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Diabetes Mellitus Types I


Diabetes Mellitus Types I & II James Bresnahan, MS1 Robert Gyory, MS1-Insulin is a peptide hormone released by the pancreas (next ). When insulin receptors are ... – PowerPoint PPT presentation

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Title: Diabetes Mellitus Types I

Diabetes Mellitus Types I II
  • James Bresnahan, MS1
  • Robert Gyory, MS1

  • 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
  • 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
  • What are some psychosocial considerations
    regarding diabetes?

(No Transcript)
Glycogen 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?
Without insulin
How do you get Type 1 Diabeetus?
  • No!!
  • Destruction of Pancreatic B-islet cells.
  • What about T2DM? Ask Rob..

What are B-Islet cells? How are they destroyed?
  • Genetic predisposition
  • Environmental stimuli
  • Lead to antibodies that attack pancreatic Beta
  • Diagnosis is bimodal with peaks at 4-6 years and
    10-14 years
  • 3M2F??
  • 23.6 per 100,000 per year.

What are the general effect
Clinical Presentation
How do you treat T1DM?
? Future?
How do Endocrinologists monitor their diabetic
patients over long periods of time?
So, 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.
Future 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.

Diabetes Mellitus Type II
But first, a biochemical interlude
Downregulation vs. Upregulation
Adapted from the common domain of Cornell
The mechanism of DM II is a complex sequence of
biochemical processes
  1. Diet high in fat and carbohydrates sedentary
    lifestyle ? highly elevated plasma glucose
  2. Chronically ? plasma glucose ? chronic
    overstimulation of ß cells and chronic
    hypersecretion of insulin
  3. Chronic hypersecretion of insulin ? down
    regulation of insulin receptors on adipocytes and
    skeletal muscles

Down 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
What 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

What are the consequences of elevated plasma
  • 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
What are the symptoms of Type II diabetes
  • 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?

How is DM II diagnosed?
  • Chronically high fasting plasma glucose
  • Elevated glycated hemoglobin pattern (HbA1C)
  • In difficult cases, insulin immunoassay

Treatments 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

Biguanides versus sulfonylureas
  • Biguanides
  • Metformin
  • Phenoformin
  • Buformin
  • Proguanil
  • Sulfonylureas
  • Carbutamide
  • Tolbutamide
  • Chlorpropamide
  • Acetohexamide
  • And others.

The prognosis and sequelae of DM II are very
similar to DM I
  • Sequelae
  • Prognosis
  • 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

Diabetes 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

Systemic Insulin Regulation
How do hormones and other factors regulate
The 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

Other 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

Learning objectives for this lecture
  1. Review the biochemistry, pathology, and medical
    treatments of diabetes mellitus 1 and 2
  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
  3. Discuss the utility of HbA1c measurement as a
    method of monitoring treatment efficacy
  4. Discuss patient, doctor, and psychosocial issues
    surrounding diabetes mellitus
  5. Discuss the prevalence of diabetes mellitus, long
    term risks to patients, and cost of care issues
  6. Discuss quality of life issues
  7. Discuss the importance of primary prevention in
    diabetes mellitus 2
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