Abstract
Background The objective of this study is to observe if mild hyperuricemia and a high-fructose diet influence the cardiovascular and metabolic systems in hypogonadic female Wistar rats compared to normogonadic female rats. Methods Fifty-six (56) adult female Wistar rats were used in the present work. Animals were divided into two groups: normogonadic (NGN) and hypogonadic (HGN). These groups were also divided into four subgroups in accordance with the treatment: control with only water (C), fructose (F), oxonic acid (OA), and fructose + oxonic acid (FOA). Lipid profile, glycemia, uric acid, and creatinine determinations were assessed. Cardiovascular changes were evaluated by measuring blood pressure, myocyte volume, fibrosis, and intima-media aortic thickness. Results HGN rats had higher levels of total cholesterol (TC) (p < 0.01) and noHDLc (p < 0.01), in addition to higher levels of uric acid (p < 0.05). The OA group significantly increased myocyte volume (p < 0.0001) and the percentage of fibrosis as well as the group receiving FOA (p < 0.001) in both gonadal conditions, being greater in the HGN group. Hypogonadic animals presented a worse lipid profile. Conclusion Mild hyperuricemia produces hypertension together with changes in the cardiac hypertrophy, fibrosis, and increased thickness of the intima media in hypogonadic rats fed high-fructose diet.
Highlights
Cardiovascular disease (CVD) remains the leading cause of death in women
All NGN animals began the experiment with similar weights (p = NS), and at the end of the experiment, a significant increase was observed between all groups (p < 0 0001)
The C and F groups were heavier than the oxonic acid (OA) and fructose + oxonic acid (FOA) groups (p < 0 001) (Table 2)
Summary
Cardiovascular disease (CVD) remains the leading cause of death in women. Apart from age, menopause status increases the prevalence of cardiometabolic risk factors as obesity, metabolic syndrome, type 2 diabetes, and hypertension [1, 2], while the exact mechanisms remain unclear. Estrogen decreases and relative hyperandrogenism could bring on changes in the body composition, with an increment in the overall fat mass, with predominance of visceral fat and ectopic fat storage (liver and skeletal muscle), as well as a peripheral fat (gluteofemoral) decrease. These conditions would lead to an increment of proinflamatory adipocytokines and a state of insulin resistance [3]. An increase of uric acid levels in menopausal women has been observed. Mild hyperuricemia produces hypertension together with changes in the cardiac hypertrophy, fibrosis, and increased thickness of the intima media in hypogonadic rats fed high-fructose diet
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