1DDX: LECTURE 50 – APRIL 20TH, 2007

DIABETES MELLITUS

Page 6
Products of glycosylation: damage is permanent. Can’t reverse glycosylation, especially in eyes.
Some nerve sensation may improve with B12. Can help in peripheral nerves

LAB TESTS
Glucose tolerance test: take blood sugar, give bolus of sugar, take blood sugar again. Looks at how well the body can
produce insulin in response to challenge. Good for people with hypoglycaemic symptoms.
Case: 19 year old has fatigue, gets a lot of headaches, just can’t seem to get enough food for energy. Normal weight, but
she forgets about eating, then eats high glycemic foods. Seems to have a problem with the timing of insulin production.
Diabetes has been ruled out. This might be a patient that would benefit from OGTT.

Slide: glucose tolerance curve. Lower is normal, upper is diabetic. If you do a random skin prick test, you have to know
when the person ate. Within 1-2 hours, enough insulin has been released to bring glucose back down to lower (normal)
level. Diabetes (Type 2) the blood sugar stays higher for much longer.
Theory: people tend to gain more weight if blood sugar spikes then drops low (The Zone diet)

Glycosylated Hb
Hemoglobin A: is most Hb in humans. Also A2, F, sickle cell, but A is majority.
A1 is 6-7% of this 90%. The A1C is the part that is glycosylated (60-70% of the A1 amount… get it?)
We all have some glycosylated Hb. Normal is 4-5.9% In someone with poor diabetic control, would see 13-20% HbA1C.
On a lab test, it is given as a percentage. Well-managed diabetes should be around 6-7%.
You are looking at what has happened in the body in the past 120 days (life of a red blood cell). Use this as a way of
regularly monitoring effect of treatment.
Higher concentration of glucose in the blood? Higher % of HbA1C. Want to keep patients in lower ranges.

URINARY KETONES AND GLUCOSE

See this in starvation states and high protein/low carb diet (eg. Atkins diet). Urine is tested for ketone to tell if the body is
burning fat.
Case: 60 year old man on Atkins diet. Loves the diet, on a strict drug regime, he doesn’t cook (orders in all the time).
Liked eating the Atkins bars. He did lose weight, but all of his joints started to hurt. What was happening to him? His
body was very acidic. More prone to injury, tighter muscles. Probably still on the diet. Absolutely resistant to changing
his diet, or to the idea that the diet wasn’t good for him. It worked for weight loss, but it may not be sustainable. Is it good
to be taking in that much protein?

Glucosuria: generally: the DM is not well-controlled, but can also present in other circumstances (gestational diabetes,
renal disease)

DIABETES MELLITUS
(we started with the signs/symptoms of the disease, now we will talk about more details of the disease)

Different types of diabetes: IDDM=insulin dependent diabetes mellitus; NIDDM=non-insulin-dependent diabetes mellitus
Secondary: can be secondary to stress/trauma.

IDDM
Will definitely be producing ketones (unlike in NIDDM). They don’t have any insulin. Islet cells destroyed.

NIDDM
Don’t tend to develop ketosis as they have some insulin in body, just resistant. Insulin prevents this pathway from
happening.

GESTATIONAL DIABETES MELLITUS

What would make you suspect it in a pregnant woman?
Has she had it before? Is she prone to fainting? Diabetes in the family? Birth weight of the previous child (over 9-10 lbs)?
Did she have previous miscarriages (baby not carried to term)?
What happens? Mother has anti-insulin hormone, secreted by placenta (human chorionic somatomammotropin). More
glucose is available to the baby so it grows larger.

DDX LECTURE 50, APRIL 20TH, 2007 – PAGE 1

MAIN FEATURES OF DIABETES

Pancreas info: FYI (but probably good to know where the insulin and glucagon comes from)
Closely associated with the blood stream (the hormones have to get in to the blood stream)
Immune response to beta cells, doesn’t seem to affect other cells, specific to betas.

Insulin: secreted when you eat.

3 main targets of insulin are LV, muscle, fat.

“Low insulin activity”: leads to problem with weight gain. Harder to lose weight. Activity of insulin on the cells in lower
than normal, but there is enough insulin in the blood to suppress lypolysis. (meaning that blood levels of insulin are not
low, but the effect that the insulin has on the cells is lower, due to impaired receptors)
Type 2 is multi-faceted: insensitivity, but can also be destruction of beta cells in long term.
Glucagon: SNS activity.

TYPE I: IDDM
Person is not producing insulin. Auto-immune illness. T-cell infiltrates. (other mechanisms: see slide)

TYPE II: NIDDM

Hallmark: weight gain.
Catch type 2 early? Can respond very well to dietary management.
(Book: The diabetic cure. Extreme, strict diet, few grains, lots of fruits and veggies, but seems to make a difference)
Often found at screening, otherwise patient is asymptomatic.

2 categories of NIDDM:
Type A: have defect in insulin receptor
Type B: have Ab to insulin receptor

Glut-2: this is the transporter that brings glucose into the cell. Insulin brings it to cell surface.
Amylin: starts to be produced I the pancreas, impairs the secretion of insulin.

Higher correlation with Type II in identical twins thank in Type 1

DDX LECTURE 50, APRIL 20TH, 2007 – PAGE 2