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Good Fats vs. Bad Fats and Their Impact on Ischemic Stroke

Monday, Oct. 24, 1-2 p.m.

CSF-1302

SEMINAR by Dr. J. Vanderluit

Obesity is a major risk factor for stroke and is associated with worse stroke outcomes. Ischemic stroke accounts for 85% of all strokes. The majority of individuals who have a stroke survive, but live with long-term disability. A stroke injury (infarct) evolves over time. Brain cells within the infarct core die immediately at the time of stroke while cells surrounding the core survive but are damaged. If untreated, the size of the infarct expands with the delayed cell death of these damaged brain cells. To understand the impact of obesity on the cellular response to stroke, my lab has developed a model of diet-induced obesity in mice. We show that feeding mice a high fat diet rich in ‘bad fats’ (60% fats based on lard) for 12 weeks results in larger infarcts. Our data suggests that the larger infarcts in obese mice is not due to differences in the initial injury, but rather to more delayed/secondary cell death in the days post-stroke. In contrast to bad fats, numerous studies have shown that diets rich in healthy ‘good’ fats such as the omega-3 polyunsaturated fatty acids (PUFA) results in better stroke outcomes.  However, little is known whether post-stroke application of omega-3 fatty acids is beneficial. To address this question, my lab examined the impact of acute application of docosahexaenoic acid (DHA), an omega-3 PUFA post-stroke. Our data shows that DHA application in the acute hours post-stroke reduces blood brain barrier breakdown, immune cell infiltration, and neuroinflammation at 24 hours post-stroke in both lean and obese mice. These findings suggest that acute post-stroke application of DHA has beneficial impact on the cellular response to an ischemic stroke.

Presented by Department of Biochemistry

Event Listing 2022-10-24 13:00:00 2022-10-24 14:00:00 America/St_Johns Good Fats vs. Bad Fats and Their Impact on Ischemic Stroke SEMINAR by Dr. J. Vanderluit Obesity is a major risk factor for stroke and is associated with worse stroke outcomes. Ischemic stroke accounts for 85% of all strokes. The majority of individuals who have a stroke survive, but live with long-term disability. A stroke injury (infarct) evolves over time. Brain cells within the infarct core die immediately at the time of stroke while cells surrounding the core survive but are damaged. If untreated, the size of the infarct expands with the delayed cell death of these damaged brain cells. To understand the impact of obesity on the cellular response to stroke, my lab has developed a model of diet-induced obesity in mice. We show that feeding mice a high fat diet rich in ‘bad fats’ (60% fats based on lard) for 12 weeks results in larger infarcts. Our data suggests that the larger infarcts in obese mice is not due to differences in the initial injury, but rather to more delayed/secondary cell death in the days post-stroke. In contrast to bad fats, numerous studies have shown that diets rich in healthy ‘good’ fats such as the omega-3 polyunsaturated fatty acids (PUFA) results in better stroke outcomes.  However, little is known whether post-stroke application of omega-3 fatty acids is beneficial. To address this question, my lab examined the impact of acute application of docosahexaenoic acid (DHA), an omega-3 PUFA post-stroke. Our data shows that DHA application in the acute hours post-stroke reduces blood brain barrier breakdown, immune cell infiltration, and neuroinflammation at 24 hours post-stroke in both lean and obese mice. These findings suggest that acute post-stroke application of DHA has beneficial impact on the cellular response to an ischemic stroke. CSF-1302 Department of Biochemistry