Zobrazeno 1 - 10
of 13
pro vyhledávání: '"Joseph G. Yu"'
Autor:
Justin Chapman, Philip D Miles, Jachelle M Ofrecio, Jaap G Neels, Joseph G Yu, Jamie L Resnik, Jason Wilkes, Saswata Talukdar, Divya Thapar, Kristen Johnson, Dorothy D Sears
Publikováno v:
PLoS ONE, Vol 5, Iss 11, p e13959 (2010)
Insulin resistance is manifested in muscle, adipose tissue, and liver and is associated with adipose tissue inflammation. The cellular components and mechanisms that regulate the onset of diet-induced insulin resistance are not clearly defined.We ini
Externí odkaz:
https://doaj.org/article/2364fd2af7e345e5bf026503469ef354
Publikováno v:
Diabetes. 54:2351-2359
Insulin resistance is predominantly characterized by decreased insulin-stimulated glucose uptake into skeletal muscle. In the current study, we have assessed various aspects of the phosphatidylinositol (PI) 3-kinase pathway in skeletal muscle biopsie
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ae06b20426fbd60583404d9a63a5a8b6
https://doi.org/10.2337/diabetes.54.8.2351
https://doi.org/10.2337/diabetes.54.8.2351
Publikováno v:
Diabetes. 49:633-639
Low plasma fibrinolytic activity in association with increased plasma plasminogen activator inhibitor 1 (PAI-1) levels has been linked to an increased risk of atherosclerosis in obesity and type 2 diabetes. We tested the hypothesis that troglitazone,
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fc9e7618c5c3f5de3416714edd65cb46
https://doi.org/10.2337/diabetes.49.4.633
https://doi.org/10.2337/diabetes.49.4.633
Publikováno v:
Diabetes Care. 23:64-69
OBJECTIVE: To characterize metabolic effects of troglitazone in type 2 diabetic, obese, and lean subjects, and examine the effects of troglitazone 2-3 weeks after discontinuation. RESEARCH DESIGN AND METHODS: Nine type 2 diabetic, nine obese, and nin
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f3cbd983fc64a6da5f14c7e303340059
https://doi.org/10.2337/diacare.23.1.64
https://doi.org/10.2337/diacare.23.1.64
Publikováno v:
Diabetes. 47:1107-1113
Impaired muscle glucose phosphorylation to glucose-6-phosphate by hexokinases (HKs)-I and -II may contribute to insulin resistance in NIDDM and obesity. HK-II expression is regulated by insulin. We tested the hypothesis that basal and insulin-stimula
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::df9883c0c27b57ec3423349adf30e9e4
https://doi.org/10.2337/diabetes.47.7.1107
https://doi.org/10.2337/diabetes.47.7.1107
Publikováno v:
Diabetes. 46:1586-1593
Impaired suppression of plasma nonesterified fatty acids (NEFAs) after glucose ingestion may contribute to glucose intolerance, but the mechanisms are unclear. Evidence that insulin inhibits hepatic glucose output (HGO), in part by suppressing plasma
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ad6835232ddc7a7bdb52e7102f3a9a2b
https://doi.org/10.2337/diacare.46.10.1586
https://doi.org/10.2337/diacare.46.10.1586
Autor:
Jamie L. Resnik, Jachelle M. Ofrecio, Jaap G. Neels, Joseph G. Yu, Philip D.G. Miles, Jason J. Wilkes, Saswata Talukdar, Kristen Johnson, Justin Chapman, Divya Thapar, Dorothy D. Sears
Publikováno v:
PLoS ONE
PLoS ONE, Vol 5, Iss 11, p e13959 (2010)
PLoS ONE, Vol 5, Iss 11, p e13959 (2010)
Background Insulin resistance is manifested in muscle, adipose tissue, and liver and is associated with adipose tissue inflammation. The cellular components and mechanisms that regulate the onset of diet-induced insulin resistance are not clearly def
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b6884ed2d7e8af56f4a8599215e9b08c
http://europepmc.org/articles/PMC2980483
http://europepmc.org/articles/PMC2980483
Autor:
Dorothy D. Sears, Joseph G. Yu, Albert Hsiao, Jachelle M. Ofrecio, Shankar Subramaniam, C. H. Courtney, Gene Hsiao, Justin Chapman
Cellular and tissue defects associated with insulin resistance are coincident with transcriptional abnormalities and are improved after insulin sensitization with thiazolidinedione (TZD) PPARγ ligands. We characterized 72 human subjects by relating
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::67e8904003a713260b2310bd24614ce6
https://europepmc.org/articles/PMC2763882/
https://europepmc.org/articles/PMC2763882/
Publikováno v:
Diabetes. 55(8)
Increased accumulation of fatty acids and their derivatives can impair insulin-stimulated glucose disposal by skeletal muscle. To characterize the nature of the defects in lipid metabolism and to evaluate the effects of thiazolidinedione treatment, w
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::138d18903e31541bffec60eac5fc1197
https://pubmed.ncbi.nlm.nih.gov/16873691
https://pubmed.ncbi.nlm.nih.gov/16873691
Autor:
Madhur K. Sinha, Yolanta T. Kruszynska, Jerrold M. Olefsky, Sandrine Javorschi, Andrea L. Hevener, Rodney A. Norman, Joseph G. Yu
Publikováno v:
Diabetes. 51(10)
The insulin-sensitizing effects of thiazolidinediones are thought to be mediated through peroxisome proliferator-activated receptor-γ, a nuclear receptor that is highly abundant in adipose tissue. It has been reported that adipocytes secrete a varie
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5b4ebb5276d00a97be964bfa03120258
https://pubmed.ncbi.nlm.nih.gov/12351435
https://pubmed.ncbi.nlm.nih.gov/12351435