Metabolic Syndrome Flashcards
intra-abdominal adiposity
elevated TGs, LDL, bp, bg, inflammation
decreased HDL’s
precursors of CV disease + type II diabetes
abd obesity: (men) >40 in waist circumference (women) >35 inch
bp>/= 130/85
TG>/=150
HDL: (men) <40 (women) <50
fasting bg: >/= 100
diagnose metabolic syndrome
increase waist circumference=
increase CHD risk
secretory products of adipose tissue that are risk factors for CVD
Adipokines
2 beneficial products of adipose tissue
Adiponectin and estrogen
driving force for metabolic syndrome
abdominal obesity
increase in visceral mass=
increase insulin resistance and can lead to type II diabetes
normal response of increased glucose after a meal:
- pancreas releases insulin
- insulin to target tissues (liver, muscle)
- GLUT-4 brings glucose in
- decrease blood glucose
when there is an increase in glucose after a meal, what does the liver do
stop making glucose
when there is an increase in glucose after a meal, what does the muscle do
converts glucose to glycogen(store) or ATP (energy)
when there is decreased glucose in blood what does pancreas beta cell do
at resting state w/ Kach channel open
when there is an increase in blood glucose, what does pancreas do (6 steps)
- glucose binds GLUT-2 on beta cell
- glycolysis and TCA—> ATP
- increase ATP closes Kach channel
- beta cell depolarized
- Ca2+ channel opens and Ca2+ influx
- insulin released
normal response of insulin at target tissue (liver, muscle) (5 steps)
- insulin binds receptor
- receptor dimerizes
- Tyr residues w/ IRS1 phosphorylate
- GLUT-4 translocation and glucose in
- glycogen synthesis too
what happens to insulin during metabolic syndrome
resistant and doesn’t bring glucose in
signaling that occurs w/ excess adipose tissue (4 things)
- release of pro-inflammatory factors and ROS
- insulin binds IRS-1
- SER residues phosphorylate
- Ang II phosphorylates SER
no GLUT-4 translocation