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Hyperglycemia causes
hypertension, neuropathy, retinopathy.
Hyperglycemia
high blood glucose levels resulting from the body not producing enough insulin
hyperinsulinemic-euglycemic clamp
tests how sensitive the body is to insulin by injecting insulin through an IV to a controlled level. At the same time, glucose is dosed as needed to keep the blood glucose level normal.
Triglyceride
three fatty acids and glycerol
Types of Cellular Receptors
Ion channel receptor, nuclear receptor, G-protein coupled receptor, receptor tyrosine kinase.
Ion channel receptor
Ligand opens ion channel
Nuclear receptor
Ligand binds transcription factor
G-Protein Coupled receptor
Ligand causes GTP-binding proteins to activate enzyme
Functions of GTP
provides energy when hydrolyzed to GDP +P, on/off switch for G proteins
GTP Translation
GTP-powered factors help the ribosome move along mRNA and bring aminoacyl-tRNAs into the ribosome as protein is made.
GTP Cell migration
GTPases help regulate cytoskeletal changes
GTP Intracellular Trafficking
GTPases help vesicles bud, move, dock, and fuse with the correct organelle
Neuromuscular primary function
contraction
Neuromuscular secondary function
Locomotion, ventilation, protection, thermoregulation, glucose storage.
Myopathies
movement disorders, immobility, death.
Malignant hyperthermia
Certain anesthesia drugs can make susceptible muscles get stuck in overdrive: they cannot relax, they burn fuel extremely fast, and the body overheats
Malignant hyperthermia symptoms
increase in co2 (Hypercapnia), muscle rigidity, acidosis, temperature increase, Tachycardia
Correlation
Do A and B occur together?
Necessary
Do we need A for B to occur?
Sufficient
Can A cause B?
Independent variable
What you intentionally change
Dependent variable
What you measure the result of
Depolarization
Na+ influx, inside of cell becomes more positive. Higher concentration outside the cell.
Repolarization
K+ efflux, inside of cell becomes more negative, higher concentration inside the cell
Neurotransmitter signalling and Cellular control of insulin
In both beta cells and presynaptic neurons, membrane depolarization opens voltage-gated Ca²⁺ channels. Ca²⁺ influx then triggers secretory vesicles to fuse with the plasma membrane and release their contents by exocytosis