Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol
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Bundalo, Maja M.Živković, Maja
Tepavčević, Snežana
Ćulafić, Tijana
Korićanac, Goran
Stanković, Aleksandra
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The renin-angiotensin system has been implicated in the development of metabolic syndrome and appears to be a key in the local tissue control of normal cardiac functions. Physiological concentrations of estrogens have been shown to be cardioprotective, especially against the damaging effects of fructose-rich diet. The aim of the study was to investigate the expression of the renin-angiotensin system molecules with potentially deleterious effect on the heart (angiotensin-converting enzyme and angiotensin II type 1 receptor) and those with potentially protective effects, (angiotensin-converting enzyme 2 and angiotensin II type 2 receptor), in ovariectomized fructose fed female rats with 17-estradiol replacement. Real-time PCR and Western blot analysis were used for quantification of gene and protein expression in the heart. Fructose diet increased the expression of angiotensin-converting enzyme and angiotensin II type 1 receptor and decreased the expression of angiotensin-converting enzy...me 2 and angiotensin II type 2 receptor. On the other hand, estradiol replacement seems to undo fructose diet effects on cardiac renin-angiotensin system. Downregulation of angiotensin-converting enzyme and angiotensin II type 1 receptor, and reversion of expression of both potentially protective molecules, angiotensin-converting enzyme 2 and angiotensin II type 2 receptor, to the control level in cardiac tissue took place. Obtained results suggest that estradiol may reverse the harmful effect of fructose-rich diet on the expression of renin-angiotensin system molecules. These findings may also be important in further research of phenotypes like insulin resistance, metabolic syndrome, and following cardiovascular pathology in females.
Keywords:
metabolic syndrome / ovariectomy / angiotensin converting enzyme / angiotensin converting enzyme 2 / angiotensin II type 1 receptor / angiotensin II type 2 receptorSource:
Hormone and Metabolic Research, 2015, 47, 7, 521-527Funding / projects:
- Genetic basis of human vascular and inflammatory diseases (RS-MESTD-Basic Research (BR or ON)-175085)
- Role of steroid hormones in neuroendocrine adaptation to stress and pathophysiology of metabolic syndrome - molecular mechanisms and clinical implications (RS-MESTD-Integrated and Interdisciplinary Research (IIR or III)-41009)
DOI: 10.1055/s-0034-1394373
ISSN: 0018-5043; 1439-4286
PubMed: 25369074
WoS: 000355332200009
Scopus: 2-s2.0-84946240884
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VinčaTY - JOUR AU - Bundalo, Maja M. AU - Živković, Maja AU - Tepavčević, Snežana AU - Ćulafić, Tijana AU - Korićanac, Goran AU - Stanković, Aleksandra PY - 2015 UR - https://vinar.vin.bg.ac.rs/handle/123456789/570 AB - The renin-angiotensin system has been implicated in the development of metabolic syndrome and appears to be a key in the local tissue control of normal cardiac functions. Physiological concentrations of estrogens have been shown to be cardioprotective, especially against the damaging effects of fructose-rich diet. The aim of the study was to investigate the expression of the renin-angiotensin system molecules with potentially deleterious effect on the heart (angiotensin-converting enzyme and angiotensin II type 1 receptor) and those with potentially protective effects, (angiotensin-converting enzyme 2 and angiotensin II type 2 receptor), in ovariectomized fructose fed female rats with 17-estradiol replacement. Real-time PCR and Western blot analysis were used for quantification of gene and protein expression in the heart. Fructose diet increased the expression of angiotensin-converting enzyme and angiotensin II type 1 receptor and decreased the expression of angiotensin-converting enzyme 2 and angiotensin II type 2 receptor. On the other hand, estradiol replacement seems to undo fructose diet effects on cardiac renin-angiotensin system. Downregulation of angiotensin-converting enzyme and angiotensin II type 1 receptor, and reversion of expression of both potentially protective molecules, angiotensin-converting enzyme 2 and angiotensin II type 2 receptor, to the control level in cardiac tissue took place. Obtained results suggest that estradiol may reverse the harmful effect of fructose-rich diet on the expression of renin-angiotensin system molecules. These findings may also be important in further research of phenotypes like insulin resistance, metabolic syndrome, and following cardiovascular pathology in females. T2 - Hormone and Metabolic Research T1 - Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol VL - 47 IS - 7 SP - 521 EP - 527 DO - 10.1055/s-0034-1394373 ER -
@article{ author = "Bundalo, Maja M. and Živković, Maja and Tepavčević, Snežana and Ćulafić, Tijana and Korićanac, Goran and Stanković, Aleksandra", year = "2015", abstract = "The renin-angiotensin system has been implicated in the development of metabolic syndrome and appears to be a key in the local tissue control of normal cardiac functions. Physiological concentrations of estrogens have been shown to be cardioprotective, especially against the damaging effects of fructose-rich diet. The aim of the study was to investigate the expression of the renin-angiotensin system molecules with potentially deleterious effect on the heart (angiotensin-converting enzyme and angiotensin II type 1 receptor) and those with potentially protective effects, (angiotensin-converting enzyme 2 and angiotensin II type 2 receptor), in ovariectomized fructose fed female rats with 17-estradiol replacement. Real-time PCR and Western blot analysis were used for quantification of gene and protein expression in the heart. Fructose diet increased the expression of angiotensin-converting enzyme and angiotensin II type 1 receptor and decreased the expression of angiotensin-converting enzyme 2 and angiotensin II type 2 receptor. On the other hand, estradiol replacement seems to undo fructose diet effects on cardiac renin-angiotensin system. Downregulation of angiotensin-converting enzyme and angiotensin II type 1 receptor, and reversion of expression of both potentially protective molecules, angiotensin-converting enzyme 2 and angiotensin II type 2 receptor, to the control level in cardiac tissue took place. Obtained results suggest that estradiol may reverse the harmful effect of fructose-rich diet on the expression of renin-angiotensin system molecules. These findings may also be important in further research of phenotypes like insulin resistance, metabolic syndrome, and following cardiovascular pathology in females.", journal = "Hormone and Metabolic Research", title = "Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol", volume = "47", number = "7", pages = "521-527", doi = "10.1055/s-0034-1394373" }
Bundalo, M. M., Živković, M., Tepavčević, S., Ćulafić, T., Korićanac, G.,& Stanković, A.. (2015). Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol. in Hormone and Metabolic Research, 47(7), 521-527. https://doi.org/10.1055/s-0034-1394373
Bundalo MM, Živković M, Tepavčević S, Ćulafić T, Korićanac G, Stanković A. Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol. in Hormone and Metabolic Research. 2015;47(7):521-527. doi:10.1055/s-0034-1394373 .
Bundalo, Maja M., Živković, Maja, Tepavčević, Snežana, Ćulafić, Tijana, Korićanac, Goran, Stanković, Aleksandra, "Fructose-Rich Diet-Induced Changes in the Expression of the Renin Angiotensin System Molecules in the Heart of Ovariectomized Female Rats Could be Reversed by Estradiol" in Hormone and Metabolic Research, 47, no. 7 (2015):521-527, https://doi.org/10.1055/s-0034-1394373 . .
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