Examining cardiomyocyte apoptosis in the presence of a high fat diet (HFD) in mice with prolonged estrogen loss
Abstract
Cardiovascular disease (CVD) is one of the leading causes of death globally and studies have shown that men and women are impacted differently. Similarly, research shows that a high intake of saturated fat increases the likelihood and severity of developing CVD. Estrogen acts as a vasodilator, a heart protective agent, which effectively protects women from CVD compared to men. However, there is a significant gap in the literature as to how CVD effects women as they begin to lose their estrogen and when combined with the presence of a high fat diet (HFD), has shown to be detrimental to women’s heart health. Cardiac apoptosis is a mechanism of cell death in heart tissue and is present as the heart is damaged by CVD. Four treatment groups were present in this study: SHAM (control), Ovariectomized (OVX), SHAM + HFD, and OVX + HFD. Animals were ovariectomized at 2.5 months old and were provided with a consistent high fat diet based on their grouping beginning at 18 months for 4 months. Animals were weighed every two weeks and echocardiograms were also performed to examine heart function. We hypothesize that cardiac apoptosis will increase in ovariectomized animals consuming a high fat diet when compared to their normal counterparts consuming a regular diet. The mice were euthanized at 24 months old, their hearts were collected, tissue was sectioned, and TUNNEL assay is actively being performed to determine the number of apoptotic cells from each group. We expect the outcomes of the TUNNEL staining to show a measurable increase in apoptotic cells in the HFD + OVX group due to the increased stress on their hearts. Overall, this experimentation has important implications in women’s cardiovascular health and therefore emphasizes the importance of furthering our understanding in this field to close the knowledge gap.
Start Time
15-4-2026 9:00 AM
End Time
15-4-2026 10:00 AM
Room Number
272
Presentation Type
Oral Presentation
Presentation Subtype
Research-in-Progress
Presentation Category
Science, Technology, and Engineering
Faculty Mentor
Foster Cerrone
Examining cardiomyocyte apoptosis in the presence of a high fat diet (HFD) in mice with prolonged estrogen loss
272
Cardiovascular disease (CVD) is one of the leading causes of death globally and studies have shown that men and women are impacted differently. Similarly, research shows that a high intake of saturated fat increases the likelihood and severity of developing CVD. Estrogen acts as a vasodilator, a heart protective agent, which effectively protects women from CVD compared to men. However, there is a significant gap in the literature as to how CVD effects women as they begin to lose their estrogen and when combined with the presence of a high fat diet (HFD), has shown to be detrimental to women’s heart health. Cardiac apoptosis is a mechanism of cell death in heart tissue and is present as the heart is damaged by CVD. Four treatment groups were present in this study: SHAM (control), Ovariectomized (OVX), SHAM + HFD, and OVX + HFD. Animals were ovariectomized at 2.5 months old and were provided with a consistent high fat diet based on their grouping beginning at 18 months for 4 months. Animals were weighed every two weeks and echocardiograms were also performed to examine heart function. We hypothesize that cardiac apoptosis will increase in ovariectomized animals consuming a high fat diet when compared to their normal counterparts consuming a regular diet. The mice were euthanized at 24 months old, their hearts were collected, tissue was sectioned, and TUNNEL assay is actively being performed to determine the number of apoptotic cells from each group. We expect the outcomes of the TUNNEL staining to show a measurable increase in apoptotic cells in the HFD + OVX group due to the increased stress on their hearts. Overall, this experimentation has important implications in women’s cardiovascular health and therefore emphasizes the importance of furthering our understanding in this field to close the knowledge gap.
