| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Franz-Volhard Clinical Research Center (A.L.B., M.Bo., F.A., K.H., G.F., F.C.L., J.J.), Charité–Campus Buch and Helios Klinikum, 13125 Berlin, Germany; and Institut National de la Santé et de la Recherche Médicale 586 (C.M., M.Be., M.L.), Institut Louis Bugnard, Université Paul Sabatier, Hôpital Rangueil, 31403 Toulouse Cedex 4, France
Address all correspondence and requests for reprints to: Jens Jordan, M.D., Franz-Volhard Clinical Research Center, Haus 129, Charité Campus Buch, Wiltbergstrasse 50, 13125 Berlin, Germany. E-mail: jordan{at}fvk.charite-buch.de.
 |
Abstract |
|---|
 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Objective: The objective was to determine the hemodynamic and metabolic response to physiologically relevant ANP concentrations.
Design: The design was a human physiological study, conducted in 2004.
Setting: The study was conducted at an academic research institute.
Participants: Fourteen healthy normal-weight men (30 ± 1.2 yr) participated in the study.
Intervention: Intravenous infusion of human ANP (h-ANP) was administered at rates of 6.25, 12.5, and 25 ng/kg·min.
Main Outcome Measures: We studied local changes in blood flow and glucose and lipid metabolism of abdominal sc adipose tissue and femoral skeletal muscle by microdialysis. Overall changes in energy expenditure and substrate oxidation rates were monitored by indirect calorimetry.
Results: The increase in serum nonesterified fatty acids and glycerol concentrations were correlated with ANP plasma concentrations (r2 = 0.86 and r2 = 0.76, respectively). In adipose tissue, glycerol increased from 53 ± 6 µmol/liter to 87±13 µmol/liter (P < 0.001). In femoral skeletal muscle, glycerol concentrations did not change, whereas lactate-to-pyruvate ratio decreased from 91 ± 23 to 32 ± 4 (P < 0.001). Indirect calorimetry indicated an increase in lipid oxidation (P < 0.05) concomitantly with a decrease in carbohydrate oxidation (P < 0.01), without changes in overall energy expenditure.
Conclusions: ANP briskly stimulates lipid mobilization and oxidation at plasma concentrations that are encountered in conditions such as heart failure. Natriuretic-peptide induced lipid mobilization might contribute to cardiac cachexia. Drugs that interfere with the natriuretic peptide system should be evaluated for potential metabolic side effects.
|
Introduction |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
|
Subjects and Methods |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Fourteen healthy men were included in our study (aged 30 ± 1.2 yr; body mass index, 24.2 ± 0.4 kg/m2; waist to hip ratio, 0.84 ± 0.01). They ingested no medications. Written informed consent was obtained before study entry. All studies were approved by the institutional review board.
Protocol
Forty-eight hours before the experiment, volunteers were asked to abstain from smoking, alcohol ingestion, caffeine-containing beverages, and vigorous exercise. The experiment took place after an overnight fast in the morning in a quiet room. After a 90-min resting phase, human ANP (Merck Bioscience AG, Clinalfa, Läufelingen, Switzerland) was infused at rates of 6.25, 12.5, and 25 ng/kg·min over 45 min each. Venous blood and microdialysis samples were collected at baseline and in 15 min intervals during the ANP infusion.
Instrumentation
One catheter (Vasocan 20G; B. Braun, Melsungen, Germany) each was placed into large antecubital veins of both arms. We used one catheter for ANP infusion and the other one for blood sampling. A microdialysis probe was inserted into abdominal sc adipose tissue and another into skeletal muscle (quadriceps femoris, vastus lateralis). Oxygen consumption and carbon dioxide production were measured by indirect calorimetry using a ventilated hood (DeltatracII; Datex Ohmeda, Duisburg, Germany) to assess energy expenditure, respiratory quotient, and carbohydrate and lipid oxidation rates. Whole-body carbohydrate and fat-oxidation rates were calculated from each period of gas collection and estimated by using stoichiometric equations (14). Heart rate was measured continuously by electrocardiogram (Cardioscreen; Medis GmbH, Ilmenau, Germany). Beat-by-beat blood pressure (Finapres; Ohmeda, Englewood, CO) and brachial arterial blood pressure (Dinamap; Critikon, Tampa, FL) were determined.
Microdialysis
Details of the microdialysis technique have been described previously (15, 16). Briefly, before insertion of the probes, we applied a local anesthetic (lidocaine) as either a cream for adipose tissue (EMLA; Astra GmbH, Wedel, Germany) or a sc injection for muscle (1% Xylocitin; Jenapharm GmbH, Jena, Germany). After probe insertion, we started the tissue perfusion with lactate-free Ringer’s solution (Serumwerk Bernburg AG, Bernburg, Germany) at a flow rate of 2 µl/min. The solution was supplemented with 50 mmol/liter ethanol (B. Braun Melsungen AG, Melsungen, Germany) for blood-flow determinations. CMA/60 microdialysis catheters and CMA/102 microdialysis pumps (both from CMA Microdialysis AB, Solna, Sweden) were used. A 60-min period was allowed for tissue recovery and for baseline calibration before ANP infusion. Two 15-min dialysate fractions were collected at baseline.
Analytical methods
ANP concentrations were determined using a RIA (Peninsula Laboratories, San Carlos, CA), and venous glycerol concentrations were determined with an ultrasensitive radiometric method (17). Venous NEFAs were assayed with an enzymatic method (Wako kit; Unipath, Dardilly, France). Catecholamines were collected in EGTA tubes (Kabevette; Kabe Labortechnik GmbH, Nümbrecht-Elsenroth, Germany) and processed immediately in a refrigerated centrifuge. The plasma was stored at –80 C until analysis. Plasma epinephrine and norepinephrine were assayed by HPLC with electrochemical (amperometric) detection. The detection limit was 5 pg/sample, and day-to-day and intraassay variability was 4 and 3%, respectively. Ethanol concentrations in perfusate (inflow) and dialysate (outflow) were measured with a standard enzymatic assay (18). Dialysate glucose, lactate, pyruvate, and glycerol concentrations were measured with a CMA/600 analyzer (CMA Microdialysis AB).
Calculations and statistics
Changes in blood flow were determined by using the ethanol-dilution technique, which is based on Fick’s principle (19, 20). Accordingly, a decrease in the outflow to inflow ratio is equivalent to an increase in blood flow and vice versa. For simplicity, the term "ethanol ratio" is substituted for the term "ethanol outflow to inflow ratio." Changes in glycerol were used to assess changes in lipolysis and/or lipid mobilization, and changes in glucose, lactate, and pyruvate were used to assess changes in carbohydrate metabolism (21, 22). In situ recovery for glycerol, glucose, lactate, and pyruvate in the dialysate was assessed by near-equilibrium dialysis (23). For all four metabolites, we found recoveries of about 30% in adipose tissue and 50% in skeletal muscle. All data are expressed as mean ± SEM. Repeated-measures ANOVA testing was used for multiple comparisons. Dunnett’s post hoc test was performed, when P < 0.05. Dose-response relationships were also analyzed by a post hoc test for the linear trend of the means. The 95% confidence interval (CI) for the difference between baseline and ANP infusion is reported for selected measurements. Linear regression analysis was performed to relate plasma ANP concentrations to metabolites. A value of P < 0.05 was considered significant.
|
Results |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Systolic blood pressure decreased dose dependently from 116 ± 3 mm Hg at baseline to 110 ± 3 mm Hg at the highest ANP infusion rate (P < 0.05). Diastolic blood pressure was 62 ± 2 mm Hg at baseline and did not change significantly with ANP infusion. Heart rate increased from 58 ± 2 beats per minute at baseline to 69 ± 4 beats per minute at the highest ANP dose (P < 0.001).
Venous measurements
At baseline, serum ANP concentration was 42 ± 3.8 pg/ml. Maximal plasma ANP concentration was 122 ± 13 pg/ml at an infusion rate of 6.25 ng/kg·min, 252 ± 30 pg/ml at an infusion rate of 12.5 ng/kg·min, and 491 ± 26 pg/ml at an infusion rate of 25 ng/kg·min ANP infusion (95% CI; 381–525 pg/ml; P < 0.001; P < 0.0001 for linear trend) (Fig. 1
, top left). Venous NEFA concentration was 8 ± 1 mg/dl (295 ± 31 µmol/liter) at baseline, with a concentration-dependent increase to 18 ± 2 mg/dl (654 ± 64 µmol/liter) after 45 min at an infusion rate of 25 ng/kg·min (95% CI; 209–442 µmol/liter; P < 0.001; P < 0.0001 for linear trend) (Fig. 1, top right). Venous glycerol concentration increased dose dependently from 0.43 ± 0.03 mg/dl (48 ± 3.3 µmol/liter) at baseline to 0.83 ± 0.09 mg/dl (92 ± 10 µmol/liter) at the highest ANP infusion rate (95% CI; 18–48 µmol/liter; P < 0.0001; P < 0.0001 for linear trend) (Fig. 1, bottom left). Venous triglyceride concentrations increased from 87 ± 15 mg/dl (0.98 ± 0.17 mmol/liter) at baseline to 101 ± 18 mg/dl (1.14 ± 0.20 mmol/liter) at the highest ANP infusion rate (P < 0.001) (Fig. 1, bottom right). Venous glucose concentration was 85 ± 2.2 mg/dl (4.7 ± 0.12 mmol/liter) at baseline and increased to 94 ± 2.3 mg/dl (5.2 ± 0.13 mmol/liter) at the highest infusion rate (95% CI; 0.28–0.73 mmol/liter; P < 0.0001; P < 0.0001 for linear trend). Norepinephrine was 365 ± 19 pg/ml (2.16 ± 0.11 nmol/liter) at baseline and 402 ± 18 pg/ml (2.38 ± 0.11 nmol/liter) at an ANP infusion rate of 25 ng/kg·min (not significant). Epinephrine was 53 ± 3 pg/ml (290 ± 16 pmol/liter) at baseline and 58 ± 5 pg/ml (320 ± 27 pmol/liter) at the highest ANP infusion rate (not significant).
|
In sc adipose tissue, ethanol ratio was 0.52 ± 0.04 at baseline and decreased to 0.45 ± 0.04 after 45 min at 25 ng/kg·min (P < 0.0001). A decrease in the ethanol ratio indicates an increase in sc blood flow (Fig. 2, top left). Dialysate glucose concentration in adipose tissue was 17.1 ± 3.1 mg/dl (0.95 ± 0.17 mmol/liter) at baseline and increased to 19.5 ± 3.4 mg/dl (1.08 ± 0.19 mmol/liter) after 45 min ANP infusion at a rate 25ng/kg·min (P < 0.01) (Fig. 2, top right). Lactate concentrations increased from 3.1 ± 0.63 mg/dl (0.34 ± 0.07 mmol/liter) at baseline to 4.0 ± 0.72 mg/dl (0.44 ± 0.08 mmol/liter) at the highest infusion rate (P < 0.001) (Fig. 2, bottom left). Dialysate glycerol in adipose tissue increased from 0.48 ± 0.05 mg/dl (53 ± 6 µmol/liter) at baseline to 0.78 ± 0.12 mg/dl (87 ± 13 µmol/liter) at the highest ANP infusion rate (P < 0.001) (Fig. 2, bottom right).
|
, top left) slightly increased at the highest infusion rate (P < 0.01), and dialysate glucose concentration (Fig. 2, top right) did not change during ANP infusion. Dialysate lactate concentrations increased from 9.6 ± 0.81 mg/dl (1.07 ± 0.09 mmol/liter) at baseline to 12.6 ± 0.9 mg/dl (1.40 ± 0.10 mmol/liter) at the highest ANP infusion rate (P < 0.001) (Fig. 2, bottom left). Dialysate glycerol concentrations tended to decrease during ANP infusion (P < 0.05) (Fig. 2, bottom right). Dialysate pyruvate concentration increased substantially from 0.17 ± 0.04 mg/dl (0.019 ± 0.004 mmol/liter) at baseline to 0.46 ± 0.06 mg/dl (0.052 ± 0.007 mmol/liter) (P < 0.001) (Fig. 3, top). Therefore, the lactate to pyruvate ratio decreased from 91 ± 23 at baseline to 32 ± 4 at the highest ANP infusion rate (P < 0.001) (Fig. 3, bottom).
|
We plotted venous plasma glycerol concentrations, venous NEFA concentrations, and dialysate glycerol concentrations against serum ANP concentrations (Fig. 4). Venous glycerol and NEFA concentrations as well as dialysate glycerol in adipose tissue were highly correlated with serum ANP concentrations. In contrast, dialysate glycerol in skeletal muscle was not related to serum ANP levels.
|
Resting energy expenditure did not change during ANP infusion (Fig. 5, top left). The respiratory quotient tended to increase at an ANP infusion rate of 6.25 ng/kg·min but started to decrease as infusion rate was further increased (Fig. 5, top right). Accordingly, carbohydrate oxidation was 5.1 ± 0.5 g/h at baseline, 6.7 ± 0.7 g/h at an ANP infusion rate of 6.25 ng/kg·min, 4.2 ± 0.8 g/6 h at an ANP infusion rate of 12.5 ng/kg·min, and 3.4 ± 0.6 g/h at an ANP infusion rate of 25 ng/kg·min (P < 0.01) (Fig. 5, bottom left). Lipid oxidation was 5.1 ± 0.4 g/h at baseline, 4.2 ± 0.5 g/h at an ANP infusion rate of 6.25 ng/kg·min, 5.4 ± 0.5 g/h at an ANP infusion rate of 12.5 ng/kg·min, and 5.9 ± 0.4 g/h at an ANP infusion rate of 25 ng/kg·min (P < 0.05) (Fig. 5, bottom right).
|
|
Discussion |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Systemic ANP infusion led to a concentration-dependent increase in venous glycerol and NEFA concentrations. The observation is consistent with increased lipolysis. Our microdialysis data suggest that ANP influences lipolysis in a tissue-dependent manner because we did not observe changes in dialysate glycerol in skeletal muscle. In adipose tissue, dialysate glycerol concentrations increased sharply. In contrast, ß-adrenoreceptor stimulation with isoproterenol stimulates lipolysis in both tissues (24, 25). The recovery of the microdialysis probe in adipose tissue was approximately 30%. Interstitial glycerol concentrations are approximately 3-fold greater than the measured dialysate concentrations. Thus, interstitial glycerol concentrations in adipose tissue substantially exceeded venous concentrations during ANP infusion. All of these findings and observations from previous studies (9, 11, 26) suggest that ANP-mediated lipid mobilization originates at least in part from an increased sc adipose tissue lipolysis.
ANP-induced increase in lipolysis could be mediated through a direct effect on natriuretic peptide receptors in adipose tissue (8, 9, 10, 11). An interaction of ANP with other regulatory systems may also be involved. Insulin potently inhibits lipolysis (27). In a previous study, ANP infusions increased circulating insulin concentrations (12), an effect that should inhibit lipolysis. Putative changes in insulin release cannot explain the ANP-mediated lipolysis. Adrenergic stimulation is well known to increase lipolysis. We measured venous catecholamine concentrations during ANP infusion. The changes in norepinephrine and epinephrine plasma concentrations were not sufficient to explain the increase in lipolysis that we observed. Moreover, locally applied ß-adrenergic blockade did not inhibit ANP-induced lipid mobilization (11). In previous studies, cortisol and growth hormone were not affected by ANP infusion (28). Direct stimulation of natriuretic peptide receptors appears to be the predominate mechanism by which systemic ANP infusion stimulates lipolysis (9, 10, 11, 26). We cannot exclude completely the possibility that other pathways are also involved.
Once NEFAs are mobilized through lipolysis, they can be re-esterified and stored or they can be oxidized. If an increase in lipolysis is perfectly compensated by an increase in NEFA re-esterification and oxidation, circulating NEFA concentrations should not change. Lipid oxidation rate and venous triglyceride concentrations tended to increase at higher ANP infusion rates. The triglyceride increase may suggest an increase in NEFA re-esterification. Nevertheless, venous NEFA concentrations increased markedly. NEFA concentrations also increased in previous studies that used pharmacological ANP doses (11, 29). The observation suggests that a mismatch exists between ANP-induced lipid mobilization and lipid utilization. Although an increment of lipid oxidation was observed, the resting muscles are not capable to increase lipid oxidation sufficiently in front of the strong lipid mobilization initiated by ANP.
In addition to marked changes in lipid metabolism, we observed consistent changes in glucose utilization with ANP infusion. Glucose oxidation was slightly increased at a low ANP infusion rate but decreased as ANP infusion rates were increased further. Lipid oxidation was slightly decreased at a low ANP infusion rate and increased at higher ANP infusion rates. A similar pattern of substrate use is observed during endurance exercise. Initially, carbohydrate oxidation predominates. With prolonged exercise, lipid oxidation is increased (30). ANP increases during exercise (26, 31). Exercise-induced ANP release is augmented during systemic ß-adrenoreceptor blockade (26, 31). We speculate that ANP might contribute to the switch between lipid and carbohydrate oxidation. Microdialysate lactate concentrations increased in both adipose tissue and skeletal muscle. However, the lactate response in skeletal muscle was associated with a marked decrease in the lactate to pyruvate ratio. These findings indicate that ANP might increase the efficiency of glycolysis because a decrease in lactate to pyruvate ratio reflects a shift from a more anaerobic to a more aerobic glycolysis. In the rat liver, ANP attenuated glycolysis and increased gluconeogenesis (32). Gluconeogenesis requires sufficient lipid oxidation. The ANP-induced increase in lipid oxidation might facilitate a secondary increase in hepatic gluconeogenesis. Additional studies are needed to address the exact mechanisms by which ANP changes carbohydrate metabolism in humans.
A potential limitation of our study is that we used an open design without a control intervention. However, the convincing dose-response relationships in our study as well as data from previous studies on ANP-mediated lipolysis suggest that our findings are not explained by a bias introduced by the open design. Therefore, we conclude that ANP within a concentration range observed in humans increases lipid mobilization from adipose tissue, which results in an increase in circulating NEFA. The response is associated with changes in carbohydrate metabolism and in the balance between carbohydrate and lipid oxidation rates. The dose response for lipid mobilization was not the same as that for the increase in lipid oxidation and the decrease in carbohydrate oxidation. It is possible that these ANP-induced metabolic alterations are mediated by different mechanisms. Our findings may have important clinical implications. Increased endogenous ANP concentrations in congestive heart failure may also promote lipid mobilization. NEFA concentrations and lipid oxidation are elevated in congestive heart failure (33). Increased ANP-mediated lipid mobilization could contribute to the loss of fat stores in patients with cardiac cachexia. Our findings do not explain the muscle wasting in cachectic patients. Furthermore, ANP-related accumulation of NEFA may contribute to the insulin resistance observed in severe congestive heart failure (34). All of these responses may be further exacerbated by medications that stimulate natriuretic peptide receptors, such as nesiritide (6). Drugs that interfere with the natriuretic peptidergic system could cause metabolic changes similar to those we encountered. We suggest that such drugs should be evaluated for their metabolic side effects.
|
Footnotes |
|---|
First Published Online March 1, 2005
Abbreviations: ANP, Atrial natriuretic peptide; CI, confidence interval; HSL, hormone-sensitive lipase; NEFA, nonesterified fatty acid; NPr, natriuretic peptide receptor.
Received October 4, 2004.
Accepted February 22, 2005.
|
References |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
(1)-adrenoreceptor stimulation in human white adipose tissue. Obes Res 10:555–558[Medline]
This article has been cited by other articles:
 |
|
 |
|
  C. Moro, M. Pasarica, K. Elkind-Hirsch, and L. M. Redman Aerobic Exercise Training Improves Atrial Natriuretic Peptide and Catecholamine-Mediated Lipolysis in Obese Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., July 1, 2009; 94(7): 2579 - 2586. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. de Glisezinski, D. Larrouy, M. Bajzova, K. Koppo, J. Polak, M. Berlan, J. Bulow, D. Langin, M. A. Marques, F. Crampes, et al. Adrenaline but not noradrenaline is a determinant of exercise-induced lipid mobilization in human subcutaneous adipose tissue J. Physiol., July 1, 2009; 587(13): 3393 - 3404. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Kita, H. Nishizawa, Y. Okuno, M. Tanaka, A. Yasui, M. Matsuda, Y. Yamada, and I. Shimomura Competitive binding of musclin to natriuretic peptide receptor 3 with atrial natriuretic peptide J. Endocrinol., May 1, 2009; 201(2): 287 - 295. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. L. Birkenfeld, P. Budziarek, M. Boschmann, C. Moro, F. Adams, G. Franke, M. Berlan, M. A. Marques, F. C.G.J. Sweep, F. C. Luft, et al. Atrial Natriuretic Peptide Induces Postprandial Lipid Oxidation in Humans Diabetes, December 1, 2008; 57(12): 3199 - 3204. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Moro, F. Pillard, I. de Glisezinski, E. Klimcakova, F. Crampes, C. Thalamas, I. Harant, M.-A. Marques, M. Lafontan, and M. Berlan Exercise-induced lipid mobilization in subcutaneous adipose tissue is mainly related to natriuretic peptides in overweight men Am J Physiol Endocrinol Metab, August 1, 2008; 295(2): E505 - E513. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Pilz, H. Scharnagl, B. Tiran, B. Wellnitz, U. Seelhorst, B. O. Boehm, and W. Marz Elevated plasma free fatty acids predict sudden cardiac death: a 6.85-year follow-up of 3315 patients after coronary angiography Eur. Heart J., November 2, 2007; 28(22): 2763 - 2769. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Moro, F. Pillard, I. de Glisezinski, F. Crampes, C. Thalamas, I. Harant, M.-A. Marques, M. Lafontan, and M. Berlan Atrial natriuretic peptide contribution to lipid mobilization and utilization during head-down bed rest in humans Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2007; 293(2): R612 - R617. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. J. Wang, M. G. Larson, M. J. Keyes, D. Levy, E. J. Benjamin, and R. S. Vasan Association of Plasma Natriuretic Peptide Levels With Metabolic Risk Factors in Ambulatory Individuals Circulation, March 20, 2007; 115(11): 1345 - 1353. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. L. Birkenfeld, M. Boschmann, C. Moro, F. Adams, K. Heusser, J. Tank, A. Diedrich, C. Schroeder, G. Franke, M. Berlan, et al. {beta}-Adrenergic and Atrial Natriuretic Peptide Interactions on Human Cardiovascular and Metabolic Regulation J. Clin. Endocrinol. Metab., December 1, 2006; 91(12): 5069 - 5075. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Engeli, M. Boschmann, P. Frings, L. Beck, J. Janke, J. Titze, F. C. Luft, M. Heer, and J. Jordan Influence of Salt Intake on Renin-Angiotensin and Natriuretic Peptide System Genes in Human Adipose Tissue Hypertension, December 1, 2006; 48(6): 1103 - 1108. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Pilz, H. Scharnagl, B. Tiran, U. Seelhorst, B. Wellnitz, B. O. Boehm, J. R. Schaefer, and W. Marz Free Fatty Acids Are Independently Associated with All-Cause and Cardiovascular Mortality in Subjects with Coronary Artery Disease J. Clin. Endocrinol. Metab., July 1, 2006; 91(7): 2542 - 2547. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Moro, J. Polak, J. Hejnova, E. Klimcakova, F. Crampes, V. Stich, M. Lafontan, and M. Berlan Atrial natriuretic peptide stimulates lipid mobilization during repeated bouts of endurance exercise Am J Physiol Endocrinol Metab, May 1, 2006; 290(5): E864 - E869. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Nishikimi, N. Maeda, and H. Matsuoka The role of natriuretic peptides in cardioprotection Cardiovasc Res, February 1, 2006; 69(2): 318 - 328. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Lafontan, C. Moro, C. Sengenes, J. Galitzky, F. Crampes, and M. Berlan An Unsuspected Metabolic Role for Atrial Natriuretic Peptides: The Control of Lipolysis, Lipid Mobilization, and Systemic Nonesterified Fatty Acids Levels in Humans Arterioscler Thromb Vasc Biol, October 1, 2005; 25(10): 2032 - 2042. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
