate of 99mTc-pertechnetate injected s.c. on the abdomen and thigh. Heart rate and blood pressure were measured and calf blood flow studied by venous occlusion plethysmography. Neurotensin-like immunoreactivity (NTLI) in serum was determined. Infusion of isotonic saline served as control. During intravenous infusion of (Gln4)-neurotensin the first order rate constants of 99mTc-pertechnetate from the abdomen decreased by 21.9 +/- 5.9% from a basal value of 8.3 +/- 0.5% min-1 (p less than 0.01). The reduction in blood flow started after a latent period of 5-10 min and persisted throughout the thirty minute observation period following infusion. A significant correlation (r=0.87, p less than 0.001) was found between the percentage decrease in blood flow from abdominal fat and the body fat content of the subjects as determined from the sum of four skinfolds. Blood flow from thigh fat did not change significantly, nor did heart rate, blood pressure or calf blood flow. During infusion of (Gln4)-neurotensin plasma neurotensin-like immunoreactivity (NTLI) increased successively. Ten minutes after starting the infusion the mean plasma NTLI level had increased from 20 +/- 5 pM to 302 +/- 31 pM; at 20 min it was 473 +/- 51 pM. These concentrations are within the range found after eating a fatty meal. The results indicate that neurotensin plays a physiological role in the regulation of human adipose tissue blood flow and may be of importance for the postprandial uptake of substrates in adipose tissue in certain regions. We suggest that neurotensin deserves consideration as an endocrine hormone affecting the regional deposition of fat postprandially.

Human adipose tissue blood flow during prolonged exercise, III. Effect of F-adrenergic blockade, nicotinic acid and glucose infusion

Subcutaneous adipose tissue blood flow (ATBF) was measured in six male subjects by the 133Xe-washout technique during 3-4 h of exercise at a work load corresponding to an oxygen uptake of about 1.71/min. The measurements were done during control conditions, during blockade of lipolysis by nicotinic acid, during acute i.v. beta-adrenergic blockade by propranolol, and during continuous i.v. infusion of glucose. The most pronounced lipid mobilization and utilization during work was seen in the control experiments where ATBF rose 3-fold on average from the initial rest period to the third hour of work. No increase in lipolysis and no increase in ATBF were found when lipolysis was blocked by nicotinic acid (0.3 g/h). Propranolol treatment (0.15 mg/kg) reduced lipolysis and nearly abolished the increase in ATBF during exercise. Intravenous administration of glucose (about 0.25 g/min) did not influence lipid metabolism (evaluated by the respiratory quotient) nor did it reduce the ATBF response to exercise. These results are inconsistent with the hypothesis that increase in ATBF during exercise is elicited via direct stimulation of vascular beta1-receptors, while they are not in disagreement with the hypothesis that adipose tissue vasodilation during exercise is secondary to metabolic events connected to lipolysis.

Human adipose tissue blood flow during prolonged exercise II.

Subcutaneous and perirenal adipose tissue blood flows (ATBF) were measured by the 133Xe washout method before, during and after 4h exercise on a bicycle ergometer. The load corresponded to about 50% of VO2 max (i.e. about 1.7l/min). Subcutaneous and perirenal ATBF increased at an average to 3--400 and 700% of their initial control values respectively. In six of nine measuring sites ATBF remained increased in the hour following work. During work plasma glycerol concentrations increased 8 fold. The core temperature increased 0.9 degree C, skin temperature did not change significantly. During passive elevation of body temperature (core temperature +1.5 degree C; skin temperature +3 degree C) neither subcutaneous ATBF nor plasma glycerol concentrations changed significantly. It is concluded that the increase in subcutaneous ATBF during exercise is not a reaction to increased body temperature.