NST 160 MT 2
Glu 6 Phosphate - ANS-Either stored as Glycogen in liver/muscle or channeled into
mitochondria & TCA cycle for energy production
First response to Hypoglycemia - ANS-Insulin DECREASED
Second response to Hypoglycemia - ANS-Glucagon INCREASED
Third response to Hypoglycemia - ANS-Epinephrine increased
IMPORTANT WHEN GLUCAGON IS LOW
stimulates glucose production and fatty acid release from adipose
Fourth response to Hypoglycemia - ANS-Cortisol/GH
IMPORTANT SIGNAL WHEN HYPOGLYCEMIA LASTS LONGER THAN 4 HOURS
downregulates insulin, reduces uptake, limits glucose utilization
Beta cells - ANS-secrete insulin, within the islet
Islets - ANS-Cluster of cells in the pancreas
-made up of insulin secreting beta cells and glucagon secreting alpha cells
Glu 2 Transporter - ANS-transports glucose into liver and beta cells
FENESTRATION - ANS-Fenestrated endothelium of the blood vessels in the islets
allows for better access to blood flow, helps with sensing of glucose in the blood
Insulin Synthesis - ANS-Synthesized as a large amino acid (86 AA)
--> proteolytically cleaved in the ER = proinsulin
--> generates C peptide, insulin A and B--> secreted by beta cells
C peptide - ANS-A cleaved portion of proinsulin that is a gr10 biomarker for insulin
because it is cleared slowly as compared to regular insulin
-Good reflection of endogenous insulin production
SIRT1 and insulin - ANS-SIRT1 increases amount of insulin from a given amount of
glucose
INHIBITS UCP2, SIRT1 directly binds to the UCP receptor, blocking UCP2, enhancing
insulin secretion
, Knocking out Sirt1= high UCP2
UCP2 inhibits ATP, ATP needed to secrete insulin
UCP2 - ANS-REGULATED BY SIRT 1
Causes defect in insulin secretion
Knocking out UCP2 restores insulin secretion, regardless of decreased sirt1
Food deprivation induces UCP2
Amyloid Polypeptides - ANS-come from beta cells
co-secreted w/ insulin
can aggregate (like in AD) and cause beta cell death
2 phases of insulin secretion - ANS-1. vesicles in cell close to membrane fuse, release
of insulin
2. vesicles inside of cell need to be transported to the membrane= slower release
Glucose transports - ANS-Facilitated transporters, active uptake SGLT1, Glu
Facilitated transport - ANS-takes up glucose continuously because hex kinase
phosphorylates glucose
Active Uptake - ANS-SGLT1s, sodium coupled glucose transporters, re-utpake for
glucose that has been filtered out from intestine and kidneys
Glu transporters - ANS-Brings glucose into cells to secrete insulin
Lipid metabolism & insulin - ANS-High levels of fatty acids can trigger release of insulin,
insulin increases LPL, generating FFA, allowing for transport of FFA into adipocytes -->
lipid droplets --> reesterification, SUPPRESSES release of FFA
Diabetes & insulin - ANS-Insulin can't suppress FFA release, no insulin= fasting
response, constant release of FFA, development of ketone bodies
Ketoacidosis - ANS-In Type 1 diabetes & fasting mode
Liver wants to drive gluconeogenesis
Can't feed acetyl CoA into TCA cycle because no oxoloacetate
Acetyl CoA turned into ketone bodies= KETOSIS= drop in blood pH
-HYPERglycemia
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