Diabetes Mellitus Flashcards
Alternative effects of insulin
Lipoproteins Smooth muscle hypertrophy Ovarian function Clotting Energy expenditure
GLUT-4 Structure Which cells have it? Where are they in cells? Increased number from?
Hydrophobic, outer part sits in membrane
Hydrophilic core= glucose enters into cells
Muscle+ adipose tissue
Membrane, but also lie in vesicles, recruited+ enhanced by insulin
Muscle cell
Proteolysis inhibited by?
Stimulated by?
Protein synthesis stimulated by?
Insulin, amino acids could be used as energy source (gluconeogenic amino acids could go to liver+ used to make glucose)
Cortisol
Insulin, Growth Hormone, IGF1
Liver cell
Glucagon effect?
Insulin effect?
- Gluconeogenic amino acids enter liver, stimulated by glucagon
- Protein synthesis (from aas), stimulated by insulin OR
- Protein lysis (protein to aas), stimulated by protein deficiency or glucagon
- Amino acids could also be converted to glucose, inhibited by insulin, stimulated by glucagon, catecholamines, cortisol= GLUCONEOGENSIS
- Glucose leaves cells into blood
Carbohydrates, Proteins, Fat
Most energy from?
Used for the longest amount of time?
Fat
Fat
Adipocyte
Insulin effect?
- Triglyceride broken down in vessels by lipoprotein lipase, stimulated by insulin= increase glycerol in blood
- NEFA (Non-esterified fatty acids) cross vessel membrane into adipocytes
- Glucose also cross into adipocytes through GLUT-4, stimulated by insulin, can be broken down into NEFAs
- Glucose can also be converted into glycerol-3-phosphate
- Glycerol+ NEFAs combine to form triglyceride in adipocytes, stimulated by insulin
- Triglycerides broken down to glycerol leaves adipocytes, inhibited by insulin, NEFAs also leave adipocytes, stimulated by glucagon, catecholamines, cortisol
Hepatic gluconeogenesis pathway
Know flashcard 4 for all pathways+ more detail
- Glycerol enters hepatocytes, converted to glycerol-3-phosphate
- Glycerol-3-phosphate converted into glucose+ leaves to blood
Energy that brain can/not use
Can use
Glucose
Ketone Bodies
Can’t use
Fatty acids
NEFA conversion to ketone bodies
Glucagon effect?
Insulin effect?
- NEFA enters hepatocyte
- Shuttle on mitchondrial membrane= converted to fatty acyl CoA
- Fatty acyl CoA→ Acetyl CoA→ Aceoacetate→ Acetone+ 3-hydroxybutarate (ketone bodies), inhibited by insulin, stimulated by glucagon
Hepatic glycogenolysis
- Glucose enters hepatocytes, converted to glucose6- phosphate
- Glucose 6 phosphate→ glycogen, stimulated by insulin (reverse reaction stimulated by glucagon, catecholamines)
- Glucose-6-phosphate→ glucose, released into liver
Fatty acids+ Glycogen+ muscle cells
Insulin effect?
- Glucose enters muscle cells by GLUT-4, stimulated by insulin, inhibited by glucagon, catecholamines, cortisol
- Glucose either converted to glycogen or acetyl-CoA
- Fatty acids also enter muscle cells+ can be converted to acetyl CoA
- Acetyl CoA enters TCA cycle for respiration
Muscle can use+ store glycogen but can’t release it again (unlike liver)
Fasted state
Low insulin: glucagon ratio
Increase NEFAs
Low amino acids when prolonged fasting
Increased proteolysis from muscles
Increased lipolysis to glycerol+ fatty acids
Increase HGO from glycogen+ gluconeogenesis
Muscle uses lipids
Brain uses glucose+ later ketones
Increased ketogenesis when prolonged fasting
Fed state
Stored insulin released High insulin: glucagon ratio Stop HGO Increase glycogen Decreased gluconeogenesis Increased protein synthesis in muscles Decreased proteolysis Increase lipogenesis in adipose
Type 1 diabetes presentation
Absolute insulin deficiency Increased proteolysis (increased amino acids)= weight loss Increased lipolysis (increased glycerol+ amino acids) Increased HGO (increased glucose+ ketones)= hyperglycaemia+ glycosuria (glucose in urine) with osmotic symptoms, ketonuria (ketones in urine)
Insulin induced hypoglycaemia
Treatment?
Increased insulin
Increased glucagon, catecholamines, cortisol
Increased growth hormone
Glucose enters muscle
Increased HGO later with glycogenolysis+ gluconeogenesis (gets better)
Increased lipolysis
Intramuscular glucagon
