Flashcards in type 2 DM Deck (10):
What is the significance of impaired glucose tolerance and impaired fasting glucose?
intermediate phase in the development of type 2 DM
incr. risk of CVD
incr. risk of neuropathy and microvascular complications (retinopathy, nephropathy)
What are the goals of treatment for type 2 DM?
HbA1C < 7% is the primary goal
also fasting glucose 70-130 mg/dl and post-prandial glucose under 180
What are some factors that contribute to the pathogenesis of type 2 DM?
obesity- reducing obesity can reverse insulin resistance
but, beta cell mass matters too- obese people with high beta cell mass don't really get DM
As insulin sensitivity decreases, you will start to see a hyperbolic relationship to beta cell activity (but beta cell activity will increase)
Eventually, thought, the curve will shift- there will be insulin resistance without beta cell compensation
insulin resistance doesn't really change over the course of the disease- but secretion does.
How is glucose taken up by body from blood?
in some places, uptake is glucose independent (brain)
to sense glucose, pancreatic cells use GLUT2 receptors. liver also uses GLUT2
GLUT4 receptors are insulin dependent and are found in muscle, fat and heart
What are some causes of insulin resistance?
obesity, esp. due to visceral adiposity and inflammation, physical inactivity (also prevents insulin-independent uptake of glucose by muscles), high fat diets, meds, glucose and lipid toxicities, aging, genetics
inflammation is imporrtant- some effect of anti-inflammatories in DM
What does fasting plasma glucose reflect?
endogenous glucose production. if fasting plasma glucose is down, first phase glucose is also down?
If you want to control HbA1C, when do you need to control glucose levels?
post-prandially- esp. below HbA1C of 8, fasting glucose levels are relatively unimportant
What is pre-diabetes?
fasting plasma glucose 100-125 mg/dl
or 2 hr post prandial glucose 140-200 or HbA1C 5.7-6.4
What is GLP-1
released from L cells in ileum and colon and stimulates insulin response form beta cells
inhibits gastric emptying
reduces food intake and body weight
inhbits glucagon secretion from alpha cells in a glucose-dependent manner
effect diminished in DM type 2