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J Sports Sci ; 38(1): 6-12, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31603027


This study aimed to examine the characteristics of electromyography (EMG) and kinematics of the supporting leg affecting energy cost while running at incline, level, and decline slopes. Twelve male Japanese middle- and long-distance runners volunteered for this study. The subjects were asked to run at 13.5 km·h-1 on a treadmill under three slope conditions. Sagittal plane kinematics and the EMG of the lower limb muscles, respiratory gases were recorded. Energy cost differed significantly between slopes, being the lowest in decline slope and the greatest in incline slope. Integrated EMG (iEMG) of leg extensor muscles was greater in the incline slope than in the decline slope, and iEMG of the gastrocnemius and soleus muscles correlated positively with energy cost. The knee and ankle joint kinematics were associated with energy cost during running. In incline slope, the knee and ankle joints were more extended (plantarflexed) to lift the body. These movements may disturb the coordination between the ankle and knee joints. The gastrocnemius muscle would do greater mechanical work to plantarflex the ankle joint rather than transfer mechanical energy as well as greater mechanical work of mono-articular muscles. These muscular activities would increase energy cost.

Metabolismo Energético/fisiologia , Extremidade Inferior/fisiologia , Corrida/fisiologia , Articulação do Tornozelo/fisiologia , Fenômenos Biomecânicos , Eletromiografia , Teste de Esforço/métodos , Articulação do Quadril/fisiologia , Humanos , Articulação do Joelho/fisiologia , Masculino , Movimento/fisiologia , Músculo Esquelético/fisiologia , Troca Gasosa Pulmonar/fisiologia , Adulto Jovem
Biol Open ; 8(5)2019 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-31023717


Non-alcoholic steatohepatitis (NASH) is a fast-growing liver disease in the Western world. Currently, only a few animal models show both the metabolic and histological features of human NASH. We aimed to explore murine NASH models in a time dependent manner that exhibit metabolic, histological and transcriptomic hallmarks of human NASH. For this, the murine strains C57BL/6J, ob/ob, and KK-Ay were used and three types of nutritional regimes were administered: normal chow diet (NCD); high-fat, high-fructose, and high-cholesterol diet (fast food diet; FFD); or choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD), for 2, 4, 8, 12, 18, 24, and 30 weeks. All strains under the FFD and CDAHFD regimes developed steatohepatitis. Among the strains treated with FFD, the non-alcoholic fatty liver disease (NAFLD) activity score, fibrosis progression and metabolic abnormalities such as hyperinsulinemia and obesity were more pronounced in ob/ob mice than in C57BL/6J and KK-Ay mice. In ob/ob mice fed FFD, the development of hepatic crown-like structures was confirmed. Furthermore, molecular pathways involved in steatohepatitis and fibrosis showed significant changes from as early as 2 weeks of starting the FFD regime. Ob/ob mice fed FFD showed metabolic, histological, and transcriptomic dysfunctions similar to human NASH, suggesting their potential as an experimental model to discover novel drugs for NASH.

Biochim Biophys Acta ; 1636(1): 69-76, 2004 Feb 27.
Artigo em Inglês | MEDLINE | ID: mdl-14984740


The effect of inhibition of acylCoA: cholesterol acyltransferase (ACAT) was studied on high density lipoprotein (HDL) metabolism. An inhibitor of ACAT, MCC-147, was given mouse peritoneal macrophages and expression of ATP-binding cassette transporter A1 (ABCA1) was examined. ABCA1 was increased both at the mRNA and protein levels, only when the cells are cholesterol-loaded and thereby the inhibitor decreased esterified cholesterol and increased unesterified cholesterol. In this condition, the ACAT inhibitor increased reversible binding of apoA-I to the cells and enhanced apoA-I-mediated release of cellular cholesterol and phospholipid, but did not influence nonspecific cellular cholesterol efflux to lipid microemulsion. It was therefore concluded that the ACAT inhibitor increased the release of cholesterol from the cholesterol-loaded macrophages by increasing the expression of ABCA1, putatively through shifting cholesterol distribution from the esterified to the free compartments.

Transportadores de Cassetes de Ligação de ATP/metabolismo , Apolipoproteína A-I/metabolismo , HDL-Colesterol/metabolismo , Inibidores Enzimáticos/farmacologia , Imidazóis/farmacologia , Macrófagos Peritoneais/metabolismo , Esterol O-Aciltransferase/metabolismo , Ureia/farmacologia , Transportadores de Cassetes de Ligação de ATP/biossíntese , Animais , Macrófagos Peritoneais/efeitos dos fármacos , Macrófagos Peritoneais/enzimologia , Camundongos , Esterol O-Aciltransferase/antagonistas & inibidores , Esterol O-Aciltransferase/biossíntese , Ureia/análogos & derivados