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Translational Studies on Mitochondrial Function and Hypoxia in Complications of Diabetes Mellitus.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Translational Studies on Mitochondrial Function and Hypoxia in Complications of Diabetes Mellitus./
Author:	Xu, Cheng.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2020,
Description:	98 p.
Notes:	Source: Dissertations Abstracts International, Volume: 82-09, Section: B.
Contained By:	Dissertations Abstracts International82-09B.
Subject:	Public health. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28420698
ISBN:	9798582530770

Translational Studies on Mitochondrial Function and Hypoxia in Complications of Diabetes Mellitus.
Xu, Cheng.

Translational Studies on Mitochondrial Function and Hypoxia in Complications of Diabetes Mellitus. - Ann Arbor : ProQuest Dissertations & Theses, 2020 - 98 p.

Source: Dissertations Abstracts International, Volume: 82-09, Section: B.

Thesis (Ph.D.)--Karolinska Institutet (Sweden), 2020.

This item must not be sold to any third party vendors.

Diabetes affects almost one out of every ten humans on earth. Yet, it is an often-overlooked disease. Diabetes is a slow killer. As the world gets more sedentary and overweight, diabetes is an ever-growing challenge, causing massive suffering and costs for individuals and society. Diabetes features high blood sugar. Sugar is processed into energy by mitochondria, little powerhouses inside the cells that make up our bodies. Mitochondria need oxygen to process sugar into energy. This process involves the production of reactive oxygen species (ROS), both as a by-product and as important messenger molecules with which different parts of the cells communicate with each other. Too much ROS, however, damages DNA, cells and leads to sickness. It is well known that high blood sugar, such as in diabetes, leads to increased ROS. This is the main cause of the various complications of diabetes that can occur over time if the diabetes is not treated well enough. These complications include heart attacks, strokes, blindness, kidney failure and wounds that risk becoming permanent and lead to limb amputations.The body contains many mechanisms to reduce damage caused by ROS. Since diabetes leads to increased ROS, the antioxidant defense of the body is insufficient to prevent ROS-inflicted damage. That is why we also investigated Coenzyme Q, an antioxidant that is also a part of the mitochondria powerhouse. We looked at how Coenzyme Q levels in different diabetic patients could explain the difference in complication rates and disease outcome. We also did experiments to see if increasing production of Coenzyme Q could improve diabetic wound healing in diabetic mice. When oxygen levels are lower in cells, for example when we consume more oxygen while exercising, the result is so called hypoxia. The cell adapts to hypoxia by adjusting many different cellular systems. An important part of these systems is hypoxia-inducible factor (HIF). Since oxygen is so important but at the same time potentially harmful in the form of ROS, HIF is a fine-tuned machinery designed to meet the challenge of oxygen levels going up and down in a cell. Many of these adjustments involve mitochondria, since mitochondria are the main consumer of oxygen in our cells. However, in diabetes this machinery is faulty because of HIF being negatively affected by high sugar levels. Temporary hypoxia happens all the time in our bodies. Then, if HIF is damaged, ROS will cause damage which builds up over time and lead to complications.We therefore set out to investigate how dysfunctional HIF can be restored to working order and so lessen the harmful effects of diabetes. Our translational studies involved subjects with diabetes, laboratory mice and cell cultures. We investigated how mitochondrial energy production, HIF and ROS interconnect in diabetes, and what can be done to correct the mechanisms which cause damage. Our findings resulted in better understanding of the nature of ROS and energy metabolism in diabetes. This newfound knowledge will contribute to future research efforts in the clinical treatment of severe complications such as diabetic foot ulcers and diabetic kidney disease.

ISBN: 9798582530770Subjects--Topical Terms:

534748
Public health.
Subjects--Index Terms:

Diabetes Mellitus (DM)

Translational Studies on Mitochondrial Function and Hypoxia in Complications of Diabetes Mellitus.
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500 $a Source: Dissertations Abstracts International, Volume: 82-09, Section: B.
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506 $a This item must not be sold to any third party vendors.
520 $a Diabetes affects almost one out of every ten humans on earth. Yet, it is an often-overlooked disease. Diabetes is a slow killer. As the world gets more sedentary and overweight, diabetes is an ever-growing challenge, causing massive suffering and costs for individuals and society. Diabetes features high blood sugar. Sugar is processed into energy by mitochondria, little powerhouses inside the cells that make up our bodies. Mitochondria need oxygen to process sugar into energy. This process involves the production of reactive oxygen species (ROS), both as a by-product and as important messenger molecules with which different parts of the cells communicate with each other. Too much ROS, however, damages DNA, cells and leads to sickness. It is well known that high blood sugar, such as in diabetes, leads to increased ROS. This is the main cause of the various complications of diabetes that can occur over time if the diabetes is not treated well enough. These complications include heart attacks, strokes, blindness, kidney failure and wounds that risk becoming permanent and lead to limb amputations.The body contains many mechanisms to reduce damage caused by ROS. Since diabetes leads to increased ROS, the antioxidant defense of the body is insufficient to prevent ROS-inflicted damage. That is why we also investigated Coenzyme Q, an antioxidant that is also a part of the mitochondria powerhouse. We looked at how Coenzyme Q levels in different diabetic patients could explain the difference in complication rates and disease outcome. We also did experiments to see if increasing production of Coenzyme Q could improve diabetic wound healing in diabetic mice. When oxygen levels are lower in cells, for example when we consume more oxygen while exercising, the result is so called hypoxia. The cell adapts to hypoxia by adjusting many different cellular systems. An important part of these systems is hypoxia-inducible factor (HIF). Since oxygen is so important but at the same time potentially harmful in the form of ROS, HIF is a fine-tuned machinery designed to meet the challenge of oxygen levels going up and down in a cell. Many of these adjustments involve mitochondria, since mitochondria are the main consumer of oxygen in our cells. However, in diabetes this machinery is faulty because of HIF being negatively affected by high sugar levels. Temporary hypoxia happens all the time in our bodies. Then, if HIF is damaged, ROS will cause damage which builds up over time and lead to complications.We therefore set out to investigate how dysfunctional HIF can be restored to working order and so lessen the harmful effects of diabetes. Our translational studies involved subjects with diabetes, laboratory mice and cell cultures. We investigated how mitochondrial energy production, HIF and ROS interconnect in diabetes, and what can be done to correct the mechanisms which cause damage. Our findings resulted in better understanding of the nature of ROS and energy metabolism in diabetes. This newfound knowledge will contribute to future research efforts in the clinical treatment of severe complications such as diabetic foot ulcers and diabetic kidney disease.
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