Contribution of BAT and skeletal muscle to thermogenesis induced by ephedrine in man

1985 ◽  
Vol 248 (5) ◽  
pp. E507-E515 ◽  
Author(s):  
A. Astrup ◽  
J. Bulow ◽  
J. Madsen ◽  
N. J. Christensen
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Local Temperature ◽  
Whole Body ◽  
Tissue Blood Flow ◽  
Muscle Oxygen ◽  
Brown Adipose ◽  
Muscle Oxygen Consumption

This investigation was performed to examine the role of brown adipose tissue (BAT) in thermogenesis induced by ephedrine in man. Light microscopy of biopsies from necropsy cases showed BAT to occur most frequently in the perirenal fat. Perirenal BAT thermogenesis was investigated in five lean men before and during stimulation with 1 mg ephedrine orally X kg body wt-1. Perirenal BAT thermogenesis was assessed by continuous measurements of local temperature and blood flow with the 133xenon clearance method. In the same study the effect of ephedrine on skeletal muscle oxygen consumption was estimated by measurements of leg blood flow and arteriovenous oxygen difference. The perirenal adipose tissue blood flow increased approximately twofold, whereas the local temperature increased approximately 0.1 degrees C on an average. Assuming that man possesses 700 g of BAT with a similar thermogenic capacity, this tissue contributed only 10 ml X min-1 to the 40 ml X min-1 increase in oxygen consumption in the subject whose perirenal BAT showed the most pronounced response to ephedrine. The leg oxygen consumption increased on an average 60% after ephedrine. By extrapolation of this value to whole body skeletal muscle, approximately 50% of the increase in oxygen consumption induced by ephedrine may take place in skeletal muscle. It is concluded that skeletal muscle is a tissue of importance with respect to the thermogenic effect of sympathomimetics in man, whereas the results do not support a major role for perirenal BAT.

alpha-Stimulation protects exercise increment in skeletal muscle oxygen consumption

1980 ◽  
Vol 238 (3) ◽  
pp. H331-H339 ◽  
Author(s):  
S. H. Nellis ◽  
S. F. Flaim ◽  
K. M. McCauley ◽  
R. Zelis
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Adrenergic Receptor ◽  
Analysis Of Covariance ◽  
Beta Blockade ◽  
Active Muscle ◽  
Muscle Oxygen ◽  
Muscle Oxygen Consumption ◽  
Exercise Induced

Oxygen consumption (VO2) in an isolated, autoperfused, statically exercising canine gracilis muscle (2.5% P0) was studied in low blood flow (Q) states induced by constant norepinephrine (NE) infusion and by mechanical occlusion (MO). Q and VO2 were evaluated at rest (Qc and VO2c), after 5 min of exercise (Qe and VO2e) and after 5 more min of exercise with either NE or MO (Qt and VO2t). Data were normalized and plotted as the VO2e-VO2t)/(VO2c-VO2e) vs. (Qe-Qt)/(Qc-Qe) and equations of the lines for NE (y = 0.090x + 0.048) and for MO (y = 0.488x + 0.070) were determined. The slopes of the lines, tested by analysis of covariance, were significantly different (P less than 0.005). These data indicate that when NE reduced Q during exercise, the exercise induced in VO2 was protected to a greater degree than when MO reduced Q under similar conditions. To determine if the effect of NE on VO2 was secondary to a beta-adrenergic-receptor-mediated of skeletal muscle metabolic processes, the experiments were repeated in the presence of beta-blockade with propranolol. In the presence of beta-blockade, the effects of NE on skeletal muscle VO2 were unchanged. It is therefore hypothesized that the mechanism of this effect of NE may be an increase in the efficiency of oxygen extraction resulting from a redistribution of blood flow to more active muscle fiber regions.

Brown adipose tissue, liver, and diet-induced thermogenesis in cafeteria diet-fed rats

1989 ◽  
Vol 67 (4) ◽  
pp. 376-381 ◽  
Author(s):  
Stephanie W. Y. Ma ◽  
David O. Foster
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Direct Determination ◽  
Metabolizable Energy ◽  
Whole Body ◽  
Tissue Blood Flow ◽  
Direct Measurements ◽  
Brown Adipose ◽  
Diet Induced Thermogenesis

Diet-induced thermogenesis (DIT) in young rats overeating a "cafeteria" (CAF) diet of palatable human foods is characterized by a chronic, propranolol-inhibitable elevation in resting metabolic rate [Formula: see text] and is associated with various changes in brown adipose tissue (BAT) that have been taken as evidence for BAT as the effector of DIT. But direct evidence for participation of BAT in DIT has been lacking. By employing a nonocclusive cannula to sample the venous effluent of interscapular BAT (IBAT) for analysis of its O2 content and measuring tissue blood flow with microspheres, we accomplished direct determination (Fick principle) of the O2 consumption of BAT in conscious CAF rats. In comparison with normophagic controls fed chow, the CAF rats exhibited a 43% increase in metabolizable energy intake, reduced food efficiency, a 22% elevation in resting [Formula: see text] at 28 °C (thermoneutrality) or 24 °C (housing temperature), and characteristic changes in the properties of their BAT (e.g., increased mass, protein content and mitochondrial GDP binding). They also exhibited the greater metabolic response to exogenous noradrenaline characteristic of CAF rats and the near elimination by propranolol of their elevation in [Formula: see text]. By the criterion of their elevated [Formula: see text], the CAF rats were exhibiting DIT at the time of the measurements of BAT blood flow and blood O2 levels. However, BAT O2 consumption was found to be no greater in the CAF rats than in the controls at either 28 or 24 °C. At 28 °C it accounted for less than 1% of whole body [Formula: see text]; at 24 °C it increased to about 10% of overall [Formula: see text] in both diet groups. Direct measurements of BAT O2 consumption during expression of the thermic response to a tube-fed meal were also made in conscious CAF and control rats. Both diet groups exhibited an approximately 15% increase in whole body [Formula: see text] at 90–120 min after the meal. The contribution by BAT to this increase was only 2–3% and did not differ significantly between groups. Thus, the results of these direct measurements of BAT O2 consumption in vivo do not support the theory that DIT in CAF rats is mainly due to increased BAT thermogenesis occurring either chronically or during assimilation of a meal. In further studies of the effector(s) of DIT in CAF rats, partial hepatectomy (two-thirds of the liver removed) was found to acutely reduce the resting [Formula: see text] of CAF rats by 1.85 mL/min, 2.3 times as much as in chow-fed controls. From this difference in response, it was estimated that in the CAF rats liver O2 consumption before hepatectomy exceeded that of the controls by about 1.5 mL/min, an amount that would be sufficient to fully account for the elevation in resting [Formula: see text] of the former. A major role for the liver in the DIT of CAF rats is thus suggested.Key words: cafeteria feeding, diet-induced thermogenesis, thermic effect of food, brown fat, liver.

Thermogenic effects of dihydrocodeine in the rat

1988 ◽  
Vol 66 (1) ◽  
pp. 61-65 ◽  
Author(s):  
Nancy J. Rothwell ◽  
Michael J. Stock ◽  
Alison E. Tedstone
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Brown Adipose Tissue ◽  
Opiate Receptors ◽  
Zucker Rats ◽  
Tissue Blood Flow ◽  
Dependent Manner ◽  
Brown Adipose ◽  
Adrenergic Antagonist

The object of this study was to assess the effects of dihydrocodeine on thermogenesis and brown adipose tissue activity in the rat from measurements of oxygen consumption and blood flow. Acute injection of dihydrocodeine tartrate (s.c.) stimulated resting oxygen consumption [Formula: see text] in Sprague–Dawley rats in a dose-dependent manner (0.5–50 mg/kg), with a peak response (40–45% increase) occurring at 10–25 mg/kg. This effect was also observed in urethane-anaesthetized rats (although the effect was reduced) and in conscious animals following gastric intubation with the drug. Pretreatment of rats with either a β-adrenergic antagonist (propranolol, 20 mg/kg), ACTH (4 g/kg), or an opiate antagonist (WIN44441-1, 2 mg/kg) significantly reduced the response to dihydrocodeine, whereas corticosterone injection (5 mg/kg) enhanced the effect. Surgical adrenalectomy or hypophysectomy (HYPX) almost completely abolished the thermogenic effect of dihydrocodeine. Dihydrocodeine also stimulated [Formula: see text] in lean (58% increase) and genetically obese Zucker rats (69% increase), and in both Zucker genotypes these responses were only slightly affected by HYPX, but enhanced in HYPX rats treated daily with corticosterone (1 mg/kg). Tissue blood flow, assessed from the distribution of radiolabelled microspheres, was unaffected in white adipose tissue, skeletal muscle, testes, kidney, brain, and liver (arterial supply) after a single injection of dihydrocodeine (25 mg/kg), but flow to interscapular and perirenal brown adipose tissue was increased by 9- to 10-fold. Surgical sympathectomy of brown adipose tissue prevented the increase in blood flow. These potent thermogenic effects of dihydrocodeine in the rat appear to result from sympathetic activation of heat production in brown fat and to involve opiate receptors, but can also be modified by pituitary and (or) adrenal hormones.

Tissue blood flow in control and cold-adapted hyperthyroid rats

1984 ◽  
Vol 62 (8) ◽  
pp. 928-933 ◽  
Author(s):  
Nancy J. Rothwell ◽  
Michael J. Stock
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Oxygen Consumption ◽  
White Adipose Tissue ◽  
Tissue Blood Flow ◽  
Cold Adapted ◽  
Brown Adipose ◽  
A Minor ◽  
Kidney Liver

Chronic injections (once daily for 10–14 days) of triiodothyronine (T3) stimulated oxygen consumption by 50 and 15% in anaesthetized, control (24 °C), and cold-adapted (5 °C) rats, respectively, compared with euthyroid controls. Tissue blood flow, determined from the distribution of radioactive microspheres, was unaffected by T3 treatment in skeletal muscle, scrotum, brain, bone, skin, diaphragm, and brown adipose tissue (BAT) of rats housed at 24 °C, but was decreased in spleen (53% of control) and significantly increased in three white adipose tissue depots (average 267% increase) and liver (56%). Blood flow to epididymal fat and leg muscle of cold-adapted rats was increased by T3 treatment (100 and 138% increases, respectively), but other tissues were unaffected. Blood oxygen extraction and oxygen consumption in vivo by interscapular BAT was increased in hyperthyroid rats compared with euthyroid controls, but was reduced by T3 treatment in cold-adapted animals. These data show that BAT makes only a minor contribution (7%) to thyroid thermogenesis, but suggest that kidney, liver, gut, and particularly white adipose tissue may be involved.

scholarly journals Total Forearm Blood Flow as an Indicator of Skeletal Muscle Blood Flow: Effect of Subcutaneous Adipose Tissue Blood Flow

1994 ◽  
Vol 87 (5) ◽  
pp. 559-566 ◽  
Author(s):  
E. E. Blaak ◽  
M. A. van Baak ◽  
G. J. Kemerink ◽  
M. T. W. Pakbiers ◽  
G. A. K. Heidendal ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Forearm Blood Flow ◽  
Muscle Blood Flow ◽  
Tissue Blood Flow ◽  
Adipose Tissue Blood Flow ◽  
Flow Through ◽  
Subcutaneous Adipose

1. In studying forearm skeletal muscle substrate exchange, an often applied method for estimating skeletal muscle blood flow is strain gauge plethysmography. A disadvantage of this method is that it only measures total blood flow through a segment of forearm and not the flow through the individual parts such as skin, adipose tissue and muscle. 2. In the present study the contribution of forearm subcutaneous adipose tissue blood flow to total forearm blood flow was evaluated in lean (% body fat 17.0 ± 2.2) and obese males (% body fat 30.9 ± 1.6) during rest and during infusion of the non-selective β-agonist isoprenaline. Measurements were obtained of body composition (hydrostatic weighing), forearm composition (magnetic resonance imaging) and of total forearm (venous occlusion plethysmography), skin (skin blood flow, laser Doppler), and subcutaneous adipose tissue blood flow (133Xe washout technique). 3. The absolute forearm area and the relative amount of fat (% of forearm area) were significantly higher in obese as compared to lean subjects, whereas the relative amounts of muscle and skin were similar. 4. During rest, the percentage contribution of adipose tissue blood flow to total forearm blood flow was significantly higher in lean compared with obese subjects (19 vs 12%, P < 0.05), whereas there were no differences in percentage contribution between both groups during isoprenaline infusion (10 vs 13%). Furthermore, the contribution of adipose tissue blood flow to total forearm blood flow was significantly lower during isoprenaline infusion than during rest in lean subjects (P < 0.05), whereas in the obese this value was similar during rest and during isoprenaline infusion. 5. In conclusion, although the overall contribution of adipose tissue blood flow to total forearm blood flow seems to be relatively small, the significance of this contribution may vary with degree of adiposity. Calculations on the contribution of adipose tissue blood flow and SBF to total forearm blood flow indicate that the contribution of non-muscular flow to total forearm blood flow may be of considerable importance and may amount in lean subjects to 35–50% of total forearm blood flow in the resting state.

Increased hemoglobin-oxygen affinity does not decrease skeletal muscle oxygen consumption

1981 ◽  
Vol 51 (4) ◽  
pp. 864-870 ◽  
Author(s):  
B. K. Ross ◽  
M. P. Hlastala
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Oxygen Affinity ◽  
Arterial Oxygen ◽  
Sodium Metabisulfite ◽  
Muscle Oxygen ◽  
Hemoglobin Oxygen Affinity ◽  
Muscle Oxygen Consumption ◽  
Stored Blood ◽  
Sodium Cyanate

The importance of hemoglobin-oxygen affinity (HOA) in affecting skeletal muscle oxygen consumption (VO2) was reevaluated using an isolated canine gracilis muscle. HOA of the blood [normal O2 half-saturation pressure of hemoglobin (P50) = 30 Torr] was increased by refrigerated storage (P50 = 22 Torr), incubation in sodium metabisulfite (P50 = 24 Torr), or in sodium cyanate (P50 = 14 Torr). Stored blood caused a significant fall in VO2 to 80% of control, with no change in venous O2 partial pressure (PvO2), substantiating previous studies. However, in contrast, blood incubated in sodium metabisulfite or sodium cyanate resulted in no impairment of VO2, with a fall in PvO2 in the latter case indicating that a critical PvO2 did not cause the reduction in VO2 with stored blood. To substantiate further the lack of existence of a critical PO2, fresh and increased HOA blood was perfused at constant flow rates and varying arterial oxygen saturations. Stored blood showed a marked reduction in VO2 as compared with normal blood over a wide range of saturations. However, carbamylated blood VO2 was identical to fresh blood VO2 values. The data suggest that the position of the oxygen dissociation curve may not be as important as originally thought in determining skeletal muscle oxygen delivery. The drop in VO2 caused by perfusion with stored blood is due to some other factor unrelated to HOA.

Adipose tissue function in the insulin-resistance syndrome

2005 ◽  
Vol 33 (5) ◽  
pp. 1045-1048 ◽  
Author(s):  
F. Karpe ◽  
G.D. Tan
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Blood Glucose Concentration ◽  
Insulin Resistance Syndrome ◽  
The Body ◽  
Tissue Blood Flow ◽  
Main Function ◽  
Adipose Tissue Blood Flow

Insulin resistance is often seen as a consequence of obesity and there are several possible links between adipose tissue function and insulin resistance determined in other organs such as skeletal muscle or liver. One such link is the regulation of NEFA (non-esterified fatty acid) delivery to the rest of the body. Simplistically, an expanded adipose tissue mass delivers more NEFA to the systemic circulation and these fatty acids compete for substrate utilization in skeletal muscle, which in turn reduces glucose utilization. This increases blood glucose concentration and provides the stimulus for increased insulin secretion and hyperinsulinaemia is a key feature of the insulin-resistance syndrome. However, there is abundant evidence that adipose tissue is exquisitely insulin sensitive and hyperinsulinaemia may therefore lead to a constant lipolytic inhibition in adipose tissue. Consequently, the main function of adipose tissue, to rapidly switch between fat uptake and fat release, will be hampered. Adipose tissue blood flow is the conveyor of signals and substrates to and from the adipose tissue. In healthy people adipose tissue blood flow is much enhanced by food intake, whereas in insulin-resistant subjects this response is blunted. This is another facet of unresponsiveness of adipose tissue in the insulin-resistance syndrome.

Sign in / Sign up

Export Citation Format

Share Document