Molecular Basis of Type 2 Diabetes Flashcards Preview

Repro-Endo > Molecular Basis of Type 2 Diabetes > Flashcards

Flashcards in Molecular Basis of Type 2 Diabetes Deck (15)
Loading flashcards...

What did the experiment with giving insulin and galactose to dogs show?

Insulin increases the volume of distribution of galactose.


What does insulin actually do to lower blood glucose?

Increases number of Glut4 receptors on the surface of muscle, fat, and heart cells.
(uptake by muscle has largest effect on blood glucose)


Is exercise useful in diabetes if there isn't weight loss?

Yes! (and in you, too) Exercise stimulates glucose uptake without insulin, and makes cells more sensitive to insulin.


What is the "euglycemic insulin clamp"?

Infusion of insulin, keep giving glucose to keep blood glucose constant.


Is fasting hyperglycemia only caused by not enough uptake of post-prandial glucose?

No. The liver is also producing more glucose.


How does insulin (and lack thereof) affect adipcytes' handling of lipids?

Insulin drives adipocytes to take up glucose and store it as fatty acids. If insulin isn't present, more free fatty acids (FFAs) get released (which may contribute to CV disease).


What does increased FFA secretion form adipose tissue cause to happen in the liver?

Increased FFAs stimulates triglyceride production in the liver, and export as VLDL (and then LDL).


The liver releases triglycerides both when fed and fasting. What's the difference between the processes in these two states?

Fasting: FFAs released from adipose go to liver (processed to VLDL/ketones).
Fed: FFAs are built from glucose in the liver.


Effect of insulin resistance on triglyceride (TG) production/export from liver?

More insulin resistance -> more TGs in the blood.
(this doesn't make sense unless you assume that the adipose is insulin-resistant, but the liver remains insulin-sensitive)


What is meant when people hypothesize that insulin resistance in the liver could be selective?

Liver fails to downregulate gluconeogenesis in response to insulin.
But, the liver continues to make TGs in response to insulin.
(compounded with insulin-resistant adipose cranking out more FFAs for the liver to use to make TGs)
(Occam's razor. Just sayin'.)


Is BMI a useful measure of adiposity at the individual level?

No! Stop emphasizing your patients' (and your) BMI. When a whole population's BMI goes up, that tells you something.


Is a big belly or a big booty better?

A big booty, of course.
Sir Mix-a-Lot was ahead of his time.


Are serum fatty acids and intracellular TGs associated with insulin resistance?

Yeah. But...


What's a relevant difference between a lean person's adipose and an obese person's adipose?

The obese person's adipose is full of macrophages, inflammatory stuff.


What is some speculation as to the purpose of inflammation of shutting off insulin signaling?

Adipose secreting inflammatory cytokines mimics infection.
If there's an infection, body wants to shunt energy away from insulin-induced anabolism toward the immune system.