Vascular maladaptations to chronic disease and physical inactivity

Abstract

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Physical inactivity due to increases in modern conveniences and access to cheap, high calorie foods have greatly contributed to the "obesity epidemic" frequently discussed in society today. Health consequences associated with obesity such as Type II diabetes (T2DM), metabolic syndrome, coronary artery disease (CAD), etc., greatly increase the morbidity and mortality rates in those constituting the obesity epidemic. Angiopathy is one of the putative primary causes of the morbidity and mortality in subjects with T2DM and CAD. Loss of the regulatory role of the vascular endothelium is a crucial initiating factor in the development of T2DM angiopathy and CAD. Consequently, understanding the physiological ramifications and underlying mechanisms for vascular dysfunction resulting from these disease states is essential for their treatment and prevention. Numerous studies exist highlighting the importance of regular physical activity and exercise on prevention of T2DM angiopathy and CAD. The following studies were conducted to investigate: Chapters 1-2) the effect of physical inactivity on vascular function and proteins during T2DM disease progression; Chapters 3-4) the effect of adipose tissue on vascular function in a CAD model; and Chapter 6) (supplemental) brief discussion on vascular function responses to angiotensin II in T2DM and role of superoxide in T2DM angiopathy.