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Flashcards in Diabetes Deck (16)
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Type 1 diabetes

-juvenile diabetes
- genetic/ environmental component
- underlying mech involves autoimmune desruction of insulin prod beta cells
-5-10% of diabetes


Type 2 diabetes

Adult onset (50% are obese)
-insulin resistant skeletal muscle
-90-95% of diabetes


complications T2DM

- lower limb amputation
-kidney failure
-cognitive dysfunction


symptoms of T2DM

-fatigue (not braking down energy sources)
-extreme thirst (to dialate glucose)
- extreme hunger
- lean body loss


flow or how muscle atrophy+ decreased insulin signaling happens due to T2DM

metabolic acidosis
increase FFA
Inflammation (IL6, TNfa)
increase glucose

all lead to decreased insulin signaling


normal insulin signaling

-when insulin binds to receptors phosphate sites open + autophosphorylation occurs
- IRS gets phosphorylates and activates P13K which converts PIP2 to PIP3
-PIP3 phosphorylates PDK1 which goes to AKT
-AKT travels to AS160 which dissociates from GLUT4


Non normal insulin signaling

-FFA will come into cell and block IRS1 and increase ROS which blocks P13K
-both cause PIP2 not to become PIP3
TNFa allso activates IKK which blocks IRS1


Ischemia affects

increase ROS, Ca, Calpain, H+, decrease ATP, inhibition of oxidative phosphorylation


reprofusion affects

increase ROS, Ca, Calpain, Caspase-3, opens MPTP which leads to cell death


both ischemia and reprofusion lead to

mitochondrial injury and cardiac cell death due to necrosis and apoptosis


exercise effects on CVD

- increase parasympathetic regulation protecting against ischemia-reprofusion injury
-promotes muscle derived myokines
-can improve myocardial regeneration capacity
- can reverse loss of muscle mass/strength
-angiogenesis (coronary collaterization)


Mediators for cardioprotection

- NO increases vasodialation (less likely for obstruction)
-HSP- increase immediatly following ex, protects pro from ROS
-ER stress pro- protects from calcium overload
cystolic antioxidants- fight against free rads in mitochondria
SODI1/2- found in matrix of mito, converts reactibe O2 rto H2O2


Endurance training effect against I-R injury

increases SOD2 which alters mito turnover and phenotype which provides cardio protection


Heart failure + symptoms

when heart is unable to pump sufficiently to maintain bf to the body
-shortness of breath, fatigue, swelling in legs, rapid/irregular heart beat


2 types of heart failure

HF w/ preserved ejection fraction
- stiff and thick chambers, maladaptive

HF w/ reduced ejection fraction
-stretched and thin chambers, can fill heart just not strong enough to pump blood out


cardiovascular improvement w endurance/Hiit

-increase Vo2 max
-decrease resting HR
-Increase LV size
-improved systolic and diastolic lv function