Title: Diabetes Mellitus Types I
1Diabetes Mellitus Types I II
- James Bresnahan, MS1
- Robert Gyory, MS1
2Introduction
- How does your body make use of glucose from the
food you eat? - What is the difference in etiology between type 1
and type 2 diabetes? How does this affect
treatment? - What is the homeostatic balance between insulin,
glucose, glucagon, and stress hormones? How does
this differ between nonaffected individuals vs.
type 1 diabetics vs. type 2 diabetcs? - Why does high blood glucose cause other
complications? - What are some psychosocial considerations
regarding diabetes?
3(No Transcript)
4Glycogen is a good form of storage. Its
condensed, easily broken down, and its byproducts
are used efficiently to make energy.
I thought T1DM is about insulin?
a-1,6-linkage
a-1,4-linkage
5Without insulin
6How do you get Type 1 Diabeetus?
- No!!
- T1DM is AUTOIMMUNE.
- Destruction of Pancreatic B-islet cells.
- What about T2DM? Ask Rob..
7What are B-Islet cells? How are they destroyed?
- Genetic predisposition
- Environmental stimuli
- Lead to antibodies that attack pancreatic Beta
cells
- Diagnosis is bimodal with peaks at 4-6 years and
10-14 years - 3M2F??
- 23.6 per 100,000 per year.
8What are the general effect
9Clinical Presentation
10How do you treat T1DM?
? Future?
11How do Endocrinologists monitor their diabetic
patients over long periods of time?
12So, high glucose is bad, what about low glucose?
-Low blood glucose is FAR more detrimental in
terms of short term problems. -Diabetic coma due
to Neuroglycopenia - Glucagon is released by
a-cells in RESPONSE to b-cells not making insulin
(a sign of high BG.) If B-cells are destroyed,
a-cells cant release glucagon.
13Future ways to monitor T1DM?
- http//www.youtube.com/watch?vw0aalblWfjU
- Take into consideration different ethical issues
ranging from cost of supplies/equipment to the
mental demands of current T1DM patients.
14Diabetes Mellitus Type II
15But first, a biochemical interlude
Downregulation vs. Upregulation
Adapted from the common domain of Cornell
University
16The mechanism of DM II is a complex sequence of
biochemical processes
- Diet high in fat and carbohydrates sedentary
lifestyle ? highly elevated plasma glucose - Chronically ? plasma glucose ? chronic
overstimulation of ß cells and chronic
hypersecretion of insulin - Chronic hypersecretion of insulin ? down
regulation of insulin receptors on adipocytes and
skeletal muscles
17Down regulation of insulin receptors exhibits a
number of negative consequences
- ? glucose uptake by cells
- ? glucose for cells to use for energy
- ?? plasma glucose
- Can cause relatively minor symptoms or serious DM
I type symptoms
Adapted from the University of Arizona Dept. of
Biological Sciences
18What are the consequences of decreased glucose
for cellular energy?
- Cells begin to burn fats for energy.
- Can cause pH problems (DKA)
- Inefficient fuel source leads to fatigue, low
energy, etc. - Important Glucose uptake is severely decreased,
but not nonexistent as in DM I
19What are the consequences of elevated plasma
glucose?
- DM Type I Symptoms
- e.g. polyuria, polydypsia, glycosuria, etc.
- Hypertrophy of ß cells
- Extremely chronic hyperstimulation can lead to ß
cell destruction - Leads to insulin dependence
Beta cells stained in green
20What are the symptoms of Type II diabetes
mellitus?
- Some patients may be asymptomatic for many years
- Others experience lighter versions of many of the
symptoms of diabetes mellitus I - Rarely, DKA and other complications can occur
such as hyperosmotic coma - Why do these symptoms differ from DM I when their
mechanisms of pathogenesis are so similar?
21How is DM II diagnosed?
- Chronically high fasting plasma glucose
- Elevated glycated hemoglobin pattern (HbA1C)
- In difficult cases, insulin immunoassay
22Treatments for DM II are widely variable
- For most people, diets lower in fats and
carbohydrates coupled with exercise will correct
the down-regulation of insulin receptors - Others need medications such as biguanides and
sulfonylureas (e.g. metformin) to decrease
endogenous glucose production - Severe cases in which beta cells have been
destroyed will need to supplement with insulin - insulin dependent diabetes
23Biguanides versus sulfonylureas
- Biguanides
- Metformin
- Phenoformin
- Buformin
- Proguanil
- Sulfonylureas
- Carbutamide
- Tolbutamide
- Chlorpropamide
- Acetohexamide
- And others.
24The prognosis and sequelae of DM II are very
similar to DM I
- In well controlled diabetics, there are very few
resulting problems - With poor control, however
- Poor circulation ? vascular disease and
cardiovascular problems - Neuropathy
- Other metabolic dysfunctions
- If a person controls their condition well, they
can either live an asymptomatic life or go into
remission altogether - With poor control, however
- Myocardial infarction, stroke, blindness,
amputation, degenerative brain disorders, renal
failure, death
25Diabetes mellitus II is one of the most
preventable disease in our society
- Obesity is the number one predictor of DM II
- Healthy diet and plenty of exercise are needed
- Patient education!!!
- Prior patient knowledge about the various genetic
and medical factors that can increase DMII
predisposition
26Systemic Insulin Regulation
27How do hormones and other factors regulate
insulin?
28The following hormone pathways work to help
regulate the action of insulin
- Epinephrine and cortisol inhibit insulin and
increase secretion of glucagon in the pancreas - HPA axis
- Growth hormone directly acts on the pancreas to
cause glucagon secretion - Glucagon inhibits insulin secretion and causes
biochemical effects that are opposite those of
insulin
29Other friends that youve met throughout the year
that effect insulin secretion
- ? insulin secretion
- Thyroxine and T3
- Norepinephrine
- Low ATP
- And others
- ? insulin secretion
- High ATP
- Somatostatin
- Leptin
- And others
30Learning objectives for this lecture
- Review the biochemistry, pathology, and medical
treatments of diabetes mellitus 1 and 2 - Provide a general overview of biochemical
dysfunction, resulting metabolic derangement,
compare and contrast the risks and sequelae, and
discuss the treatments for both diseases and why
treatments are specific to only one disease and
not the other - Discuss the utility of HbA1c measurement as a
method of monitoring treatment efficacy - Discuss patient, doctor, and psychosocial issues
surrounding diabetes mellitus - Discuss the prevalence of diabetes mellitus, long
term risks to patients, and cost of care issues - Discuss quality of life issues
- Discuss the importance of primary prevention in
diabetes mellitus 2