Effects of epinephrine on human muscle glucose and protein metabolism

1995 ◽  
Vol 268 (1) ◽  
pp. E55-E59 ◽  
Author(s):  
D. A. Fryburg ◽  
R. A. Gelfand ◽  
L. A. Jahn ◽  
D. Oliveras ◽  
R. S. Sherwin ◽  
...  
Keyword(s):  
Plasma Insulin ◽  
Forearm Blood Flow ◽  
Muscle Protein ◽  
Human Muscle ◽  
Whole Body ◽  
Epinephrine Infusion ◽  
Healthy Human ◽  
Human Volunteers ◽  
Human Forearm ◽  
Forearm Muscle

Systemic epinephrine infusion causes hypoaminoacidemia and inhibits whole body leucine flux (proteolysis) in humans. Its specific action on muscle protein is not known and is difficult to assess during systemic epinephrine infusions, which affect plasma insulin, amino acid, and free fatty acid concentrations. During a steady-state infusion of L-[ring-2,6-3H]phenylalanine, we examined the effect of locally infused epinephrine on the metabolism of protein and glucose in forearm muscle of 10 healthy human volunteers. During local epinephrine infusion, systemic concentrations of glucose, phenylalanine, insulin, and epinephrine were unchanged and lactate declined (P < 0.02). Compared with baseline, epinephrine induced significant increases in forearm blood flow (P < 0.01) and net lactate release (P < 0.001) and a decrease in glucose uptake (P < 0.01) at both 2 and 4 h. At 2 and 4 h phenylalanine release from muscle proteolysis was suppressed (P < 0.01), and at 4 h the net phenylalanine balance was less negative than baseline (P < 0.02), indicating an anticatabolic effect on muscle protein. We conclude that in human forearm muscle epinephrine, at physiological concentrations, has a catabolic effect on muscle glycogen but an anticatabolic action on muscle protein. The mechanism of this latter effect is not known.

Interactions between local and reflex influences on human forearm skin blood flow

1976 ◽  
Vol 41 (6) ◽  
pp. 826-831 ◽  
Author(s):  
J. M. Johnson ◽  
G. L. Brengelmann ◽  
L. B. Rowell
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Forearm Blood Flow ◽  
Lower Body Negative Pressure ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Vasoconstrictor Response ◽  
Human Forearm ◽  
Forearm Skin ◽  
Forearm Muscle

A three-part experiment was designed to examine interactions between local and reflex influences on forearm skin blood flow (SkBF). In part I locally increasing arm skin temperature (Tsk) to 42.5 degrees C was not associated with increases in underlying forearm muscle blood flow, esophageal temperature (Tes), or forearm blood flow in the contralateral cool arm. In part II whole-body Tsk was held at 38 or 40 degrees C and the surface temperature of one arm held at 38 or 42 degrees C for prolonged periods. SkBF in the heated arm rose rapidly with the elevation in body Tsk and arm Tsk continued to rise as Tes rose. SkBF in the arm kept at 32 degrees C paralleled rising Tes. In six studies, SkBF in the cool arm ultimately converged with SkBF in the heated arm. In eight other studies, heated arm SkBF maintained an offset above cool arm SkBF throughout the period of whole-body heating. In part III, local arm Tsk of 42.5 degrees C did not abolish skin vasoconstrictor response to lower body negative pressure. We conclude that local and reflex influences to skin interact so as to modify the degree but not the pattern of skin vasomotor response.

Glycerol exchange across the human forearm assessed by a combination of tracer and arteriovenous exchange techniques

1993 ◽  
Vol 84 (1) ◽  
pp. 99-104 ◽  
Author(s):  
M. Elia ◽  
K. Khan ◽  
G. Calder ◽  
A. Kurpad
Keyword(s):  
Isotopic Exchange ◽  
Venous Blood ◽  
Human Muscle ◽  
The Other ◽  
Whole Body ◽  
Free Glycerol ◽  
Tracer Method ◽  
Concentration Difference ◽  
Human Forearm ◽  
Forearm Muscle

1. Whole-body kinetics and regional exchange of glycerol across forearm muscle were assessed in eight lean subjects by a combination of a tracer method (infusion of [2H5]glycerol) and arteriovenous catheterization. 2. During an apparent steady state, the enrichment of glycerol in deep venous blood from the muscle bed of the forearm was about half (4.40 ± 1.72 atom per cent excess) that observed in arterialized blood (8.41 ± 4.30 atom per cent excess). Under the same conditions, the circulating concentrations of glycerol in arterialized (91 ± 24 μmol/l) and venous (87 ± 32 μmol/l) blood were similar. 3. In a further group of 37 subjects it was found that about half had a positive arteriovenous concentration difference and the other had half a negative arteriovenous concentration difference (mean −1.6 ± 11.9 μmol/l; range −25 to +22 μmol/l). 4. These results suggest: (a) that human muscle does not always release glycerol and may take it up; (b) that there is substantial isotopic exchange of glycerol across forearm muscle tissue, which is not reflected by the net exchange of glycerol; this could be due to slow equilibrium of enriched glycerol from the circulation, with unenriched free glycerol in the muscle pool, or due to the simultaneous metabolic utilization of enriched glycerol and metabolic production of unenriched glycerol; (c) that the estimation of glycerol flux rates is strongly dependent on whether the blood is arterialized or deep venous.

Characterization of endothelium-derived hyperpolarizing factor in the human forearm microcirculation

2001 ◽  
Vol 280 (6) ◽  
pp. H2470-H2477 ◽  
Author(s):  
Julian P. J. Halcox ◽  
Suresh Narayanan ◽  
Laura Cramer-Joyce ◽  
Rita Mincemoyer ◽  
Arshed A. Quyyumi
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Human Subjects ◽  
Epoxyeicosatrienoic Acid ◽  
Healthy Human ◽  
Human Forearm ◽  
Oxide Synthase ◽  
Cytochrome P 450

The identity of endothelium-dependent hyperpolarizing factor (EDHF) in the human circulation remains controversial. We investigated whether EDHF contributes to endothelium-dependent vasomotion in the forearm microvasculature by studying the effect of K+ and miconazole, an inhibitor of cytochrome P-450, on the response to bradykinin in healthy human subjects. Study drugs were infused intra-arterially, and forearm blood flow was measured using strain-gauge plethysmography. Infusion of KCl (0.33 mmol/min) into the brachial artery caused baseline vasodilation and inhibited the vasodilator response to bradykinin, but not to sodium nitroprusside. Thus the incremental vasodilation induced by bradykinin was reduced from 14.3 ± 2 to 7.1 ± 2 ml · min−1 · 100 g−1( P < 0.001) after KCl infusion. A similar inhibition of the bradykinin ( P = 0.014), but not the sodium nitroprusside (not significant), response was observed with KCl after the study was repeated during preconstriction with phenylephrine to restore resting blood flow to basal values after KCl. Miconazole (0.125 mg/min) did not inhibit endothelium-dependent or -independent responses to ACh and sodium nitroprusside, respectively. However, after inhibition of cyclooxygenase and nitric oxide synthase with aspirin and N G-monomethyl-l-arginine, the forearm blood flow response to bradykinin ( P = 0.003), but not to sodium nitroprusside (not significant), was significantly suppressed by miconazole. Thus nitric oxide- and prostaglandin-independent, bradykinin-mediated forearm vasodilation is suppressed by high intravascular K+ concentrations, indicating a contribution of EDHF. In the human forearm microvasculature, EDHF appears to be a cytochrome P-450 derivative, possibly an epoxyeicosatrienoic acid.

Racial differences in lipid metabolism in women with abdominal obesity

2000 ◽  
Vol 279 (3) ◽  
pp. R944-R950 ◽  
Author(s):  
Susan B. Racette ◽  
Jeffrey F. Horowitz ◽  
Bettina Mittendorfer ◽  
Samuel Klein
Keyword(s):  
Fatty Acid ◽  
Black Women ◽  
Racial Differences ◽  
Abdominal Obesity ◽  
Plasma Insulin ◽  
White Women ◽  
Abdominal Fat ◽  
Fat Free Mass ◽  
Whole Body ◽  
Epinephrine Infusion

We evaluated palmitate rate of appearance (Ra) in plasma during basal conditions and during a four-stage epinephrine infusion plus pancreatic hormonal clamp in nine white and nine black women with abdominal obesity, who were matched on fat-free mass, total and percent body fat, and waist-to-hip circumference ratio. On the basis of single-slice magnetic resonance imaging analysis, black women had the same amount of subcutaneous abdominal fat but less intra-abdominal fat than white women (68 ± 9 vs. 170 ± 14 cm2, P < 0.05). Basal palmitate Rawas lower in black than in white women (1.95 ± 0.26 vs. 2.88 ± 0.23 μmol · kg fat-free mass−1 · min−1, P < 0.005), even though plasma insulin and catecholamine concentrations were the same in both groups. Palmitate Ra across a physiological range of plasma epinephrine concentrations remained lower in black women, because the increase in palmitate Ra during epinephrine infusion was the same in both groups. We conclude that basal and epinephrine-stimulated palmitate Ra is lower in black than in white women with abdominal obesity. The differences in basal palmitate kinetics are not caused by alterations in plasma insulin or catecholamine concentrations or lipolytic sensitivity to epinephrine. The lower rate of whole body fatty acid flux and smaller intra-abdominal fat mass may have clinical benefits because of the relationship between excessive fatty acid availability and metabolic diseases.

Effect of starvation on human muscle protein metabolism and its response to insulin

1990 ◽  
Vol 259 (4) ◽  
pp. E477-E482 ◽  
Author(s):  
D. A. Fryburg ◽  
E. J. Barrett ◽  
R. J. Louard ◽  
R. A. Gelfand
Keyword(s):  
Amino Acid ◽  
Muscle Protein ◽  
Acid Output ◽  
Nitrogen Loss ◽  
Whole Body ◽  
Glucose Disposal ◽  
Catabolic State ◽  
Muscle Protein Metabolism ◽  
Forearm Muscle ◽  
Net Release

Although starvation is known to impair insulin-stimulated glucose disposal, whether it also induces resistance to insulin's antiproteolytic action on muscle is unknown. To assess the effect of fasting on muscle protein turnover in the basal state and in response to insulin, we measured forearm amino acid kinetics, using [3H]phenylalanine (Phe) and [14C]leucine (Leu) infused systemically, in eight healthy subjects after 12 (postabsorptive) and 60 h of fasting. After a 150-min basal period, forearm local insulin concentration was selectively raised by approximately 25 muU/ml for 150 min by intra-arterial insulin infusion (0.02 mU.kg-1. min-1). The 60-h fast increased urine nitrogen loss and whole body Leu flux and oxidation (by 50-75%, all P less than 0.02). Post-absorptively, forearm muscle exhibited a net release of Phe and Leu, which increased two- to threefold after the 60-h fast (P less than 0.05); this effect was mediated exclusively by accelerated local rates of amino acid appearance (Ra), with no reduction in rates of disposal (Rd). Local hyperinsulinemia in the postabsorptive condition caused a twofold increase in forearm glucose uptake (P less than 0.01) and completely suppressed the net forearm output of Phe and Leu (P less than 0.02). After the 60-h fast, forearm glucose disposal was depressed basally and showed no response to insulin; in contrast, insulin totally abolished the accelerated net forearm release of Phe and Leu. The action of insulin to reverse the augmented net release of Phe and Leu was mediated exclusively by approximately 40% suppression of Ra (P less than 0.02) rather than a stimulation of Rd. We conclude that in short-term fasted humans 1) muscle amino acid output accelerates due to increased proteolysis rather than reduced protein synthesis, and 2) despite its catabolic state and a marked impairment in insulin-mediated glucose disposal, muscle remains sensitive to insulin's antiproteolytic action.

Oral citrulline does not affect whole body protein metabolism in healthy human volunteers: Results of a prospective, randomized, double-blind, cross-over study

2011 ◽  
Vol 30 (6) ◽  
pp. 807-811 ◽  
Author(s):  
Ronan Thibault ◽  
Laurent Flet ◽  
Fabienne Vavasseur ◽  
Marie Lemerle ◽  
Véronique Ferchaud-Roucher ◽  
...  
Keyword(s):  
Protein Metabolism ◽  
Whole Body ◽  
Healthy Human ◽  
Double Blind ◽  
Body Protein ◽  
Human Volunteers

Exercise augments the acute anabolic effects of intradialytic parenteral nutrition in chronic hemodialysis patients

2004 ◽  
Vol 286 (4) ◽  
pp. E589-E597 ◽  
Author(s):  
Lara B. Pupim ◽  
Paul J. Flakoll ◽  
Deanna K. Levenhagen ◽  
T. Alp Ikizler
Keyword(s):  
Parenteral Nutrition ◽  
Muscle Protein ◽  
Chronic Hemodialysis ◽  
Whole Body ◽  
Constant Infusion ◽  
Acid Uptake ◽  
Protein Homeostasis ◽  
Body Protein ◽  
Forearm Muscle ◽  
Intradialytic Parenteral Nutrition

Decreased dietary protein intake and hemodialysis (HD)-associated protein catabolism are among several factors that predispose chronic hemodialysis (CHD) patients to uremic malnutrition and associated muscle wasting. Intradialytic parenteral nutrition (IDPN) acutely reverses the net negative whole body and forearm muscle protein balances observed during the HD procedure. Exercise has been shown to improve muscle protein homeostasis, especially if performed with adequately available intramuscular amino acids. We hypothesized that exercise performance would provide additive anabolic effects to the beneficial effects of IDPN. We studied six CHD patients at two separate HD sessions: 1) IDPN administration only and 2) IDPN + exercise. Patients were studied 2 h before, during, and 2 h after an HD session by use of a primed constant infusion of l-[1-13C]leucine and l-[ ring-2H5] phenylalanine. Exercise combined with IDPN promoted additive twofold increases in forearm muscle essential amino acid uptake (455 ± 105 vs. 229 ± 38 nmol·100 ml-1·min-1, P < 0.05) and net muscle protein accretion (125 ± 37 vs. 56 ± 30 μg·100 ml-1·min-1, P < 0.05) during HD compared with IDPN alone. Measurements of whole body protein homeostasis and energy expenditure were not altered by exercise treatment. In conclusion, exercise in the presence of adequate nutritional supplementation has potential as a therapeutic intervention to blunt the loss of muscle mass in CHD patients.

Independent stimulation of glucose metabolism and Na+-K+ exchange by insulin in the human forearm

1988 ◽  
Vol 255 (6) ◽  
pp. E953-E958 ◽  
Author(s):  
E. Ferrannini ◽  
S. Taddei ◽  
D. Santoro ◽  
A. Natali ◽  
C. Boni ◽  
...  
Keyword(s):  
Blood Flow ◽  
Glucose Uptake ◽  
Forearm Blood Flow ◽  
Potassium Uptake ◽  
Human Forearm ◽  
Net Uptake ◽  
Forearm Technique ◽  
Forearm Muscle ◽  
Local Levels

Insulin promotes potassium uptake into skeletal muscle by stimulating the activity of the Na+-K+ pump. To test whether insulin-induced glucose and potassium uptake are linked processes in vivo, we used the perfused forearm technique in healthy volunteers. Local hyperinsulinemia (125 +/- 11 microU/ml for 100 min) induced a net uptake of glucose and potassium (4.79 +/- 0.61 and 0.76 +/- 0.22 mumol.min-1.100 ml-1 of forearm volume, respectively). When an intra-arterial ouabain infusion (0.72 microgram.min-1.100 ml-1, producing local levels of approximately 0.5 mM) was superimposed on the insulin infusion, potassium uptake was blocked (0.026 +/- 0.190 ml.min-1.100 ml-1, P less than 0.02), and glucose uptake was decreased (to 3.31 +/- 0.34 mumol.min-1.100 ml-1, P less than 0.03). The latter change was explained by a 30% fall in forearm blood flow (from 2.95 +/- 0.10 to 2.01 +/- 0.18 ml.min-1.100 ml-1, P less than 0.001). To separate out the effect of blood flow, in another series of studies forearm blood flow was clamped by co-infusing propranolol and phentolamine (7 and 8 micrograms.min-1.100 ml-1, respectively). Under these conditions of fixed flow (7.0 +/- 0.8 ml.min-1.100 ml-1), ouabain still abolished the stimulatory effect of insulin on potassium uptake but had only a small (and statistically insignificant) effect on forearm glucose extraction (from 20 +/- 2 to 16 +/- 2%, P = N>). We conclude that in human forearm muscle ouabain inhibits Na+-K+ exchange and depresses insulin-induced glucose uptake via an adrenergic-mediated limitation of blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

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