Dates of Funding: 2023-2025
I am currently a postdoctoral fellow in the department of medicine, division of endocrinology, metabolism, and diabetes. I am currently funded by a NIH F32 and aspire to be an independent nutrient sensing scientist. My graduate training from James Madison University and Auburn University focused on nutrient supplementation strategies during and after exercise. To further understand how nutrients are sensed to promote cellular responses, I pursued my first postdoctoral fellowship at Penn State College of Medicine. I investigated how the stress-response protein family known as Sestrins affect how glucose contributes to cellular growth. Results from these studies suggested a strong role for Sestrins in regulating metabolism.

Dysfunction of skeletal muscle metabolism underpins many disease states including Diabetes Mellitus. Correcting dysfunctional skeletal muscle metabolism has proven to improve disease prognosis. Sestrin1-3 are a family of stress-responsive proteins that have been shown to directly affect the activation status of adenosine monophosphate-activated protein kinase (AMPK) and mechanistic target of rapamycin in complex 1 (mTORC1) to maintain bioenergetic homeostasis. AMPK and mTORC1 are master regulators of bioenergetics such that their activation status is dysfunctional in many disease states. Given that Sestrins affect the activation status of both AMPK and mTORC1, Sestrins have been promising therapeutic targets to improve disease prognosis. Sestrin1/2 have been most studied; however, Sestrin3 is suggested to be the most impactful for metabolic regulation. Canonically, Sestrins have been thought to directly affect AMPK and mTORC1 activation to regulate metabolic processes; however, preliminary data suggests AMPK and mTORC1 activation is an indirect consequence of Sestrin-regulated glycolytic enzyme activity. Using translational models, cellular and molecular techniques, and stable isotope tracing, the precise function of Sestrin3-regulation on metabolism will be unveiled. Moreover, the proposed experiments will provide excellent training and a pathway to independence. It is anticipated that these findings can be leveraged to identify unique pharmacological targets and promote an area of research that is ripe for future investigation.

Dates of Funding: 2023-2025
I am currently a postdoctoral fellow in the department of medicine, division of endocrinology, metabolism, and diabetes. I am currently funded by a NIH F32 and aspire to be an independent nutrient sensing scientist. My graduate training from James Madison University and Auburn University focused on nutrient supplementation strategies during and after exercise. To further understand how nutrients are sensed to promote cellular responses, I pursued my first postdoctoral fellowship at Penn State College of Medicine. I investigated how the stress-response protein family known as Sestrins affect how glucose contributes to cellular growth. Results from these studies suggested a strong role for Sestrins in regulating metabolism.

Dysfunction of skeletal muscle metabolism underpins many disease states including Diabetes Mellitus. Correcting dysfunctional skeletal muscle metabolism has proven to improve disease prognosis. Sestrin1-3 are a family of stress-responsive proteins that have been shown to directly affect the activation status of adenosine monophosphate-activated protein kinase (AMPK) and mechanistic target of rapamycin in complex 1 (mTORC1) to maintain bioenergetic homeostasis. AMPK and mTORC1 are master regulators of bioenergetics such that their activation status is dysfunctional in many disease states. Given that Sestrins affect the activation status of both AMPK and mTORC1, Sestrins have been promising therapeutic targets to improve disease prognosis. Sestrin1/2 have been most studied; however, Sestrin3 is suggested to be the most impactful for metabolic regulation. Canonically, Sestrins have been thought to directly affect AMPK and mTORC1 activation to regulate metabolic processes; however, preliminary data suggests AMPK and mTORC1 activation is an indirect consequence of Sestrin-regulated glycolytic enzyme activity. Using translational models, cellular and molecular techniques, and stable isotope tracing, the precise function of Sestrin3-regulation on metabolism will be unveiled. Moreover, the proposed experiments will provide excellent training and a pathway to independence. It is anticipated that these findings can be leveraged to identify unique pharmacological targets and promote an area of research that is ripe for future investigation.

Dates of Funding: 2023-2025
I am currently a postdoctoral fellow in the department of medicine, division of endocrinology, metabolism, and diabetes. I am currently funded by a NIH F32 and aspire to be an independent nutrient sensing scientist. My graduate training from James Madison University and Auburn University focused on nutrient supplementation strategies during and after exercise. To further understand how nutrients are sensed to promote cellular responses, I pursued my first postdoctoral fellowship at Penn State College of Medicine. I investigated how the stress-response protein family known as Sestrins affect how glucose contributes to cellular growth. Results from these studies suggested a strong role for Sestrins in regulating metabolism.

Dysfunction of skeletal muscle metabolism underpins many disease states including Diabetes Mellitus. Correcting dysfunctional skeletal muscle metabolism has proven to improve disease prognosis. Sestrin1-3 are a family of stress-responsive proteins that have been shown to directly affect the activation status of adenosine monophosphate-activated protein kinase (AMPK) and mechanistic target of rapamycin in complex 1 (mTORC1) to maintain bioenergetic homeostasis. AMPK and mTORC1 are master regulators of bioenergetics such that their activation status is dysfunctional in many disease states. Given that Sestrins affect the activation status of both AMPK and mTORC1, Sestrins have been promising therapeutic targets to improve disease prognosis. Sestrin1/2 have been most studied; however, Sestrin3 is suggested to be the most impactful for metabolic regulation. Canonically, Sestrins have been thought to directly affect AMPK and mTORC1 activation to regulate metabolic processes; however, preliminary data suggests AMPK and mTORC1 activation is an indirect consequence of Sestrin-regulated glycolytic enzyme activity. Using translational models, cellular and molecular techniques, and stable isotope tracing, the precise function of Sestrin3-regulation on metabolism will be unveiled. Moreover, the proposed experiments will provide excellent training and a pathway to independence. It is anticipated that these findings can be leveraged to identify unique pharmacological targets and promote an area of research that is ripe for future investigation.

Dates of Funding: 2023-2025
I am currently a postdoctoral fellow in the department of medicine, division of endocrinology, metabolism, and diabetes. I am currently funded by a NIH F32 and aspire to be an independent nutrient sensing scientist. My graduate training from James Madison University and Auburn University focused on nutrient supplementation strategies during and after exercise. To further understand how nutrients are sensed to promote cellular responses, I pursued my first postdoctoral fellowship at Penn State College of Medicine. I investigated how the stress-response protein family known as Sestrins affect how glucose contributes to cellular growth. Results from these studies suggested a strong role for Sestrins in regulating metabolism.

Dysfunction of skeletal muscle metabolism underpins many disease states including Diabetes Mellitus. Correcting dysfunctional skeletal muscle metabolism has proven to improve disease prognosis. Sestrin1-3 are a family of stress-responsive proteins that have been shown to directly affect the activation status of adenosine monophosphate-activated protein kinase (AMPK) and mechanistic target of rapamycin in complex 1 (mTORC1) to maintain bioenergetic homeostasis. AMPK and mTORC1 are master regulators of bioenergetics such that their activation status is dysfunctional in many disease states. Given that Sestrins affect the activation status of both AMPK and mTORC1, Sestrins have been promising therapeutic targets to improve disease prognosis. Sestrin1/2 have been most studied; however, Sestrin3 is suggested to be the most impactful for metabolic regulation. Canonically, Sestrins have been thought to directly affect AMPK and mTORC1 activation to regulate metabolic processes; however, preliminary data suggests AMPK and mTORC1 activation is an indirect consequence of Sestrin-regulated glycolytic enzyme activity. Using translational models, cellular and molecular techniques, and stable isotope tracing, the precise function of Sestrin3-regulation on metabolism will be unveiled. Moreover, the proposed experiments will provide excellent training and a pathway to independence. It is anticipated that these findings can be leveraged to identify unique pharmacological targets and promote an area of research that is ripe for future investigation.

Dates of Funding: 2023-2025
I am currently a postdoctoral fellow in the department of medicine, division of endocrinology, metabolism, and diabetes. I am currently funded by a NIH F32 and aspire to be an independent nutrient sensing scientist. My graduate training from James Madison University and Auburn University focused on nutrient supplementation strategies during and after exercise. To further understand how nutrients are sensed to promote cellular responses, I pursued my first postdoctoral fellowship at Penn State College of Medicine. I investigated how the stress-response protein family known as Sestrins affect how glucose contributes to cellular growth. Results from these studies suggested a strong role for Sestrins in regulating metabolism.

Dysfunction of skeletal muscle metabolism underpins many disease states including Diabetes Mellitus. Correcting dysfunctional skeletal muscle metabolism has proven to improve disease prognosis. Sestrin1-3 are a family of stress-responsive proteins that have been shown to directly affect the activation status of adenosine monophosphate-activated protein kinase (AMPK) and mechanistic target of rapamycin in complex 1 (mTORC1) to maintain bioenergetic homeostasis. AMPK and mTORC1 are master regulators of bioenergetics such that their activation status is dysfunctional in many disease states. Given that Sestrins affect the activation status of both AMPK and mTORC1, Sestrins have been promising therapeutic targets to improve disease prognosis. Sestrin1/2 have been most studied; however, Sestrin3 is suggested to be the most impactful for metabolic regulation. Canonically, Sestrins have been thought to directly affect AMPK and mTORC1 activation to regulate metabolic processes; however, preliminary data suggests AMPK and mTORC1 activation is an indirect consequence of Sestrin-regulated glycolytic enzyme activity. Using translational models, cellular and molecular techniques, and stable isotope tracing, the precise function of Sestrin3-regulation on metabolism will be unveiled. Moreover, the proposed experiments will provide excellent training and a pathway to independence. It is anticipated that these findings can be leveraged to identify unique pharmacological targets and promote an area of research that is ripe for future investigation.

Dates of Funding: 2023-2025
I am currently a postdoctoral fellow in the department of medicine, division of endocrinology, metabolism, and diabetes. I am currently funded by a NIH F32 and aspire to be an independent nutrient sensing scientist. My graduate training from James Madison University and Auburn University focused on nutrient supplementation strategies during and after exercise. To further understand how nutrients are sensed to promote cellular responses, I pursued my first postdoctoral fellowship at Penn State College of Medicine. I investigated how the stress-response protein family known as Sestrins affect how glucose contributes to cellular growth. Results from these studies suggested a strong role for Sestrins in regulating metabolism.

Dysfunction of skeletal muscle metabolism underpins many disease states including Diabetes Mellitus. Correcting dysfunctional skeletal muscle metabolism has proven to improve disease prognosis. Sestrin1-3 are a family of stress-responsive proteins that have been shown to directly affect the activation status of adenosine monophosphate-activated protein kinase (AMPK) and mechanistic target of rapamycin in complex 1 (mTORC1) to maintain bioenergetic homeostasis. AMPK and mTORC1 are master regulators of bioenergetics such that their activation status is dysfunctional in many disease states. Given that Sestrins affect the activation status of both AMPK and mTORC1, Sestrins have been promising therapeutic targets to improve disease prognosis. Sestrin1/2 have been most studied; however, Sestrin3 is suggested to be the most impactful for metabolic regulation. Canonically, Sestrins have been thought to directly affect AMPK and mTORC1 activation to regulate metabolic processes; however, preliminary data suggests AMPK and mTORC1 activation is an indirect consequence of Sestrin-regulated glycolytic enzyme activity. Using translational models, cellular and molecular techniques, and stable isotope tracing, the precise function of Sestrin3-regulation on metabolism will be unveiled. Moreover, the proposed experiments will provide excellent training and a pathway to independence. It is anticipated that these findings can be leveraged to identify unique pharmacological targets and promote an area of research that is ripe for future investigation.

Dates of Funding: 2023-2025
I am currently a postdoctoral fellow in the department of medicine, division of endocrinology, metabolism, and diabetes. I am currently funded by a NIH F32 and aspire to be an independent nutrient sensing scientist. My graduate training from James Madison University and Auburn University focused on nutrient supplementation strategies during and after exercise. To further understand how nutrients are sensed to promote cellular responses, I pursued my first postdoctoral fellowship at Penn State College of Medicine. I investigated how the stress-response protein family known as Sestrins affect how glucose contributes to cellular growth. Results from these studies suggested a strong role for Sestrins in regulating metabolism.

Dysfunction of skeletal muscle metabolism underpins many disease states including Diabetes Mellitus. Correcting dysfunctional skeletal muscle metabolism has proven to improve disease prognosis. Sestrin1-3 are a family of stress-responsive proteins that have been shown to directly affect the activation status of adenosine monophosphate-activated protein kinase (AMPK) and mechanistic target of rapamycin in complex 1 (mTORC1) to maintain bioenergetic homeostasis. AMPK and mTORC1 are master regulators of bioenergetics such that their activation status is dysfunctional in many disease states. Given that Sestrins affect the activation status of both AMPK and mTORC1, Sestrins have been promising therapeutic targets to improve disease prognosis. Sestrin1/2 have been most studied; however, Sestrin3 is suggested to be the most impactful for metabolic regulation. Canonically, Sestrins have been thought to directly affect AMPK and mTORC1 activation to regulate metabolic processes; however, preliminary data suggests AMPK and mTORC1 activation is an indirect consequence of Sestrin-regulated glycolytic enzyme activity. Using translational models, cellular and molecular techniques, and stable isotope tracing, the precise function of Sestrin3-regulation on metabolism will be unveiled. Moreover, the proposed experiments will provide excellent training and a pathway to independence. It is anticipated that these findings can be leveraged to identify unique pharmacological targets and promote an area of research that is ripe for future investigation.

Dates of Funding: 2023-2025
I am currently a postdoctoral fellow in the department of medicine, division of endocrinology, metabolism, and diabetes. I am currently funded by a NIH F32 and aspire to be an independent nutrient sensing scientist. My graduate training from James Madison University and Auburn University focused on nutrient supplementation strategies during and after exercise. To further understand how nutrients are sensed to promote cellular responses, I pursued my first postdoctoral fellowship at Penn State College of Medicine. I investigated how the stress-response protein family known as Sestrins affect how glucose contributes to cellular growth. Results from these studies suggested a strong role for Sestrins in regulating metabolism.

Dysfunction of skeletal muscle metabolism underpins many disease states including Diabetes Mellitus. Correcting dysfunctional skeletal muscle metabolism has proven to improve disease prognosis. Sestrin1-3 are a family of stress-responsive proteins that have been shown to directly affect the activation status of adenosine monophosphate-activated protein kinase (AMPK) and mechanistic target of rapamycin in complex 1 (mTORC1) to maintain bioenergetic homeostasis. AMPK and mTORC1 are master regulators of bioenergetics such that their activation status is dysfunctional in many disease states. Given that Sestrins affect the activation status of both AMPK and mTORC1, Sestrins have been promising therapeutic targets to improve disease prognosis. Sestrin1/2 have been most studied; however, Sestrin3 is suggested to be the most impactful for metabolic regulation. Canonically, Sestrins have been thought to directly affect AMPK and mTORC1 activation to regulate metabolic processes; however, preliminary data suggests AMPK and mTORC1 activation is an indirect consequence of Sestrin-regulated glycolytic enzyme activity. Using translational models, cellular and molecular techniques, and stable isotope tracing, the precise function of Sestrin3-regulation on metabolism will be unveiled. Moreover, the proposed experiments will provide excellent training and a pathway to independence. It is anticipated that these findings can be leveraged to identify unique pharmacological targets and promote an area of research that is ripe for future investigation.

Dates of Funding: 2023-2025
I am currently a postdoctoral fellow in the department of medicine, division of endocrinology, metabolism, and diabetes. I am currently funded by a NIH F32 and aspire to be an independent nutrient sensing scientist. My graduate training from James Madison University and Auburn University focused on nutrient supplementation strategies during and after exercise. To further understand how nutrients are sensed to promote cellular responses, I pursued my first postdoctoral fellowship at Penn State College of Medicine. I investigated how the stress-response protein family known as Sestrins affect how glucose contributes to cellular growth. Results from these studies suggested a strong role for Sestrins in regulating metabolism.

Dysfunction of skeletal muscle metabolism underpins many disease states including Diabetes Mellitus. Correcting dysfunctional skeletal muscle metabolism has proven to improve disease prognosis. Sestrin1-3 are a family of stress-responsive proteins that have been shown to directly affect the activation status of adenosine monophosphate-activated protein kinase (AMPK) and mechanistic target of rapamycin in complex 1 (mTORC1) to maintain bioenergetic homeostasis. AMPK and mTORC1 are master regulators of bioenergetics such that their activation status is dysfunctional in many disease states. Given that Sestrins affect the activation status of both AMPK and mTORC1, Sestrins have been promising therapeutic targets to improve disease prognosis. Sestrin1/2 have been most studied; however, Sestrin3 is suggested to be the most impactful for metabolic regulation. Canonically, Sestrins have been thought to directly affect AMPK and mTORC1 activation to regulate metabolic processes; however, preliminary data suggests AMPK and mTORC1 activation is an indirect consequence of Sestrin-regulated glycolytic enzyme activity. Using translational models, cellular and molecular techniques, and stable isotope tracing, the precise function of Sestrin3-regulation on metabolism will be unveiled. Moreover, the proposed experiments will provide excellent training and a pathway to independence. It is anticipated that these findings can be leveraged to identify unique pharmacological targets and promote an area of research that is ripe for future investigation.