Zobrazeno 1 - 10
of 20
pro vyhledávání: '"Joan J. Guinovart"'
Publikováno v:
The Journal of Biological Chemistry
Hepatic glycogen metabolism is impaired in diabetes. We previously demonstrated that strategies to increase liver glycogen content in a high-fat-diet mouse model of obesity and insulin resistance led to a reduction in food intake and ameliorated obes
Autor:
Felipe Slebe, Mar García-Rocha, Rosa Gasa, Jordi Duran, Ramon Gomis, Joan J. Guinovart, Joan Mir-Coll
Publikováno v:
Diabetologia. 59:1012-1020
Glycogen accumulation occurs in beta cells of diabetic patients and has been proposed to partly mediate glucotoxicity-induced beta cell dysfunction. However, the role of glycogen metabolism in beta cell function and its contribution to diabetes patho
Autor:
Ainhoa Garcia, Sandra A. Rebuffat, Delia Zafra, Deborah J. Burks, Rosa Gasa, Susana G. Kalko, Joana Moitinho Oliveira, Joan J. Guinovart, Ramon Gomis
Publikováno v:
AJP-Endocrinology and Metabolism
AJP-Endocrinology and Metabolism, American Physiological Society, 2014, 306 (1), pp.E36-E47. ⟨10.1152/ajpendo.00409.2013⟩
AJP-Endocrinology and Metabolism, American Physiological Society, 2014, 306 (1), pp.E36-E47. ⟨10.1152/ajpendo.00409.2013⟩
Pancreatic β-cells play a central role in type 2 diabetes (T2D) development, which is characterized by the progressive decline of the functional β-cell mass that is associated mainly with increased β-cell apoptosis. Thus, understanding how to enha
Autor:
J.P. Pontigo, Juan C. Slebe, Ilona I. Concha, Romina Bertinat, Rody San Martín, Moisés Pérez, Alejandro J. Yáñez, Joan J. Guinovart
Publikováno v:
JOURNAL OF CELLULAR BIOCHEMISTRY
Artículos CONICYT
CONICYT Chile
instacron:CONICYT
MOLECULAR AND CELLULAR BIOCHEMISTRY
Artículos CONICYT
CONICYT Chile
instacron:CONICYT
MOLECULAR AND CELLULAR BIOCHEMISTRY
Using a streptozotocin-induced type 1 diabetic rat model, we analyzed and separated the effects of hyperglycemia and hyperinsulinemia over the in vivo expression and subcellular localization of hepatic fructose 1,6-bisphosphatase (FBPase) in the mult
Publikováno v:
Diabetologia. 54:2639-2648
Glycogen deposition is impaired in diabetes, thus contributing to the development of hyperglycaemia. Several glucose-lowering strategies have attempted to increase liver glycogen deposition by modulating targets, which eventually trigger the activati
Autor:
Joan Ballester, Teresa Rigau, Jorge Domínguez, Joan E. Rodríguez-Gil, Meritxell Sensat, Joan J. Guinovart, M. Carmen Muñoz
Publikováno v:
Journal of Andrology. 26:706-715
Oral administration of sodium tungstate to adult male streptozotocin-diabetic rats for 3 months normalized serum levels of glucose, insulin, luteinizing hormone, and follicle-stimulating hormone. These effects were accompanied by an increase in repro
Autor:
Delia Zafra, Joan J. Guinovart, Ciro Mercurio, Rosario Perona, Albert Barberà, Isabel Sánchez-Pérez, Jorge Domínguez, Martine Caron, Mª Carmen Muñoz, Susanna Baqué, Ramon Gomis
Publikováno v:
Digital.CSIC. Repositorio Institucional del CSIC
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Sodium tungstate is a powerful antidiabetic agent when administered orally. In primary cultured hepatocytes, tungstate showed insulin-like actions, which led to an increase in glycogen synthesis and accumulation. However, this compound did not signif
Publikováno v:
Diabetologia. 40:143-149
The effects of oral administration of tungstate to an animal model of non-insulin-dependent diabetes mellitus (NIDDM), the neonatally streptozotocin-induced diabetic rat was studied. Islet insulin content and beta-cell mass were lowered in these anim
Publikováno v:
Biochemical Journal. 304:449-453
The ability of amylin to impair hepatic insulin action is controversial. We have found that the effect of amylin in primary cultured hepatocytes is strongly dependent on the culture conditions. Only in hepatocytes preincubated in the presence of feta
Autor:
Helena Corominola, Joan J. Guinovart, Alberto Gómez-Ramos, Ramon Gomis, Jesús Avila, Delia Zafra, Jorge Domínguez
Publikováno v:
Digital.CSIC. Repositorio Institucional del CSIC
instname
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Tungstate treatment increases the phosphorylation of glycogen synthase kinase-3β (GSK3β) at serine 9, which triggers its inactivation both in cultured neural cells and in vivo. GSK3 phosphorylation is dependent on the activation of extracellular si
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ba40704a2f7aabe449156e1464dcc6b5
http://hdl.handle.net/10261/252378
http://hdl.handle.net/10261/252378