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1.
Nutr Metab Cardiovasc Dis ; 34(7): 1681-1691, 2024 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-38553359

RESUMEN

BACKGROUND & AIMS: Bariatric surgery is highly effective against obesity. Pre-surgical exercise programs are recommended to prepare the candidate physically and metabolically for surgery-related rapid weight loss. However, the ideal exercise prescription in this population is unknown. This study aimed to compare the metabolic effects of moderate-intensity constant (MICT) vs. a high-intensity interval training (HIIT) program in candidates to undergo bariatric surgery. METHODS AND RESULTS: Twenty-five candidates (22 women) to undergo sleeve gastrectomy aged from 18 to 60 years old were recruited. At baseline, we measured body composition, physical activity levels, grip strength, and aerobic capacity. Further, we assessed metabolic function through glycemia and insulinemia (both fasting and after oral glucose tolerance test (OGTT)), homeostatic model assessment for insulin resistance (HOMA-IR), lipid profile, glycated haemoglobin (HbA1c), transaminases, fibroblast growth factor 21 (FGF21), growth differentiation factor 15 (GDF15), apelin, and adiponectin. Afterward, participants were randomized into MICT (n = 14) or HIIT (n = 11). Both training programs consisted of 10 sessions (2-3 times/week, 30 min per session) distributed during 4 weeks before the surgery. After this, all outcomes were measured again at the end of the training programs and 1 month after the surgery (follow-up). A mixed effect with Tukey's post-hoc analysis was performed to compare values at baseline vs. post-training vs. postsurgical follow-up. Both training programs increased aerobic capacity after training (p < 0.05), but only after MICT these changes were kept at follow-up (p < 0.05). However, only MICT decreased fat mass and increased total muscle mass and physical activity levels (p < 0.05). Metabolically, MICT decreased insulinemia after OGTT (p < 0.05), whereas HIIT increased adiponectin after training and GDF15 at follow-up (both p < 0.05). CONCLUSIONS: Both MICT and HIIT conferred benefits in candidates to undergo bariatric surgery, however, several of those effects were program-specific, suggesting that exercise intensity should be considered when preparing these patients. Future studies should explore the potential benefits of prescribing MICT or HIIT in a customized fashion depending on a pretraining screening, along with possible summatory effects by combining these two exercise programs (MICT + HIIT). CLINICAL TRIAL REGISTRATION: International Traditional Medicine Clinical Trial Registry, N° ISRCTN42273422.


Asunto(s)
Biomarcadores , Glucemia , Gastrectomía , Entrenamiento de Intervalos de Alta Intensidad , Pérdida de Peso , Humanos , Femenino , Masculino , Persona de Mediana Edad , Adulto , Resultado del Tratamiento , Biomarcadores/sangre , Factores de Tiempo , Adulto Joven , Gastrectomía/efectos adversos , Glucemia/metabolismo , Adolescente , Cirugía Bariátrica , Insulina/sangre , Resistencia a la Insulina , Obesidad/cirugía , Obesidad/fisiopatología , Obesidad/sangre
2.
Cell Metab ; 8(5): 384-98, 2008 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-19046570

RESUMEN

The unconventional myosin Myo1c has been implicated in insulin-regulated GLUT4 translocation to the plasma membrane in adipocytes. We show that Myo1c undergoes insulin-dependent phosphorylation at S701. Phosphorylation was accompanied by enhanced 14-3-3 binding and reduced calmodulin binding. Recombinant CaMKII phosphorylated Myo1c in vitro and siRNA knockdown of CaMKIIdelta abolished insulin-dependent Myo1c phosphorylation in vivo. CaMKII activity was increased upon insulin treatment and the CaMKII inhibitors CN21 and KN-62 or the Ca(2+) chelator BAPTA-AM blocked insulin-dependent Myo1c phosphorylation and insulin-stimulated glucose transport in adipocytes. Myo1c ATPase activity was increased after CaMKII phosphorylation in vitro and after insulin stimulation of CHO/IR/IRS-1 cells. Expression of wild-type Myo1c, but not S701A or ATPase dead mutant K111A, rescued the inhibition of GLUT4 translocation by siRNA-mediated Myo1c knockdown. These data suggest that insulin regulates Myo1c function via CaMKII-dependent phosphorylation, and these events play a role in insulin-regulated GLUT4 trafficking in adipocytes likely involving Myo1c motor activity.


Asunto(s)
Adipocitos/metabolismo , Proteína Quinasa Tipo 2 Dependiente de Calcio Calmodulina/fisiología , Transportador de Glucosa de Tipo 4/metabolismo , Insulina/fisiología , Miosinas/metabolismo , 1-(5-Isoquinolinesulfonil)-2-Metilpiperazina/análogos & derivados , 1-(5-Isoquinolinesulfonil)-2-Metilpiperazina/farmacología , Proteínas 14-3-3/metabolismo , Animales , Proteína Quinasa Tipo 2 Dependiente de Calcio Calmodulina/antagonistas & inhibidores , Línea Celular , Cricetinae , Ratones , Miosina Tipo I , Fosforilación , Transporte de Proteínas
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