Bastyr University

Poorly Controlled Type 2 Diabetes Mellitus

Dawn Dailidenas, Mickinzie Lopez, Mindy Lu, Stephanie Michael, Cheryl ODell
Macronutrients & Research Methods, Bastyr University, Kenmore, WA

Introduction
Type 2 diabetes mellitus (T2DM) is characterized by insulin
resistance and beta cell dysfunction, resulting in
metabolically altered pathways relating to glucose
metabolism in the brain, liver, adipose, pancreas, and skeletal
muscle.
Signs & Symptoms (NDIC, 2008)
Fatigue
Polyuria
Polyphasia/Polydipsia
Weight loss
Blurred vision
Slow wound healing

Methods/Questions
We performed an in-depth literature review analyzing peerreviewed case studies, scientific journals, textbooks, and
government agencies such as the American Diabetes
Association (ADA) to investigate the implications of
uncontrolled T2DM and determine the most effective forms
of treatment.

Skeletal Muscle

Questions that we considered include:

Reduced glucose uptake and metabolism.

How is the metabolism altered in this condition?

Liver

What treatment is typically applied?

Increased circulation of free fatty acids lead to fatty liver

Results

Treatment
In addition to diet and exercise, poorly controlled T2DM
requires medication and other interventions.
The initial prescription drug is predominantly Metformin,
followed by other anti-diabetic prescriptions to reduce
HbA1c levels.

Genetic predisposition
Women with history of gestational diabetes

Diabetes Disease Management Programs (DDMP) result in

improved glycemic control and health-related quality of
life (HR-QOL) (Rasekaba, 2012).

Pre-diabetes
Diagnosis (NDIC, 2011)

Random glucose test: >200 mg/dL

Impaired glucose uptake (Kirk, 2013).

Inhibition of gluconeogenesis and glycogenolysis leads to

hyperglycemia.

Overweight, sedentary

Glucose tolerance test: >200 mg/dL

Hypoinsulinemia leads to decreased translocation of

GLUT 4 (Kirk, 2013).

What happens metabolically and where?

Risk Factors

Blood glucose level test: a fasting glucose >126 mg/dL

Results

Pancreas
In response to high levels of glucose, beta cells release
more insulin (Kirk, 2013).
Overworked beta cells lead to dysfunction (Kirk, 2013)
Brain
Removal of appetite regulation leads to difficulty
controlling dietary habits (Gropper, 2013).
The vagus nerve continues to signal hepatic glucose
output, contributing to hyperglycemia (Gropper, 2013)
Adipose
Lipogenesis continues (Gropper, 2013)
Circulating free fatty acids and proinflammatory
chemokines bind to receptors, leading to insulin resistance
(Kirk, 2013)

Some patients may require subcutaneous insulin

injections (Sirnivasan, 2008).

Discussion
BLURB