RESUMEN
So far, the relationship between wind and athletics performance has been studied mainly for 100 m sprint, based on simulation of biomechanical models, requiring several assumptions. In this study, this relationship is quantified empirically for all five horizontal jump and sprint events where wind is measured, with freely available competition results. After systematic scraping several elite and sub-elite results sites, the obtained results (n = 150,169) were filtered and matched to athletes. A quadratic mixed effects model with athlete and season as random effects was applied to express the influence of wind velocity on performance in each event. Whether this effect differs with performance level was investigated by applying the model on subgroups based on performance level. In the fitted quadratic model, the linear coefficients were significant (p < .001) for all events; the quadratic coefficients were significant for all events (p < .001) except long jump (p = .138). A 2.0â mâ s-1 tail wind provides an average advantage of 0.125, 0.140 and 0.146-s for the 100, 200 and 100/110 m hurdles, respectively, and an advantage of 0.058 and 0.102 m for long jump and triple jump, respectively. Performance level had a significant effect on the wind influence only for 100 m (p < .001). Amateur athletes (â¼13â s) benefit 69% more from a 2.0â mâ s-1 tail wind than elite athletes (â¼10â s). Practical formulas are presented for each event. These can easily be used correct results for wind speed, allowing better talent scouting and championship selection. This study demonstrates the efficacy of answering scientific questions empirically, through freely available data.
Asunto(s)
Rendimiento Atlético , Atletismo , Viento , Atletas , Humanos , Modelos TeóricosRESUMEN
UniProtKB/Swiss-Prot, a curated protein database, and dictyBase, the Model Organism Database for Dictyostelium discoideum, have established a collaboration to improve data sharing. One of the major steps in this effort was the 'Dicty annotation marathon', a week-long exercise with 30 annotators aimed at achieving a major increase in the number of D. discoideum proteins represented in UniProtKB/Swiss-Prot. The marathon led to the annotation of over 1000 D. discoideum proteins in UniProtKB/Swiss-Prot. Concomitantly, there were a large number of updates in dictyBase concerning gene symbols, protein names and gene models. This exercise demonstrates how UniProtKB/Swiss-Prot can work in very close cooperation with model organism databases and how the annotation of proteins can be accelerated through those collaborations.
RESUMEN
The ob gene product is known to control food intake and energy expenditure. To determine whether thermogenic agents directly control ob gene expression, the effects of beta-adrenoceptor agonists on the level of the ob gene messenger RNA (mRNA) and on leptin secretion have been studied in mouse brown adipocytes differentiated in culture. These cells highly expressed the beta 3-adrenoceptor, the uncoupling protein, and the ob gene mRNAs. The ob gene was expressed in mouse brown adipocytes earlier than in mouse white adipocytes under the same culture conditions and to a similar level. The beta 3-, beta L-, and beta 2-adrenoceptor agonists BRL 37344, dobutamine, and terbutaline inhibited ob gene expression in mouse brown adipocytes differentiated in culture with EC50 values of 0.3, 1.0, and 85 nM, respectively. Leptin secretion by the cells under basal conditions was 78 +/- 10 pg/microgram DNA-4 h and was decreased by exposure to the beta-adrenoceptor agonists. The ob gene mRNA half-life was 9.4 h and was decreased to 2.4 h by 1 nM BRL 37344, indicating that the inhibitory effect of the beta 3-agonist might be due to destabilization of ob gene mRNA. (Bu)2cAMP (10-100 microM) and forskolin (20 microM) mimicked the effect of the beta-adrenoceptor agonists. FFA (150-800 microM) had only a small inhibitory effect on ob gene mRNA expression. The results suggest the existence in brown adipose tissue of a retroregulatory pathway by which leptin production in inhibited when the sympathetic nervous system is stimulated.
Asunto(s)
Adipocitos/metabolismo , Expresión Génica/efectos de los fármacos , Obesidad/genética , Proteínas/metabolismo , ARN Mensajero/metabolismo , Receptores Adrenérgicos beta/fisiología , Adipocitos/citología , Tejido Adiposo Pardo/citología , Tejido Adiposo Pardo/metabolismo , Agonistas Adrenérgicos beta/farmacología , Animales , Bucladesina/farmacología , Diferenciación Celular , Células Cultivadas , Dobutamina/farmacología , Etanolaminas/farmacología , Cinética , Leptina , Ratones , Ratones Endogámicos BALB C , Receptores de Leptina , Terbutalina/farmacologíaRESUMEN
1. The possible existence of a beta 3-adrenoceptor in human brown and white adipose tissues was investigated by mRNA expression and binding studies. 2. The relative amounts of beta 1-, beta 2- and beta 3-adrenoceptor mRNA, as determined by total RNA Northern blot analysis in newborn brown adipose tissue, were 28, 63 and 9% respectively of the total beta-adrenoceptor mRNA. 3. The beta 1/beta 2-adrenoceptors of human brown adipose tissue plasma membranes were characterized using [3H]-CGP 12177 as a ligand. Their Kd and Bmax values were 1.9 nM and 156 fmol mg-1 of membrane proteins, respectively. The beta 3-adrenoceptor was characterized by use of the new specific radioligand [3H]-SB 206606. The binding of this ligand was stereospecifically displaced by the active R,R- or the inactive S,S-enantiomer of BRL 37344 up to a concentration of about 10 microM. The Kd and Bmax values of the brown adipose tissue membrane beta 3-adrenoceptors were 87 nM and 167 fmol mg-1 of proteins, respectively. A low affinity [3H]-CGP 12177 binding site population was also detected in these membranes. 4. In human omental white adipose tissue, no beta 3-adrenoceptor mRNA could be detected in total RNA Northern blots and the beta 1-and beta 2-adrenoceptor mRNAs represented 9 and 91%, respectively of the total beta-adrenoceptor mRNA, and no specific binding of [3H]-SB 206606 could be measured.
Asunto(s)
Tejido Adiposo Pardo/metabolismo , Tejido Adiposo/metabolismo , ARN Mensajero/metabolismo , Receptores Adrenérgicos beta/metabolismo , Agonistas Adrenérgicos beta/metabolismo , Antagonistas Adrenérgicos beta/metabolismo , Adulto , Anciano , Sitios de Unión , Etanolaminas/metabolismo , Femenino , Humanos , Masculino , Persona de Mediana Edad , Propanolaminas/metabolismo , ARN Mensajero/genética , Receptores Adrenérgicos beta/genética , Receptores Adrenérgicos beta 1/genética , Receptores Adrenérgicos beta 1/metabolismo , Receptores Adrenérgicos beta 2/genética , Receptores Adrenérgicos beta 2/metabolismo , Receptores Adrenérgicos beta 3 , EstereoisomerismoRESUMEN
Changes in intracellular calcium concentration [Ca2+]i in response to norepinephrine (NE) and to various adrenergic agonists were monitored by dual excitation microfluorimetry in single human adipocytes differentiated in culture and loaded with fura-2 acetoxymethyl ester (fura-2 AM). The addition of NE elicited increases in [Ca2+]i that were depending on the cell, (1) either rapid (time to peak: 9 +/- 3 s), large, and transient; or (2) slow (time to peak: 125 +/- 8 s), small, and sustained. The rapid and large [Ca+]i response, which was inhibited by 90% by the alpha 1-antagonist prazosin and only by 20% by the non-specific beta antagonist (-)-propranolol, was considered to be mediated by the alpha 1-adrenoceptor. In fact, an alpha 1A-adrenoceptor was found to be expressed in human white adipose tissue. Consecutive additions of beta-agonists specific for each subtype of alpha-adrenoceptor enabled the characterization of four cell populations with different response patterns: 47% of the cells had alpha 1- and beta 1-, beta 2- and beta 3-induced [Ca2+]i responses; 29% had only beta 1-, beta 2-, beta 3-responses; 14% had alpha 1- and beta 3-responses, and 10% had only an alpha 1-response. Taken together, these results show that in differentiated human adipocytes: (1) alpha 1- and beta-adrenergic stimulations induce [Ca2+]i increases with different kinetics and amplitudes; (2) there is a beta 3-adrenergic response similar to the beta 1- or beta 2-adrenergic responses; and (3) there is a marked adrenoceptor heterogeneity.
Asunto(s)
Adipocitos/fisiología , Calcio/análisis , Receptores Adrenérgicos alfa/genética , Receptores Adrenérgicos beta/genética , Adipocitos/química , Adipocitos/citología , Agonistas alfa-Adrenérgicos/farmacología , Agonistas Adrenérgicos beta/farmacología , Secuencia de Bases , Diferenciación Celular/efectos de los fármacos , Diferenciación Celular/fisiología , Células Cultivadas/química , Células Cultivadas/citología , Células Cultivadas/fisiología , Citosol/química , Fura-2 , Heterogeneidad Genética , Humanos , Datos de Secuencia Molecular , Norepinefrina/farmacología , Epiplón/patologíaRESUMEN
The ob gene mRNA expression in rat brown adipose tissue (BAT) and epididymal white adipose tissue (WAT) was measured on Northern blots hybridized with a rat ob gene probe. The level of ob gene mRNA in BAT was about 40% of that in WAT. Fasting (36 h) or semi-starvation (10 days) decreased the ob gene mRNA level in both tissues by 62-68%, and cold exposure at 6 degrees C (24 h) decreased it in BAT (-84%) but not in WAT. Acute administration of the beta 3-adrenergic agonist Ro 16-8714 decreased the ob gene mRNA level in BAT (-51%) and WAT (-28%) of lean Zucker rats and only in BAT (-74%) of obese falfa rats. This study demonstrates that, in the rat, the ob gene is not only expressed in WAT but also in BAT, and suggests that in these two tissues, the modulation of the ob gene expression might be more closely associated with known alterations in cell lipid content than with changes in sympathetic activity.
Asunto(s)
Tejido Adiposo Pardo/metabolismo , Tejido Adiposo/metabolismo , Expresión Génica , Obesidad/genética , Biosíntesis de Proteínas , Animales , Secuencia de Bases , Cartilla de ADN , Epidídimo , Ayuno , Leptina , Masculino , Datos de Secuencia Molecular , Especificidad de Órganos , Reacción en Cadena de la Polimerasa , ARN Mensajero/análisis , ARN Mensajero/biosíntesis , Ratas , Ratas Mutantes , Ratas Sprague-Dawley , InaniciónRESUMEN
The results of this study suggest that the atypical beta-adrenergic receptor (beta 3 subtype) is expressed in human white adipose tissue. A beta 3-adrenergic receptor mRNA could be detected in human omental fat poly(A)+ RNA by polymerase chain reaction amplification with appropriate primers. The expression of the beta 3-adrenergic receptor in human fat was confirmed by Northern blot analysis; however, the level of its mRNA was lower than those of the beta 1- and beta 2-adrenergic receptors. Two populations of ((-)-4-(3-t-butylamino-2-hydroxypropoxy)-[5,7-3H]benzimidazole-2-one) ([3H]CGP 12177)-binding sites were identified in human omental fat membranes, one with a high affinity (Kd = 1.7 nM) and the other with a low affinity (Kd = 22 nM). The low affinity binding site population, which should represent the beta 3-adrenergic receptor, was predominant (75% of the total binding sites).
Asunto(s)
Tejido Adiposo/metabolismo , Receptores Adrenérgicos beta/biosíntesis , Anciano , Secuencia de Bases , Sitios de Unión , Northern Blotting , ADN de Cadena Simple , Humanos , Masculino , Persona de Mediana Edad , Datos de Secuencia Molecular , Epiplón , Reacción en Cadena de la Polimerasa , ARN Mensajero/metabolismo , Receptores Adrenérgicos beta/genéticaRESUMEN
The aim of the study was to examine in the obese Zucker (fa/fa) rats the effect of a peroxisome proliferator nafenopin on liver and brown adipose tissue peroxisomal and mitochondrial beta-oxidation enzyme activities and on the overall energy dissipation. A 17-day nafenopin treatment increased liver wet weight 2.1-fold and liver total acyl-CoA oxidase and mitochondria beta-oxidative activities 32- and 4.6-fold, respectively. It increased the interscapular brown adipose tissue (IBAT) acyl-CoA oxidase activity 2.1-fold but had no effect on the mitochondria beta-oxidative activity. Because nafenopin was found to decrease food intake by 22%, obese nafenopin-treated rats were compared with a group of obese pair-fed rats. Both food restriction and nafenopin treatment decreased body weight gain, but a decrease (14%) in fat content was only observed in nafenopin-treated rats. Food restriction of obese rats decreased the mean metabolic rate by 13%, and nafenopin treatment prevented this decrease. Both food restriction and nafenopin treatment decreased the mean daily respiratory quotient (RQ). However, the RQ of nafenopin-treated rats was steadily lower than that of control, whereas that of food-restricted rats was the same as that of control animals during the feeding period and decreased when food supply was exhausted. The increase in liver and IBAT fatty acid beta-oxidative activities may be the cause of the decreased lipid accretion measured in obese rats.
Asunto(s)
Metabolismo Energético , Microcuerpos/efectos de los fármacos , Nafenopina/farmacología , Obesidad/metabolismo , Tejido Adiposo/patología , Tejido Adiposo Pardo/metabolismo , Tejido Adiposo Pardo/ultraestructura , Animales , Composición Corporal , Metabolismo Energético/efectos de los fármacos , Hígado/metabolismo , Hígado/ultraestructura , Microcuerpos/metabolismo , Microcuerpos/fisiología , Mitocondrias/metabolismo , Obesidad/patología , Oxidación-Reducción , Ratas , Ratas Zucker , Valores de ReferenciaRESUMEN
1. The effect of changes in fatty acid beta-oxidation activity on triglyceride and cholesteryl ester synthesis were studied in cultured smooth muscle cells (SMC) and in a macrophage cell line IC-21 in the presence of oleic acid (100 microM). 2. Etomoxir, an inhibitor of carnitine palmitoyltransferase I, stimulated the incorporation of [2-3H]glycerol into triglycerides in SMC and in macrophages 6.2- and 8.2-fold, respectively, and the incorporation of [4-14C]cholesterol into cholesteryl esters in macrophages 3.5-fold. 3. L-Carnitine, a cofactor of fatty acid beta-oxidation, decreased the incorporation of [2-3H]glycerol into triglycerides in smooth muscle cells by 69% and the incorporation of [4-14C]cholesterol into cholesteryl esters by 52%. L-Carnitine had no effect on the macrophages.
Asunto(s)
Ácidos Grasos/metabolismo , Metabolismo de los Lípidos , Macrófagos/metabolismo , Músculo Liso Vascular/metabolismo , Animales , Carnitina/farmacología , Carnitina O-Palmitoiltransferasa/antagonistas & inhibidores , Línea Celular , Células Cultivadas , Colesterol/metabolismo , Ésteres del Colesterol/biosíntesis , Vasos Coronarios , Compuestos Epoxi/farmacología , Glicerol/metabolismo , Macrófagos/efectos de los fármacos , Músculo Liso Vascular/efectos de los fármacos , Oxidación-Reducción , Porcinos , Triglicéridos/biosíntesisRESUMEN
In cultured pig coronary smooth muscle cells phorbol 12-myristate 13-acetate (PMA) stimulated the conversion of [4-14C]cholesterol into cholesteryl esters and the incorporation of [2-3H]glycerol into triglycerides 6.4- and 4.5-fold, respectively. The maximal effects occurred after 3 h of treatment and there was a return to basal values after 72 h. In the presence of 400 microM oleic acid, PMA stimulated the conversion of [4-14C]cholesterol into cholesteryl esters and that of [2-3H]glycerol into triglycerides 5.3- and 2.3-fold, respectively. The stimulatory effects were more sustained (still significant after 72 h) and their maxima were delayed (peaks after 24 h). PMA was also found to increase 2-fold the amount of triglyceride that accumulated in the cells in the presence of oleic acid after 24 h. In macrophages IC-21, the effects of PMA were observed only in the presence of oleic acid. They consisted of a 1.9-fold stimulation in the conversion of [4-14C]cholesterol into cholesteryl esters after 72 h and of a 1.7-fold stimulation in the incorporation of [2-3H]glycerol into triglycerides after 24 h. PMA also increased the amount of triglyceride that accumulated in the cells 1.9-fold after 72 h. It is concluded that PMA, and possibly growth factors, may promote lipid storage in smooth muscle cells and that fatty acids favor long lasting effects of PMA in smooth muscle cells and are necessary for any effect of PMA in macrophages.
Asunto(s)
Ésteres del Colesterol/biosíntesis , Acetato de Tetradecanoilforbol/farmacología , Triglicéridos/biosíntesis , Animales , Células Cultivadas , Colesterol/metabolismo , Ácidos Grasos no Esterificados/metabolismo , Glicerol/metabolismo , Macrófagos/efectos de los fármacos , Macrófagos/metabolismo , Músculo Liso Vascular/efectos de los fármacos , Músculo Liso Vascular/metabolismo , Ácido Oléico , Ácidos Oléicos/farmacologíaRESUMEN
The induction of hypothyroidism in rats by methimazole affects interscapular brown adipose tissue (IBAT) mitochondrial and peroxisomal enzyme activities in opposite directions. Hypothyroidism, indeed, decreases both mitochondrial succinate dehydrogenase and beta-oxidation total activities by 35 and 45%, respectively and increases peroxisomal catalase and acyl coenzyme A (acyl CoA) oxidase total activities 3.2- and 1.6-fold, respectively. Administration of a thyroid hormone analogue (3'-isopropyl-3,5-diiodo-L-thyronine) prevents these enzymatic modifications. The effects of hypothyroidism on IBAT mitochondrial enzyme activities seem to be direct, i.e. due to the lack of thyroid hormones, while those on peroxisomal enzyme activities might be indirect, i.e. secondary to the increased thermogenic needs of the rat and mediated by adrenergic stimulation. It is noteworthy that the indirect effects of hypothyroidism on peroxisomes are not observed in liver where acyl CoA oxidase activity is in fact decreased by 40%. In hypothyroid rat IBAT, administration of the peroxisome proliferator nafenopin does not further stimulate the already increased peroxisomal enzyme activities and does not inhibit the already decreased mitochondrial enzyme activities.