NURS 165 Study Guide - Final Guide: Polyphagia, Dyslipidemia, Hypoglycemia
Diabetes Pathophysiology Study Guide
• Normal glucose
o Big polar hydrophilic molecule → can’t get across plasma membrane
▪ Enters via facilitated diffusion via GLUT transporter
▪ Against gradient w/ SGLT & sodium
o GLUT 2 is on liver cells
▪ After eating, it transports glucose into the cell
▪ During fasting, these liver cells make glucose
• Gluconeogenesis
• Glycogenolysis
• These pathways raise glucose in cell → so, it diffuses
out of cell w/ concentration gradient
• Now, that transporter facilitates glucose leaving cell
o GLUT 4 is on muscle cells
▪ GLUT 4 is a special transporter that is sensitive to insulin
▪ Person eats → glucose & insulin increase → GLUT 4 inserted
into muscle cells to take up glucose → glucose moves into cell
• When insulin isn’t present, GLUT 4 isn’t inserted and
blood glucose isn’t taken up!
▪ Remember: GLUT 2 on liver cells, GLUT 4 on muscle cells!
o Normally, there is no glucose in urine
▪ Glucose that enters renal tubules is removed by sodium-
glucose transport proteins
• There are normally enough glucose transporters to
control this
• BUT, when not enough transporters OR too much
glucose, kidneys get overwhelmed → glucose in urine
o Glucose is major energy source for cells!
▪ Glucose cycle – G6P → pyruvate → acetyl CoA → Krebs → ETC
• Anabolism = energy storage
o Insulin controls storage of dietary fuels – HOW?
▪ Glucose uptake, glycogen synthesis
▪ Breakdown of glucose that isn’t used for glycogen → more
Acetyl CoA
▪ Oh btw this happens in liver – shown below
find more resources at oneclass.com
find more resources at oneclass.com
o Acetyl CoA from excess glucose synthesizes triglycerides → forms
VLDLs
o Triglyceride uptake via lipoproteins to adipose
LOOK AT THIS PICTURE IT’S V HELPFUL!!
☺
o GLUT 4 NEEDS insulin; GLUT 2 is FASTER with insulin
o Lipoprotein lipase: breaks down triglycerides from VLDLs and
chylomicrons → fatty acids that diffuse into adipocyte → re-form
triglycerides
▪ Insulin promotes this activity (fat storage)
▪ Think why people on insulin can gain weight!
• Catabolism – Energy Release
o Producing G6P and then removing the phosphate → free glucose
▪ Hepatic glucose production depends on this
o When G6P enters cells, it gets trapped
▪ But this is reversible in liver, due to G6P enzyme
o ALL CELLS: Glucose + Phosphate → glucose-6-phosphate
▪ Liver cells can carry reverse reaction
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Vldls: triglyceride uptake via lipoproteins to adipose. Look at this picture it"s v helpful!: glut 4 needs insulin; glut 2 is faster with insulin, lipoprotein lipase: breaks down triglycerides from vldls and chylomicrons fatty acids that diffuse into adipocyte re-form triglycerides. Increase uptake of amino acids and protein synthesis. Inhibited by: glucose and insulin, glucagon-like-peptide-1 (glp 1, glucagon acts primarily on the liver. Inc. glycogenolysis (to raise bg) so this makes sense: when insulin isn"t there more glucagon high bg. Insulin normally has paracrine effect, inhibiting glucagon: well duh because steroids like cortisol and epinephrine power you through stressors so they need glucose in the blood and not up-taken by cells, cortisol, steroid anti-insulin. Epidemiology: type 1 is all over the world, now, more type 2 cases are being diagnosed, family history both types, but now more with type 2, recessive gene, genetics of type 2.
