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Hi everyone,

I'm new to this forum but have found reading the posts here very helpful for my studying.

I have two related questions from both NBME 12 and 13:

the first question was (nbme 12): "a previously healthy 7 year old girl is brought to the physician by her parents because of a 1- month history of excessive urination; she has also had a 2.3 kg weight loss... fruits odor to breath....high blood serum glucose concentration....
the question asks "what is most likely to be decreased?"
A. arterial PCO2
B. Arterial PO2
C. serum acetone concentration
D. serum K+ concentration
E. serum triglyceride concentration
F. serum BUN

anyways so we know shes in ketosis, but isn't there increased activation of lipoprotein lipase, increased breakdown of triglycerides, therefore increased ketones?

Why are triglyceride levels not decreased for this reason?

NBME 13: "a 48 year old man comes to the physician because he is concerned about his weight....lab values show fasting serum glucose and insulin that are increased and remain increased 2 hours after the patient receives 75 g of glucose. Which lab values is found in the patient's serum?"

So there is a chart with arrows up and down, and apparently this is the answer:

A. triglycerides increased, HDL-cholesterol decreased, free fatty acids increased

again, can someone please explain the lipid profile in diabetics and also in ketosis?

thank you!
 

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Hi everyone,

I'm new to this forum but have found reading the posts here very helpful for my studying.

I have two related questions from both NBME 12 and 13:

the first question was (nbme 12): "a previously healthy 7 year old girl is brought to the physician by her parents because of a 1- month history of excessive urination; she has also had a 2.3 kg weight loss... fruits odor to breath....high blood serum glucose concentration....
the question asks "what is most likely to be decreased?"
A. arterial PCO2
B. Arterial PO2
C. serum acetone concentration
D. serum K+ concentration
E. serum triglyceride concentration
F. serum BUN

anyways so we know shes in ketosis, but isn't there increased activation of lipoprotein lipase, increased breakdown of triglycerides, therefore increased ketones?

Why are triglyceride levels not decreased for this reason?

NBME 13: "a 48 year old man comes to the physician because he is concerned about his weight....lab values show fasting serum glucose and insulin that are increased and remain increased 2 hours after the patient receives 75 g of glucose. Which lab values is found in the patient's serum?"

So there is a chart with arrows up and down, and apparently this is the answer:

A. triglycerides increased, HDL-cholesterol decreased, free fatty acids increased

again, can someone please explain the lipid profile in diabetics and also in ketosis?

thank you!
first one is decreased arterial pco2 ,as we know in diabetic patient due to built of acetone there is decrease in ph, and is compensated by hyperventilation so called kusumal breathing.so you exaling alot of co2 out .
second
one as we know in diabetic patient they are resistant to insulin .though there is enough glucose in blood stream it cant be reached to different tissue whuch are glucose dependent example skeletal muscle,so despite high glucose body sense as hypoglycemia leads to release of stress hormone like epinephrine which break down fatty acid stored in adipose tissue and skeletal muscle resulting increase in triglyceride.
hope it clear to some extent .
 

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Question Number 1:

Like you said LPL increases the breakdown of triglycerides but that is to breakdown the triglycerides from VLDLS and Chylomicrons and then store them in the tissue. So basically LPL does anabolism by storing fats in tissue and we all know that INSULIN is the hormone of anabolism.So insulin deficiency in Q1 will lead to less function of LPL so the Triglycerides from VLDLs,IDLs etc wont be utilized anymore by the tissue so when doing serum triglyceride level it will increase.

Answer is A arterial PCO2

A. arterial PCO2
The patient suffers from ketoacidosis a type of metabolic acidosis and we all know to deal with metabolic acidosis the body tries to hyperventilate to get rid of CO2 which is resp alkalosis. So PCO2 decreases

B. Arterial PO2
Not affected

C. serum acetone concentration
Acetone and other ketoacid levels will increase in the blood due to more utilization of Fatty acids which occurs due to actiavtion of hormone sensetive lipase by glucagon and absence of insulin

D. serum K+ concentration
Remember how glucose enters the beta cells of islet of langerhans and cause insulin release by Atp production which causes retention of K+ ions in the cell so low insulin means more K+ ion leaving the cell so increased serum K+ levels

E. serum triglyceride concentration
See my logic above it will increase

F. serum BUN
This one is a guess but from what I think Diabetics cannot use glucose as a main source of energy so will use proteins to and more the breakdown of protein the more urea formation

Question Number 2:

Insulin is high but the person is resistant to insulin, means the receptors are underegulated or modified so that cannot detect insulin anymore.

No effect of insulin ---> High triglycerides
No effect of insulin will also trigger the stress hormones like glucagon,epinephrine etc and they will stimulate the hormone sensitive lipase and cause breakdown of triglycerides in the adipose tissue to release free fatty acids into the bloodstream.

Hope this helps :cool:
 

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I am Confused

But wait this is confusing,
You are saying the following

"No effect of insulin ---> High triglycerides
No effect of insulin will also trigger the stress hormones like glucagon,epinephrine etc and they will stimulate the hormone sensitive lipase and cause breakdown of triglycerides in the adipose tissue to release free fatty acids into the bloodstream."

So you are saying there is increased triglycerides in the first line and then you are saying decreased triglycerides in the second line, how does that work?
I thought HSL (Hormone Sensitive Lipase) is inhibited by insulin which in type 2 diabetes there is insulin so HSL should be inhibited and fat breakdown should be inhibited as a result. Can you clarify what is really going on in type 2 diabetes when there is insulin but there is resistance to it (and by the way in type 2 diabetes there is resistance to insulin is to GLUT4 but not to HSL)
 
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