scholarly journals Major differences in noradrenaline action on lipolysis and blood flow rates in skeletal muscle and adipose tissue in vivo

Diabetologia ◽  
2005 ◽  
Vol 48 (5) ◽  
pp. 946-953 ◽  
Author(s):  
V. Quisth ◽  
S. Enoksson ◽  
E. Blaak ◽  
E. Hagström-Toft ◽  
P. Arner ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Flow Rates

No apparent suppression by insulin of in vivo skeletal muscle lipolysis in nonobese women

2002 ◽  
Vol 283 (2) ◽  
pp. E295-E301 ◽  
Author(s):  
Erik Moberg ◽  
Stefan Sjöberg ◽  
Eva Hagström-Toft ◽  
Jan Bolinder
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Insulin Infusion ◽  
Muscle Blood Flow ◽  
Tissue Blood Flow ◽  
Glycerol Release ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Flow Rates

To investigate the antilipolytic effect of insulin in skeletal muscle and adipose tissue in vivo, the rates of glycerol release from the two tissues were compared in 10 nonobese women during a two-step euglycemic hyperinsulinemic clamp. Tissue interstitial glycerol levels were determined by microdialysis, and tissue blood flow was assessed with the 133Xe clearance technique. Absolute rates of glycerol release were estimated according to Fick's principle. In both adipose tissue and muscle, glycerol levels decreased significantly already during the low insulin infusion rate. The fractional release of glycerol (difference between interstitial glycerol and arterialized venous plasma glycerol) was reduced by more than one-half in adipose tissue ( P < 0.0001) in response to insulin, whereas it remained unaltered in skeletal muscle. Muscle blood flow rates increased by 60% ( P < 0.02) during insulin infusion; in adipose tissue, blood flow rates did not change significantly in response to insulin. The basal rate of glycerol release from skeletal muscle amounted to ∼15% of that from adipose tissue. After insulin infusion, the rate of adipose tissue glycerol release was markedly suppressed, whereas in skeletal muscle the rate of glycerol mobilization did not change significantly in response to insulin. It is concluded that insulin does not inhibit the rate of lipolysis in skeletal muscle of nonobese women.

scholarly journals Microdialysis: use in human exercise studies

1999 ◽  
Vol 58 (4) ◽  
pp. 913-917 ◽  
Author(s):  
Peter Arner
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Brain Function ◽  
Water Soluble ◽  
Tissue Blood Flow ◽  
Microdialysis Probe ◽  
Peripheral Tissues

Microdialysis has been used for 25 years to study brain function in vivo. Recently, it has been developed for investigations on peripheral tissues. A microdialysis catheter is an artificial blood vessel system which can be placed in the extracellular space of various tissues such as adipose tissue and skeletal muscle in order to examine these tissues in situ. Molecules are collected from the tissue by the device and their true interstitial concentration can be estimated. Metabolically-active molecules can be delivered to the interstitial space through the microdialysis probe and their action on the tissue can be investigated locally without producing generalized effects. It is also possible to study local tissue blood flow with microdialysis by adding a flow marker (usually ethanol) to the microdialysis solvent. The microdialysis technique is particularly useful for studies of small and water-soluble molecules. A number of important observations on the in vivo regulation of lipolysis, carbohydrate metabolism and blood flow in human skeletal muscle and adipose tissue have been made recently using microdialysis.

scholarly journals Catecholamine Regulation of Local Lactate Production in Vivo in Skeletal Muscle and Adipose Tissue: Role of β-Adrenoreceptor Subtypes

2008 ◽  
Vol 93 (1) ◽  
pp. 240-246 ◽  
Author(s):  
Veronica Qvisth ◽  
Eva Hagström-Toft ◽  
Staffan Enoksson ◽  
Jan Bolinder
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Lactate Production ◽  
Normal Weight ◽  
Receptor Subtype ◽  
Local Blood Flow ◽  
Muscle Lactate ◽  
Fractional Release

Abstract Context: The regulation of lactate production in skeletal muscle (SM) and adipose tissue (AT) is not fully elucidated. Objective: Our objective was to investigate the catecholamine-mediated regulation of lactate production and blood flow in SM and AT in healthy, normal-weight subjects by using microdialysis. Methods: First, lactate levels in SM and AT were measured during an iv norepinephrine infusion (n = 11). Local blood flow was determined with the 133Xe-clearance technique. Second, muscle lactate was measured during hypoglycemia and endogenous epinephrine stimulation (n = 12). Third, SM was perfused with selective β1–3-adrenoreceptor agonists in situ (n = 8). Local blood flow was measured with the ethanol perfusion technique. Results: In response to iv norepinephrine, the fractional release of lactate (difference between tissue and arterial lactate) increased by 40% in SM (P = 0.001), whereas remaining unchanged in AT. Blood flow decreased by 40% in SM (P &lt; 0.005) and increased by 50% in AT (P &lt; 0.05). In response to hypoglycemia, epinephrine increased 10-fold, and the fractional release of lactate in SM doubled (P &lt; 0.0001). The blood flow remained unchanged. The β2-agonist, terbutaline, caused a marked concentration-dependent increase of muscle lactate and blood flow (P &lt; 0.0001). The β1-agonist, dobutamine, induced a discrete increase of muscle lactate (P &lt; 0.0001), and the blood flow remained unchanged. The β3-agonist, CPG 12177, did not affect muscle lactate or blood flow. Conclusions: Catecholamines stimulate lactate production in SM, but not in AT. In SM, the β2-adrenoreceptor is the most important β-adrenergic receptor subtype in the regulation of lactate production.

Lactate release from adipose tissue and skeletal muscle in vivo: defective insulin regulation in insulin-resistant obese women

2007 ◽  
Vol 292 (3) ◽  
pp. E709-E714 ◽  
Author(s):  
Veronica Qvisth ◽  
Eva Hagström-Toft ◽  
Erik Moberg ◽  
Stefan Sjöberg ◽  
Jan Bolinder
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Lactate Production ◽  
Obese Women ◽  
Local Blood Flow ◽  
Lactate Release ◽  
Insulin Resistant ◽  
Insulin Regulation

To study the local tissue lactate production in the normal state and its possible disturbances in insulin resistance, rates of lactate release from adipose tissue (AT) and skeletal muscle (SM) were compared postabsorptively and during a hyperinsulinemic euglycemic clamp in 11 healthy nonobese and 11 insulin-resistant obese women. A combination of microdialysis, to measure interstitial lactate, and the 133Xe clearance technique, to determine local blood flow, were used. In the controls, local blood flow increased by 40% in SM ( P < 0.05) and remained unchanged in AT, whereas the interstitial-plasma difference in lactate doubled in AT ( P < 0.005) and was unaffected in SM during hyperinsulinemia. In the obese, blood flow and interstitial-plasma difference in lactate remained unchanged in both tissues during hyperinsulinemia. The lactate release (μmol100 g−1min−1) was 1.17 ± 0.22 in SM and 0.43 ± 0.11 in AT among the controls ( P < 0.01) and 0.86 ± 0.23 in SM and 0.83 ± 0.25 in AT among the obese women in the postabsorptive state. During insulin infusion, lactate release in the controls increased to 1.92 ± 0.26 in SM ( P < 0.005) and to 1.14 ± 0.22 in AT ( P < 0.005) but remained unchanged in the obese women. It is concluded that AT and SM are both significant sources of lactate release postabsorptively, and AT is at least as responsive to insulin as SM. The ability to increase lactate release in response to insulin is impaired in AT and SM in insulin-resistant obese women, involving defective insulin regulation of both tissue lactate metabolism and local blood flow.

scholarly journals Adipose tissue and skeletal muscle insulin-mediated glucose uptake in insulin resistance: role of blood flow and diabetes

2018 ◽  
Vol 108 (4) ◽  
pp. 749-758 ◽  
Author(s):  
Ele Ferrannini ◽  
Patricia Iozzo ◽  
Kirsi A Virtanen ◽  
Miikka-Juhani Honka ◽  
Marco Bucci ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Blood Supply ◽  
Insulin Resistant ◽  
Femoral Muscle

Abstract Background Adipose tissue glucose uptake is impaired in insulin-resistant states, but ex vivo studies of human adipose tissue have yielded heterogeneous results. This discrepancy may be due to different regulation of blood supply. Objective The aim of this study was to test the flow dependency of in vivo insulin-mediated glucose uptake in fat tissues, and to contrast it with that of skeletal muscle. Design We reanalyzed data from 159 individuals in which adipose tissue depots—subcutaneous abdominal and femoral, and intraperitoneal—and femoral skeletal muscle were identified by MRI, and insulin-stimulated glucose uptake ([18F]-fluoro-2-deoxyglucose) and blood flow ([15O]-H2O) were measured simultaneously by positron emission tomography scanning. Results Individuals in the bottom tertile of whole-body glucose uptake [median (IQR) 36 (17) µmol. kg fat-free mass (kgFFM)−1 . min−1 .nM−1] displayed all features of insulin resistance compared with the rest of the group [median (IQR) 97 (71) µmol . kgFFM−1 .min−1 . nM−1]. Rates of glucose uptake were directly related to the degree of insulin resistance in all fat depots as well as in skeletal muscle. However, blood flow was inversely related to insulin sensitivity in each fat depot (all P ≤ 0.03), whereas femoral muscle blood flow was not significantly different between insulin-resistant and insulin-sensitive subjects, and was not related to insulin sensitivity. Furthermore, in subjects performing one-leg exercise, blood flow increased 5- to 6-fold in femoral muscle but not in the overlying adipose tissue. The presence of diabetes was associated with a modest increase in fat and muscle glucose uptake independent of insulin resistance. Conclusions Reduced blood supply is an important factor for the impairment of in vivo insulin-mediated glucose uptake in both subcutaneous and visceral fat. In contrast, the insulin resistance of glucose uptake in resting skeletal muscle is predominantly a cellular defect. Diabetes provides a modest compensatory increase in fat and muscle glucose uptake that is independent of insulin resistance.

scholarly journals Effects of aging and exercise training on spinotrapezius muscle microvascular Po2 dynamics and vasomotor control

2011 ◽  
Vol 110 (3) ◽  
pp. 695-704 ◽  
Author(s):  
Danielle J. McCullough ◽  
Robert T. Davis ◽  
James M. Dominguez ◽  
John N. Stabley ◽  
Christian S. Bruells ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Exercise Training ◽  
Sodium Nitroprusside ◽  
Vascular Function ◽  
Treadmill Running ◽  
Aged Rats ◽  
Phosphorescence Quenching

With advancing age, there is a reduction in exercise tolerance, resulting, in part, from a perturbed ability to match O2 delivery to uptake within skeletal muscle. In the spinotrapezius muscle (which is not recruited during incline treadmill running) of aged rats, we tested the hypotheses that exercise training will 1) improve the matching of O2 delivery to O2 uptake, evidenced through improved microvascular Po2 (PmO2), at rest and throughout the contractions transient; and 2) enhance endothelium-dependent vasodilation in first-order arterioles. Young (Y, ∼6 mo) and aged (O, >24 mo) Fischer 344 rats were assigned to control sedentary (YSED; n = 16, and OSED; n = 15) or exercise-trained (YET; n = 14, and OET; n = 13) groups. Spinotrapezius blood flow (via radiolabeled microspheres) was measured at rest and during exercise. Phosphorescence quenching was used to quantify PmO2 in vivo at rest and across the rest-to-twitch contraction (1 Hz, 5 min) transition in the spinotrapezius muscle. In a follow-up study, vasomotor responses to endothelium-dependent (acetylcholine) and -independent (sodium nitroprusside) stimuli were investigated in vitro. Blood flow to the spinotrapezius did not increase above resting values during exercise in either young or aged groups. Exercise training increased the precontraction baseline PmO2 (OET 37.5 ± 3.9 vs. OSED 24.7 ± 3.6 Torr, P < 0.05); the end-contracting PmO2 and the time-delay before PmO2 fell in the aged group but did not affect these values in the young. Exercise training improved maximal vasodilation in aged rats to acetylcholine (OET 62 ± 16 vs. OSED 27 ± 16%) and to sodium nitroprusside in both young and aged rats. Endurance training of aged rats enhances the PmO2 in a nonrecruited skeletal muscle and is associated with improved vascular smooth muscle function. These data support the notion that improvements in vascular function with exercise training are not isolated to the recruited muscle.

scholarly journals Microdialysis of skeletal muscle at rest

1999 ◽  
Vol 58 (4) ◽  
pp. 919-923 ◽  
Author(s):  
Jan Henriksson
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Human Skeletal Muscle ◽  
Human Metabolism ◽  
High Expectations ◽  
Perfusate Flow ◽  
Muscle Research ◽  
Interstitial Glucose

Techniques in human skeletal muscle research are by necessity predominantly 'descriptive'.Microdialysis has raised high expectations that it could meet the demand for a method that allows 'mechanistic' investigations to be performed in human skeletal muscle. In the present review, some views are given on how well the initial expectations on the use of the microdialysis technique in skeletal muscle have been fulfilled, and the areas in which additional work is needed in order to validate microdialysis as an important metabolic technique in this tissue. The microdialysis catheter has been equated to an artificial blood vessel, which is introduced into the tissue. By means of this 'vessel' the concentrations of compounds in the interstitial space can be monitored. The concentration of substances in the collected samples is dependent on the rate of perfusate flow. When perfusate flow is slow enough to allow complete equilibration between interstitial and perfusate fluids, the concentration in the perfusate is maximal and identical to the interstitial concentration. Microdialysis data may be influenced by changes in blood flow, especially in instances where the tissue diffusivity limits the recovery in vivo, i.e. when recovery in vitro is 100 %, whereas the recovery in vivo is less than 100 %. Microdialysis data indicate that a significant arterial-interstitial glucose concentration gradient exists in skeletal muscle but not in adipose tissue at rest. While the concentrations of glucose and lactate in the dialysate from skeletal muscle are close to the expected values, the glycerol values obtained for muscle are still puzzling. Ethanol added to the perfusate will be cleared by the tissue at a rate that is determined by the nutritive blood flow (the microdialysis ethanol technique). It is concluded that microdialysis of skeletal muscle has become an important technique for mechanistic studies in human metabolism and nutrition.

Endothelium regulates skeletal muscle microcirculation by a blood flow velocity-sensing mechanism

1990 ◽  
Vol 258 (3) ◽  
pp. H916-H920 ◽  
Author(s):  
A. Koller ◽  
G. Kaley
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Blood Flow ◽  
Flow Velocity ◽  
Cremaster Muscle ◽  
Positive Linear Correlation ◽  
Skeletal Muscle Microcirculation ◽  
Per Se ◽  
Dependent Flow

In rat cremaster muscle, utilizing parallel arteriolar occlusion, we found that an increase in red blood cell (RBC) velocity (3.5-26.5 mm/s) per se induced an increase in diameter (1.5-9.4 microns) of arterioles (mean control diam 21.5 +/- 0.6 microns; n = 25). The dilation of arterioles appeared only when RBC velocity increased and started always with a delay (mean 8.4 +/- 0.5 s) after the increase in flow velocity. A positive linear correlation was found between peak changes in RBC velocity and diameter (r = 0.87, P less than 0.05). The velocity sensor as well as the mechanism(s) that mediates this response is likely to be located in endothelial cells, because the dilation to increased RBC velocity was completely eliminated after impairment of arteriolar endothelium with light-dye (L-D) treatment. The in vivo demonstration of this phenomenon in arterioles suggests the existence of a new endothelium-dependent, flow velocity-sensitive mechanism for the regulation of blood flow in the microcirculation.

scholarly journals IL-4 and SDF-1 Increase Adipose Tissue-Derived Stromal Cell Ability to Improve Rat Skeletal Muscle Regeneration

2020 ◽  
Vol 21 (9) ◽  
pp. 3302
Author(s):  
Małgorzata Zimowska ◽  
Karolina Archacka ◽  
Edyta Brzoska ◽  
Joanna Bem ◽  
Areta M. Czerwinska ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Muscle Regeneration ◽  
Structure And Function ◽  
Skeletal Muscle Regeneration ◽  
Stem Cell Markers ◽  
Myogenic Factors ◽  
And Function

Skeletal muscle regeneration depends on the satellite cells, which, in response to injury, activate, proliferate, and reconstruct damaged tissue. However, under certain conditions, such as large injuries or myopathies, these cells might not sufficiently support repair. Thus, other cell populations, among them adipose tissue-derived stromal cells (ADSCs), are tested as a tool to improve regeneration. Importantly, the pro-regenerative action of such cells could be improved by various factors. In the current study, we tested whether IL-4 and SDF-1 could improve the ability of ADSCs to support the regeneration of rat skeletal muscles. We compared their effect at properly regenerating fast-twitch EDL and poorly regenerating slow-twitch soleus. To this end, ADSCs subjected to IL-4 and SDF-1 were analyzed in vitro and also in vivo after their transplantation into injured muscles. We tested their proliferation rate, migration, expression of stem cell markers and myogenic factors, their ability to fuse with myoblasts, as well as their impact on the mass, structure and function of regenerating muscles. As a result, we showed that cytokine-pretreated ADSCs had a beneficial effect in the regeneration process. Their presence resulted in improved muscle structure and function, as well as decreased fibrosis development and a modulated immune response.

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