Key result
A single dose of estradiol in obese male rats significantly decreased transverse diameters of cardiomyocytes (P<.001) and heart mass (P<.05) compared with untreated obese rats.
Why the study?
Does estradiol reduce obesity-induced cardiac hypertrophy in a high-fat diet rat model?
Does estradiol reduce obesity-induced cardiac hypertrophy in a high-fat diet rat model?
p-value: p=< .001
A single dose of estradiol in obese rats reduces obesity-induced cardiac hypertrophy and improves biochemical parameters via Akt activation.
Should not change practice; hypothesis-generating for estradiol effects on obesity-related hypertrophy in rats.
We studied the in vivo effects of estradiol on size and biochemical parameters of cardiomyocytes in pathophysiological conditions such as obesity and insulin resistance. Male Wistar rats were normally fed (controls, n = 7) or fed with high-fat diet (obese, n = 14). Half of the obese rats (obese + estradiol, n = 7) were treated with a single dose of estradiol (40 μg/kg, intraperitoneally) and 24 hours after treatment all the rats were killed. Estradiol in vivo in obese rats resulted in a significant increase in protein kinase B (Akt) activation (P < .05) and decrease in heart mass (P < .05), ratio of the heart mass/body mass (P < .05), transverse diameters of cardiomyocytes (P < .001), concentration of serum high-sensitivity C-reactive protein (P < .001), and total cholesterol (P < .01) compared with obese nontreated rats. Our results suggest that estradiol in obese/IR rats affects the size of cardiomyocytes and its actions lead in vivo to a reduction in obesity-induced cardiac hypertrophy, via Akt.
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Obradović et al. (2013) studied Obesity and insulin resistance (n=21). Estradiol vs. Obese nontreated rats was evaluated on Transverse diameters of cardiomyocytes (p=< .001). A single dose of estradiol in obese male rats significantly decreased transverse diameters of cardiomyocytes (P<.001) and heart mass (P<.05) compared with untreated obese rats.
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