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1.
J Strength Cond Res ; 30(6): 1688-99, 2016 06.
Artículo en Inglés | MEDLINE | ID: mdl-26562712

RESUMEN

This study examined whether the existing duration of type-2 diabetes influenced patient responses to progressive resistance training. Twenty-six women with type-2 diabetes were stratified into short- (3 ± 2 years; n = 12) or long-standing (10 ± 3 years; n = 14) disease groups. Patients participated in a high daily or high weekly frequency elastic band resistance training program that consisted of 2 daily sessions, 5 d·wk for 12 weeks. Glucose control, body composition, and physical function were evaluated pre- and posttraining. No significant diabetes duration × training interactions were detected for blood markers of glucose control (p > 0.05); however, there were significant main effects of training driven by comparable improvements in both cohorts (hemoglobin A1c, -13 to 18%; fasting glucose, -23 to 31%; postprandial glucose, -36 to 40%; insulin, -34 to 40%; C-peptide, -38 to 51%; p ≤ 0.05). Anthropometrics and body composition were also favorably modified in both the groups after training (weight, -5 to 9%; body mass index, -6 to 9%; waist-to-hip ratio, -3 to 5%; percent fat, -14 to 20%; p ≤ 0.05). Likewise, indices of physical function improved in both the groups after training (bicep curl repetitions, +15-33%; sit-and-stand repetitions, +45-47%; p ≤ 0.05). A few exceptions were noted in which patients with long-standing disease demonstrated greater pre-to-post gains (p ≤ 0.05) in grip strength (+11-13%) and peak exercise time (+19%) and load (+21%) during graded exercise, whereas those with shorter disease duration did not. Overall, these data suggest that patients with a long history of diabetes respond positively to resistance training and in a manner comparable to their recently diagnosed counterparts. Therefore, current inactivity in patients with long-standing disease should not deter from beginning an exercise program.


Asunto(s)
Glucemia/metabolismo , Composición Corporal/fisiología , Diabetes Mellitus Tipo 2/terapia , Ejercicio Físico/fisiología , Entrenamiento de Fuerza/métodos , Anciano , Antropometría , Biomarcadores/sangre , Diabetes Mellitus Tipo 2/fisiopatología , Impedancia Eléctrica , Prueba de Esfuerzo , Femenino , Hemodinámica/fisiología , Humanos , Persona de Mediana Edad , Factores de Tiempo
3.
Fish Shellfish Immunol ; 27(2): 360-4, 2009 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-19540346

RESUMEN

Granulocyte-colony stimulating factor (G-CSF) is a cytokine that stimulates the proliferation and differentiation of hematopoietic progenitor cells committed to the neutrophil/granulocyte lineage. Here, we report the two distinct granulocyte colony stimulating factor homologues from black rockfish Sebastes schlegelii. The G-CSF homologue cDNAs were isolated from the black rockfish LPS or Con A/PMA stimulated leukocyte cDNA libraries. The cDNA for the Black rockfish G-CSF-1 homologue predicts a peptide of 202 amino acids that is the closest to the Bastard halibut (Paralichthys olivaceus) G-CSF, whereas the cDNA of the Black rockfish G-CSF-2 homologue predicts a peptide of 212 amino acids that is the closest to the Fugu (Takifugu rubripes). In a healthy fish, the mRNAs of both G-CSF homologues were predominantly expressed in leukocytes, spleen, and gill. Expression of the black rockfish G-CSF-1 homologue was induced in peripheral blood leukocytes (PBLs) after stimulation with LPS, Con A/PMA, or Poly I:C, and G-CSF-2 homologue was strongly induced in PBLs after stimulation with Con A/PMA for 24 h only.


Asunto(s)
Peces/genética , Peces/metabolismo , Factor Estimulante de Colonias de Granulocitos/genética , Factor Estimulante de Colonias de Granulocitos/metabolismo , Adyuvantes Inmunológicos/farmacología , Secuencia de Aminoácidos , Animales , Secuencia de Bases , Clonación Molecular , ADN Complementario/metabolismo , Perfilación de la Expresión Génica , Regulación de la Expresión Génica/efectos de los fármacos , Factor Estimulante de Colonias de Granulocitos/química , Datos de Secuencia Molecular , Filogenia
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