Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation
Authorized Users Only
2012
Authors
Korićanac, G.Tepavčević, S.
Romić, S.
Živković, M.
Stojiljković, Mojca
Milosavljević, T.
Stanković, A.
Petković, M.
Kamčeva, T.
Žakula, Z.
Article (Published version)
Metadata
Show full item recordAbstract
Fructose rich diet increases hepatic triglycerides production and has deleterious cardiac effects. Estrogens are involved in regulation of lipid metabolism as well, but their effects are cardio beneficial. In order to study effects of fructose rich diet on the main heart fatty acid transporter CD36 and the role of estrogens, we subjected ovariectomized female rats to the standard diet or fructose rich diet, with or without estradiol (E2) replacement. The following parameters were analyzed: feeding behavior, visceral adipose tissue mass, plasma lipids, cardiac CD36 expression, localization and insulin regulation, as well as the profile of cardiac lipids. Results show that fructose rich diet significantly increased plasma triglycerides and decreased plasma free fatty acid (FFA) concentration, while E2 additionally emphasized FFA decrease. The fructose diet increased cardiac plasma membrane content of CD36 in the basal and insulin-stimulated states, and decreased its low density microsome...s content. The E2 in fructose-fed rats raised the total cardiac protein content of CD36, its presence in plasma membranes and low density microsomes, and cardiac deposition of triglycerides, as well. Although E2 counteracts fructose in some aspects of lipid metabolism, and separately they have opposite cardiac effects, in combination with fructose rich diet, E2 additionally enhances CD36 presence in plasma membranes of cardiac cells and triglycerides accumulation, which paradoxically might promote deleterious effects of fructose diet on cardiac lipid metabolism. Taken together, the results presented in this work are of high importance for clinical administration of estrogens in females with a history of type 2 diabetes.
Keywords:
Heart / Fructose / Estradiol / CD36 fatty acid transporter / Cardiac lipidsSource:
European Journal of Pharmacology, 2012, 694, 1-3, 127-134Funding / projects:
- Genetic basis of human vascular and inflammatory diseases (RS-MESTD-Basic Research (BR or ON)-175085)
- Mechanistic studies of the reactions of transition metal ion complexes with biologically relevant molecules (RS-MESTD-Basic Research (BR or ON)-172011)
DOI: 10.1016/j.ejphar.2012.08.007
ISSN: 0014-2999
PubMed: 22960064
WoS: 000310177000017
Scopus: 2-s2.0-84867333702
Collections
Institution/Community
Institut za molekularnu genetiku i genetičko inženjerstvoTY - JOUR AU - Korićanac, G. AU - Tepavčević, S. AU - Romić, S. AU - Živković, M. AU - Stojiljković, Mojca AU - Milosavljević, T. AU - Stanković, A. AU - Petković, M. AU - Kamčeva, T. AU - Žakula, Z. PY - 2012 UR - https://imagine.imgge.bg.ac.rs/handle/123456789/576 AB - Fructose rich diet increases hepatic triglycerides production and has deleterious cardiac effects. Estrogens are involved in regulation of lipid metabolism as well, but their effects are cardio beneficial. In order to study effects of fructose rich diet on the main heart fatty acid transporter CD36 and the role of estrogens, we subjected ovariectomized female rats to the standard diet or fructose rich diet, with or without estradiol (E2) replacement. The following parameters were analyzed: feeding behavior, visceral adipose tissue mass, plasma lipids, cardiac CD36 expression, localization and insulin regulation, as well as the profile of cardiac lipids. Results show that fructose rich diet significantly increased plasma triglycerides and decreased plasma free fatty acid (FFA) concentration, while E2 additionally emphasized FFA decrease. The fructose diet increased cardiac plasma membrane content of CD36 in the basal and insulin-stimulated states, and decreased its low density microsomes content. The E2 in fructose-fed rats raised the total cardiac protein content of CD36, its presence in plasma membranes and low density microsomes, and cardiac deposition of triglycerides, as well. Although E2 counteracts fructose in some aspects of lipid metabolism, and separately they have opposite cardiac effects, in combination with fructose rich diet, E2 additionally enhances CD36 presence in plasma membranes of cardiac cells and triglycerides accumulation, which paradoxically might promote deleterious effects of fructose diet on cardiac lipid metabolism. Taken together, the results presented in this work are of high importance for clinical administration of estrogens in females with a history of type 2 diabetes. T2 - European Journal of Pharmacology T1 - Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation EP - 134 IS - 1-3 SP - 127 VL - 694 DO - 10.1016/j.ejphar.2012.08.007 ER -
@article{ author = "Korićanac, G. and Tepavčević, S. and Romić, S. and Živković, M. and Stojiljković, Mojca and Milosavljević, T. and Stanković, A. and Petković, M. and Kamčeva, T. and Žakula, Z.", year = "2012", abstract = "Fructose rich diet increases hepatic triglycerides production and has deleterious cardiac effects. Estrogens are involved in regulation of lipid metabolism as well, but their effects are cardio beneficial. In order to study effects of fructose rich diet on the main heart fatty acid transporter CD36 and the role of estrogens, we subjected ovariectomized female rats to the standard diet or fructose rich diet, with or without estradiol (E2) replacement. The following parameters were analyzed: feeding behavior, visceral adipose tissue mass, plasma lipids, cardiac CD36 expression, localization and insulin regulation, as well as the profile of cardiac lipids. Results show that fructose rich diet significantly increased plasma triglycerides and decreased plasma free fatty acid (FFA) concentration, while E2 additionally emphasized FFA decrease. The fructose diet increased cardiac plasma membrane content of CD36 in the basal and insulin-stimulated states, and decreased its low density microsomes content. The E2 in fructose-fed rats raised the total cardiac protein content of CD36, its presence in plasma membranes and low density microsomes, and cardiac deposition of triglycerides, as well. Although E2 counteracts fructose in some aspects of lipid metabolism, and separately they have opposite cardiac effects, in combination with fructose rich diet, E2 additionally enhances CD36 presence in plasma membranes of cardiac cells and triglycerides accumulation, which paradoxically might promote deleterious effects of fructose diet on cardiac lipid metabolism. Taken together, the results presented in this work are of high importance for clinical administration of estrogens in females with a history of type 2 diabetes.", journal = "European Journal of Pharmacology", title = "Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation", pages = "134-127", number = "1-3", volume = "694", doi = "10.1016/j.ejphar.2012.08.007" }
Korićanac, G., Tepavčević, S., Romić, S., Živković, M., Stojiljković, M., Milosavljević, T., Stanković, A., Petković, M., Kamčeva, T.,& Žakula, Z.. (2012). Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation. in European Journal of Pharmacology, 694(1-3), 127-134. https://doi.org/10.1016/j.ejphar.2012.08.007
Korićanac G, Tepavčević S, Romić S, Živković M, Stojiljković M, Milosavljević T, Stanković A, Petković M, Kamčeva T, Žakula Z. Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation. in European Journal of Pharmacology. 2012;694(1-3):127-134. doi:10.1016/j.ejphar.2012.08.007 .
Korićanac, G., Tepavčević, S., Romić, S., Živković, M., Stojiljković, Mojca, Milosavljević, T., Stanković, A., Petković, M., Kamčeva, T., Žakula, Z., "Estradiol enhances effects of fructose rich diet on cardiac fatty acid transporter CD36 and triglycerides accumulation" in European Journal of Pharmacology, 694, no. 1-3 (2012):127-134, https://doi.org/10.1016/j.ejphar.2012.08.007 . .