Poster Title

The Role of mitoNEET and Pioglitazone in Energy Metabolism: Illuminating a Flawed System in Type 2 Diabetes Patients

Presenter Information

Callie FreemanFollow

Grade Level at Time of Presentation

Secondary School

Institution

Western Kentucky University

KY House District #

3 and 4

KY Senate District #

3 and 4

Department

Dept. of Biology

Abstract

The Role of mitoNEET and Pioglitazone in Energy Metabolism: Illuminating a Flawed System in Type 2 Diabetes Patients

By: Callie Freeman (callieafreeman@gmail.com)

Mentor: Dr. Michael Menze, Department of Biology at the University of Louisville (michael.menze@louisville.edu)

Type 2 Diabetes affects over 29 million people in the United States, making it a foremost concern within the medical community. Pioglitazone, a drug commonly used to treat type 2 diabetes, has been shown to interact with the outer-mitochondrial membrane protein mitoNEET, which contains an electron transferring iron – sulfur cluster. Pioglitazone interferes with mitoNEET’s ability to transfer electrons within the electron transport chain, causing an interruption in ATP (and later glucose energy) production. We hypothesized that Pioglitazone’s ability to interact with the mitoNEET protein is the reason for its effectiveness as a blood glucose lowering medication, suggesting that mitoNEET plays a key role in cellular respiration (as it is able to control ATP production). This hypothesis was tested by measuring the rate of oxygen consumption in Hep G2 cells via a respirometer, a machine used to measure both oxygen concentration and oxygen consumption. Measuring the rate of oxygen consumption allowed the amount of cellular respiration occurring to be determined; we considered higher rates of oxygen consumption to correlate with higher amounts of cellular respiration (and thus ATP production). By treating the cells with Pioglitazone, the rate of oxygen consumption decreased an average 27.33 ± 5.04 pmol O2 * s-1 * 106 cells (n = 3, ± SE). This suggested that mitoNEET does indeed affect ATP production and is a key element of type 2 diabetes research. By understanding exactly how the drug Pioglitazone functions, our research will allow the pharmaceutical industry to develop anti-diabetes drugs more effectively. Before now, little was known about the mitoNEET protein and its integral role in cellular metabolism; through the mitoNEET protein, there is another mechanism by which diabetes can be treated.

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The Role of mitoNEET and Pioglitazone in Energy Metabolism: Illuminating a Flawed System in Type 2 Diabetes Patients

The Role of mitoNEET and Pioglitazone in Energy Metabolism: Illuminating a Flawed System in Type 2 Diabetes Patients

By: Callie Freeman (callieafreeman@gmail.com)

Mentor: Dr. Michael Menze, Department of Biology at the University of Louisville (michael.menze@louisville.edu)

Type 2 Diabetes affects over 29 million people in the United States, making it a foremost concern within the medical community. Pioglitazone, a drug commonly used to treat type 2 diabetes, has been shown to interact with the outer-mitochondrial membrane protein mitoNEET, which contains an electron transferring iron – sulfur cluster. Pioglitazone interferes with mitoNEET’s ability to transfer electrons within the electron transport chain, causing an interruption in ATP (and later glucose energy) production. We hypothesized that Pioglitazone’s ability to interact with the mitoNEET protein is the reason for its effectiveness as a blood glucose lowering medication, suggesting that mitoNEET plays a key role in cellular respiration (as it is able to control ATP production). This hypothesis was tested by measuring the rate of oxygen consumption in Hep G2 cells via a respirometer, a machine used to measure both oxygen concentration and oxygen consumption. Measuring the rate of oxygen consumption allowed the amount of cellular respiration occurring to be determined; we considered higher rates of oxygen consumption to correlate with higher amounts of cellular respiration (and thus ATP production). By treating the cells with Pioglitazone, the rate of oxygen consumption decreased an average 27.33 ± 5.04 pmol O2 * s-1 * 106 cells (n = 3, ± SE). This suggested that mitoNEET does indeed affect ATP production and is a key element of type 2 diabetes research. By understanding exactly how the drug Pioglitazone functions, our research will allow the pharmaceutical industry to develop anti-diabetes drugs more effectively. Before now, little was known about the mitoNEET protein and its integral role in cellular metabolism; through the mitoNEET protein, there is another mechanism by which diabetes can be treated.