Dates of Funding: 2023-2025
There is an ongoing obesity pandemic. Currently affecting close to half of all adults in the U.S., obesity is an independent driver of a number of chronic diseases including type II diabetes, non-alcoholic fatty liver disease and heart failure. In obesity, the large fat stores undergo lipolysis, releasing excess fats into the blood stream, a condition known as dyslipidemia. Dyslipidemia subsequently causes deposition of fat in peripheral organs, such as the heart and liver, contributing to their functional decline.

I have identified a new reversible post-translational modification on the enzyme hormone sensitive lipase (HSL), the rate-limiting enzyme regulating lipolysis. This post-translational modification inhibits HSL and lipolysis in fat cells. Following extensive cellular and molecular based research characterizing this new molecular pathway to block lipolysis, we have created a knock-in mouse with HSL that is resistant to this inhibitory modification. My NORC Pilot award will allow us to fully phenotype and characterize the brand-new mouse model at baseline and in the context of obesity. We predict this mouse will be dyslipidemia at baseline and will have worsened liver and heart function when fed a high fat diet.

Targeting this new pathway to block lipolysis in fat cells could mitigate the detrimental effects of obesity in peripheral organs, such as the heart, and prolong the healthy lifespan for obese individuals.

I am a senior postdoctoral fellow in the Division of Cardiology. Since arriving in Colorado in 2020, I have received additional funding from the American Heart Association and the Colorado Clinical and Translational Sciences Institute (CCTSI) to support myself and my research. Working together with the outstanding NORC faculty and core facilities has greatly enhanced and accelerated my work in understanding the pathological interaction between fat, the heart and other organs in obesity and metabolic disease.

Dates of Funding: 2023-2025
There is an ongoing obesity pandemic. Currently affecting close to half of all adults in the U.S., obesity is an independent driver of a number of chronic diseases including type II diabetes, non-alcoholic fatty liver disease and heart failure. In obesity, the large fat stores undergo lipolysis, releasing excess fats into the blood stream, a condition known as dyslipidemia. Dyslipidemia subsequently causes deposition of fat in peripheral organs, such as the heart and liver, contributing to their functional decline.

I have identified a new reversible post-translational modification on the enzyme hormone sensitive lipase (HSL), the rate-limiting enzyme regulating lipolysis. This post-translational modification inhibits HSL and lipolysis in fat cells. Following extensive cellular and molecular based research characterizing this new molecular pathway to block lipolysis, we have created a knock-in mouse with HSL that is resistant to this inhibitory modification. My NORC Pilot award will allow us to fully phenotype and characterize the brand-new mouse model at baseline and in the context of obesity. We predict this mouse will be dyslipidemia at baseline and will have worsened liver and heart function when fed a high fat diet.

Targeting this new pathway to block lipolysis in fat cells could mitigate the detrimental effects of obesity in peripheral organs, such as the heart, and prolong the healthy lifespan for obese individuals.

I am a senior postdoctoral fellow in the Division of Cardiology. Since arriving in Colorado in 2020, I have received additional funding from the American Heart Association and the Colorado Clinical and Translational Sciences Institute (CCTSI) to support myself and my research. Working together with the outstanding NORC faculty and core facilities has greatly enhanced and accelerated my work in understanding the pathological interaction between fat, the heart and other organs in obesity and metabolic disease.

Dates of Funding: 2023-2025
There is an ongoing obesity pandemic. Currently affecting close to half of all adults in the U.S., obesity is an independent driver of a number of chronic diseases including type II diabetes, non-alcoholic fatty liver disease and heart failure. In obesity, the large fat stores undergo lipolysis, releasing excess fats into the blood stream, a condition known as dyslipidemia. Dyslipidemia subsequently causes deposition of fat in peripheral organs, such as the heart and liver, contributing to their functional decline.

I have identified a new reversible post-translational modification on the enzyme hormone sensitive lipase (HSL), the rate-limiting enzyme regulating lipolysis. This post-translational modification inhibits HSL and lipolysis in fat cells. Following extensive cellular and molecular based research characterizing this new molecular pathway to block lipolysis, we have created a knock-in mouse with HSL that is resistant to this inhibitory modification. My NORC Pilot award will allow us to fully phenotype and characterize the brand-new mouse model at baseline and in the context of obesity. We predict this mouse will be dyslipidemia at baseline and will have worsened liver and heart function when fed a high fat diet.

Targeting this new pathway to block lipolysis in fat cells could mitigate the detrimental effects of obesity in peripheral organs, such as the heart, and prolong the healthy lifespan for obese individuals.

I am a senior postdoctoral fellow in the Division of Cardiology. Since arriving in Colorado in 2020, I have received additional funding from the American Heart Association and the Colorado Clinical and Translational Sciences Institute (CCTSI) to support myself and my research. Working together with the outstanding NORC faculty and core facilities has greatly enhanced and accelerated my work in understanding the pathological interaction between fat, the heart and other organs in obesity and metabolic disease.

Dates of Funding: 2023-2025
There is an ongoing obesity pandemic. Currently affecting close to half of all adults in the U.S., obesity is an independent driver of a number of chronic diseases including type II diabetes, non-alcoholic fatty liver disease and heart failure. In obesity, the large fat stores undergo lipolysis, releasing excess fats into the blood stream, a condition known as dyslipidemia. Dyslipidemia subsequently causes deposition of fat in peripheral organs, such as the heart and liver, contributing to their functional decline.

I have identified a new reversible post-translational modification on the enzyme hormone sensitive lipase (HSL), the rate-limiting enzyme regulating lipolysis. This post-translational modification inhibits HSL and lipolysis in fat cells. Following extensive cellular and molecular based research characterizing this new molecular pathway to block lipolysis, we have created a knock-in mouse with HSL that is resistant to this inhibitory modification. My NORC Pilot award will allow us to fully phenotype and characterize the brand-new mouse model at baseline and in the context of obesity. We predict this mouse will be dyslipidemia at baseline and will have worsened liver and heart function when fed a high fat diet.

Targeting this new pathway to block lipolysis in fat cells could mitigate the detrimental effects of obesity in peripheral organs, such as the heart, and prolong the healthy lifespan for obese individuals.

I am a senior postdoctoral fellow in the Division of Cardiology. Since arriving in Colorado in 2020, I have received additional funding from the American Heart Association and the Colorado Clinical and Translational Sciences Institute (CCTSI) to support myself and my research. Working together with the outstanding NORC faculty and core facilities has greatly enhanced and accelerated my work in understanding the pathological interaction between fat, the heart and other organs in obesity and metabolic disease.

Dates of Funding: 2023-2025
There is an ongoing obesity pandemic. Currently affecting close to half of all adults in the U.S., obesity is an independent driver of a number of chronic diseases including type II diabetes, non-alcoholic fatty liver disease and heart failure. In obesity, the large fat stores undergo lipolysis, releasing excess fats into the blood stream, a condition known as dyslipidemia. Dyslipidemia subsequently causes deposition of fat in peripheral organs, such as the heart and liver, contributing to their functional decline.

I have identified a new reversible post-translational modification on the enzyme hormone sensitive lipase (HSL), the rate-limiting enzyme regulating lipolysis. This post-translational modification inhibits HSL and lipolysis in fat cells. Following extensive cellular and molecular based research characterizing this new molecular pathway to block lipolysis, we have created a knock-in mouse with HSL that is resistant to this inhibitory modification. My NORC Pilot award will allow us to fully phenotype and characterize the brand-new mouse model at baseline and in the context of obesity. We predict this mouse will be dyslipidemia at baseline and will have worsened liver and heart function when fed a high fat diet.

Targeting this new pathway to block lipolysis in fat cells could mitigate the detrimental effects of obesity in peripheral organs, such as the heart, and prolong the healthy lifespan for obese individuals.

I am a senior postdoctoral fellow in the Division of Cardiology. Since arriving in Colorado in 2020, I have received additional funding from the American Heart Association and the Colorado Clinical and Translational Sciences Institute (CCTSI) to support myself and my research. Working together with the outstanding NORC faculty and core facilities has greatly enhanced and accelerated my work in understanding the pathological interaction between fat, the heart and other organs in obesity and metabolic disease.

Dates of Funding: 2023-2025
There is an ongoing obesity pandemic. Currently affecting close to half of all adults in the U.S., obesity is an independent driver of a number of chronic diseases including type II diabetes, non-alcoholic fatty liver disease and heart failure. In obesity, the large fat stores undergo lipolysis, releasing excess fats into the blood stream, a condition known as dyslipidemia. Dyslipidemia subsequently causes deposition of fat in peripheral organs, such as the heart and liver, contributing to their functional decline.

I have identified a new reversible post-translational modification on the enzyme hormone sensitive lipase (HSL), the rate-limiting enzyme regulating lipolysis. This post-translational modification inhibits HSL and lipolysis in fat cells. Following extensive cellular and molecular based research characterizing this new molecular pathway to block lipolysis, we have created a knock-in mouse with HSL that is resistant to this inhibitory modification. My NORC Pilot award will allow us to fully phenotype and characterize the brand-new mouse model at baseline and in the context of obesity. We predict this mouse will be dyslipidemia at baseline and will have worsened liver and heart function when fed a high fat diet.

Targeting this new pathway to block lipolysis in fat cells could mitigate the detrimental effects of obesity in peripheral organs, such as the heart, and prolong the healthy lifespan for obese individuals.

I am a senior postdoctoral fellow in the Division of Cardiology. Since arriving in Colorado in 2020, I have received additional funding from the American Heart Association and the Colorado Clinical and Translational Sciences Institute (CCTSI) to support myself and my research. Working together with the outstanding NORC faculty and core facilities has greatly enhanced and accelerated my work in understanding the pathological interaction between fat, the heart and other organs in obesity and metabolic disease.

Dates of Funding: 2023-2025
There is an ongoing obesity pandemic. Currently affecting close to half of all adults in the U.S., obesity is an independent driver of a number of chronic diseases including type II diabetes, non-alcoholic fatty liver disease and heart failure. In obesity, the large fat stores undergo lipolysis, releasing excess fats into the blood stream, a condition known as dyslipidemia. Dyslipidemia subsequently causes deposition of fat in peripheral organs, such as the heart and liver, contributing to their functional decline.

I have identified a new reversible post-translational modification on the enzyme hormone sensitive lipase (HSL), the rate-limiting enzyme regulating lipolysis. This post-translational modification inhibits HSL and lipolysis in fat cells. Following extensive cellular and molecular based research characterizing this new molecular pathway to block lipolysis, we have created a knock-in mouse with HSL that is resistant to this inhibitory modification. My NORC Pilot award will allow us to fully phenotype and characterize the brand-new mouse model at baseline and in the context of obesity. We predict this mouse will be dyslipidemia at baseline and will have worsened liver and heart function when fed a high fat diet.

Targeting this new pathway to block lipolysis in fat cells could mitigate the detrimental effects of obesity in peripheral organs, such as the heart, and prolong the healthy lifespan for obese individuals.

I am a senior postdoctoral fellow in the Division of Cardiology. Since arriving in Colorado in 2020, I have received additional funding from the American Heart Association and the Colorado Clinical and Translational Sciences Institute (CCTSI) to support myself and my research. Working together with the outstanding NORC faculty and core facilities has greatly enhanced and accelerated my work in understanding the pathological interaction between fat, the heart and other organs in obesity and metabolic disease.

Dates of Funding: 2023-2025
There is an ongoing obesity pandemic. Currently affecting close to half of all adults in the U.S., obesity is an independent driver of a number of chronic diseases including type II diabetes, non-alcoholic fatty liver disease and heart failure. In obesity, the large fat stores undergo lipolysis, releasing excess fats into the blood stream, a condition known as dyslipidemia. Dyslipidemia subsequently causes deposition of fat in peripheral organs, such as the heart and liver, contributing to their functional decline.

I have identified a new reversible post-translational modification on the enzyme hormone sensitive lipase (HSL), the rate-limiting enzyme regulating lipolysis. This post-translational modification inhibits HSL and lipolysis in fat cells. Following extensive cellular and molecular based research characterizing this new molecular pathway to block lipolysis, we have created a knock-in mouse with HSL that is resistant to this inhibitory modification. My NORC Pilot award will allow us to fully phenotype and characterize the brand-new mouse model at baseline and in the context of obesity. We predict this mouse will be dyslipidemia at baseline and will have worsened liver and heart function when fed a high fat diet.

Targeting this new pathway to block lipolysis in fat cells could mitigate the detrimental effects of obesity in peripheral organs, such as the heart, and prolong the healthy lifespan for obese individuals.

I am a senior postdoctoral fellow in the Division of Cardiology. Since arriving in Colorado in 2020, I have received additional funding from the American Heart Association and the Colorado Clinical and Translational Sciences Institute (CCTSI) to support myself and my research. Working together with the outstanding NORC faculty and core facilities has greatly enhanced and accelerated my work in understanding the pathological interaction between fat, the heart and other organs in obesity and metabolic disease.

Dates of Funding: 2023-2025
There is an ongoing obesity pandemic. Currently affecting close to half of all adults in the U.S., obesity is an independent driver of a number of chronic diseases including type II diabetes, non-alcoholic fatty liver disease and heart failure. In obesity, the large fat stores undergo lipolysis, releasing excess fats into the blood stream, a condition known as dyslipidemia. Dyslipidemia subsequently causes deposition of fat in peripheral organs, such as the heart and liver, contributing to their functional decline.

I have identified a new reversible post-translational modification on the enzyme hormone sensitive lipase (HSL), the rate-limiting enzyme regulating lipolysis. This post-translational modification inhibits HSL and lipolysis in fat cells. Following extensive cellular and molecular based research characterizing this new molecular pathway to block lipolysis, we have created a knock-in mouse with HSL that is resistant to this inhibitory modification. My NORC Pilot award will allow us to fully phenotype and characterize the brand-new mouse model at baseline and in the context of obesity. We predict this mouse will be dyslipidemia at baseline and will have worsened liver and heart function when fed a high fat diet.

Targeting this new pathway to block lipolysis in fat cells could mitigate the detrimental effects of obesity in peripheral organs, such as the heart, and prolong the healthy lifespan for obese individuals.

I am a senior postdoctoral fellow in the Division of Cardiology. Since arriving in Colorado in 2020, I have received additional funding from the American Heart Association and the Colorado Clinical and Translational Sciences Institute (CCTSI) to support myself and my research. Working together with the outstanding NORC faculty and core facilities has greatly enhanced and accelerated my work in understanding the pathological interaction between fat, the heart and other organs in obesity and metabolic disease.

Dates of Funding: 2023-2025
There is an ongoing obesity pandemic. Currently affecting close to half of all adults in the U.S., obesity is an independent driver of a number of chronic diseases including type II diabetes, non-alcoholic fatty liver disease and heart failure. In obesity, the large fat stores undergo lipolysis, releasing excess fats into the blood stream, a condition known as dyslipidemia. Dyslipidemia subsequently causes deposition of fat in peripheral organs, such as the heart and liver, contributing to their functional decline.

I have identified a new reversible post-translational modification on the enzyme hormone sensitive lipase (HSL), the rate-limiting enzyme regulating lipolysis. This post-translational modification inhibits HSL and lipolysis in fat cells. Following extensive cellular and molecular based research characterizing this new molecular pathway to block lipolysis, we have created a knock-in mouse with HSL that is resistant to this inhibitory modification. My NORC Pilot award will allow us to fully phenotype and characterize the brand-new mouse model at baseline and in the context of obesity. We predict this mouse will be dyslipidemia at baseline and will have worsened liver and heart function when fed a high fat diet.

Targeting this new pathway to block lipolysis in fat cells could mitigate the detrimental effects of obesity in peripheral organs, such as the heart, and prolong the healthy lifespan for obese individuals.

I am a senior postdoctoral fellow in the Division of Cardiology. Since arriving in Colorado in 2020, I have received additional funding from the American Heart Association and the Colorado Clinical and Translational Sciences Institute (CCTSI) to support myself and my research. Working together with the outstanding NORC faculty and core facilities has greatly enhanced and accelerated my work in understanding the pathological interaction between fat, the heart and other organs in obesity and metabolic disease.