Diabetes Flashcards
what percentage of the population has diabetes
8.3%
what percentage of people older than 60 have diabetes
26.9%
what are the 3 effects of inability to move glucose form ciruclation into energy stories
- energy stores are not refilled after a meal, tissues are chronically starved
- high conc of glucose in the circulation damages blood and renal vessels
- high osmotic pressure of extracellular fluids leads to dehydration of tissues
what are the 3 main chronic morbiditeis with diabetes
blindness
nephropahthy
neuropathy
what percentage of cases of diabetes are type 1
10-20%
what are major risk factors for type 2 diabetes
central obesity
sedentary lifestyle
what usually leads to the onset to type I diabetes
viral infection that causes immune system to turn on insulin producing cells
what do drugs that treat type II diabetes do
stimulate insulin secretion
sensitize peripheral tissues to insulin
reduce intestinal absorption of glucose
repress gluconeogensis
how does insulin sensitivity change during pregnancy
its downregulated to allow for fetal metabolism to compete for glucose
how does insulin increase glucose permeability of plasma membranes
increase number of GLUT4 receptors
how does insulin affect fatty acid homeostasis
stimulate synthesis of fatty acids adn triglycerid
repress fat mobilization in adipose tissue by inhibiting HSL
how does high glucose conc affect protein
spontaneous glycation of protein
when do you see sorbitol
when high conc of glucose, polyol pathway generates sorbitol from glucose
why is sortibol dangerous
it’s osmotically active, draws water into cells, changes cell structure
what does the polyol pathway drain
NADPH pool
how do you get sorbitol to change into fructose
polyol dehydrogenase
when do you get nonketotic hyperosmolar syndrome or hyperosmolar hyperglycemic state
type 2 diabetic with dehydration and hyderglycemia affecting the CNS
what can hyperglycemia cause in extremem cases
non0ketotic hyperglycemin hyperosmolar coma (NKHHC)
how does insulin affect potassium
stimulates K+ uptake into cells, so you get a drop in serum potassium
incrase in serum lipoproteins and fatty acids during hyperlipidemia is due to what two factors
- expression of LPL is regulated by insulin, absence of LIPL are not released from chylomicrons and VLDLs
- absence of inuslin, HSL stays active, so aipocytes keep releasing FAs into ciruclation.
how does insulin affect ketons
represses ketone body production
when would a type I diabetic experience hypoglycermia
accidently overdosing
what forms insulin
pre-proinsulin by proteolytic processing
where is mature insuline stored
secretory vesicles
what does insulin bind to on the target cell
kinase insulin recptor
what does the kinase insule receptor do
phosphorylates itself and IRS1
what does the initial phosphorylation reactive activate
kinase cades
how does insuline affect glycogen synthase
increase glycogen synthesis
how does insulin affect phosphorylase kinase
decrease glycogen degration
how does insulin affect glycogen phosphorylase
decrease glycogen degradation
how does insulin affect pyruvate dehydrogenase, pyruvate kinase, and PFK2
incrase glycolysis
how does insulin affect fructose 26 bisphosphate
decrease gluconeogensis
how does insulin affect acetyl-CoA carboxylase
increase FA synthesis
how does insulin affect HMG-CoA reductase
incrase cholesterol synthesis
how does insulin affect hSL
decrease mobilization of fat
how does insulin affect carntine acyltransferase
decrease ketogensis