Description
Diabetes mellitus (DM) is a disease characterized by chronically elevated levels of glucose in the bloodstream. Glucose is a form of sugar that is used as fuel by the body’s cells. Blood glucose levels are usually tightly controlled and regulated through a negative feedback system. When this system fails, however, glucose can accumulate in the bloodstream. This system failure typically results from insufficient insulin release due to malfunctioning pancreatic beta cells or the body has developed a resistance to insulin. Excessive glucose accumulation contributes to chronic inflammation and the hardening of blood vessels in the body. This inflammation contributes to a multitude of debilitating health issues such as neuropathy, nephropathy, retinopathy, renal failure, and/or gangrene of the limbs. Additionally, DM is the 7th leading cause of death in the United States and its treatment comes with a significant economic deficit. While there is currently no cure, pharmaceuticals, dietary modification, physical activity, and weight control are the four main approaches for DM intervention and control. These four approaches each operate to regulate glucose using different biological pathways in order to reduce and regulate blood glucose levels. These pathways include improving insulin sensitivity and correcting pancreatic beta cell function. The purpose of this paper will be to provide an overview of type II diabetes mellitus (T2DM) as well as to review the physiological mechanisms involved with glucose control and finally to discuss the use and effectiveness of the main interventional approaches used with the treatment of T2DM: pharmaceuticals, dietary control, physical activity and weight control.
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Details
Title
- TYPE II DIABETES MELLITUS: INTERVENTIONS FOR BLOOD GLUCOSE CONTROL
Contributors
- Woods, Jessica M (Author)
- Swan, Pamela (Thesis director)
- Larson, Rachel (Committee member)
- College of Health Solutions (Contributor)
- Barrett, The Honors College (Contributor)
Date Created
The date the item was original created (prior to any relationship with the ASU Digital Repositories.)
2019-05
Resource Type
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