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Endocrine > Bridges - Endocrine Pancreas > Flashcards

Bridges - Endocrine Pancreas Flashcards

1
Q

What is gluconeogenesis?

A
  • Use of amino acids and fatty acids to generate glucose in the liver
  • Stimulated by GLUCAGON
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2
Q

How does glucose uptake happen in different tissues?

A
  • Passive glucose uptake: brain, liver, kidneys
    1. Higher concentration gradient outside the cell to a lower concentration inside the cell
    2. In the liver, when you are making glucose, the opposite would be happening, i.e., spitting out glucose passively
  • Stimulated glucose uptake: muscle, adipose (via GLUT-4 -> see attached image)
    1. This is still PASSIVE transport -> you just need the transporter to enable this
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3
Q

What are the orders of fuel utilization in fasting and storage in the fed state?

A
  • Energy production (fasting):
    1. Creatine phosphate
    2. Glycolysis
    3. Glycogenolysis
    4. Gluconeogenesis
    5. Fat oxidation
  • Fuel storage (fed state):
    1. Glucose uptake/oxidation
    2. Glycogenesis
    3. Lipogenesis
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4
Q

What are the responses to overfeeding?

A
  • Most of this carbohydrate oxidation is going to occur in the muscle
  • Liver is more for storage than for ATP generation
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5
Q

Why is this image so important?

A
  • Both insulin and C-peptide packaged in IC vesicles, and released at the same time. If you had a defect in this enzyme, you would effectively be T1D
  • If you want to know insulin production in someone taking exogenous insulin, you can measure the C PEPTIDE to see how much insulin they are making
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6
Q

What are the key pancreatic cells? What hormones do they release?

A
  • Beta: insulin
  • Alpha: glucagon
  • Delta: somatostatin
  • Ductal: exocrine
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7
Q

What are the functions of insulin?

A
  • Promotes uptake of glucose from blood into muscle and adipose tissue
  • Enhances synthesis of glycogen and TGs in liver, adipose, and muscle tissue
  • INH gluconeogenesis from non-glucose precursors like amino acids and lipids
  • Promotes glucose breakdown, and prevents lipid breakdown
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8
Q

What causes insulin secretion (molecular pathway: iamge)?

A
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9
Q

What is this?

A

Pancreatic insulin with glucagon (red) and insulin (green) staining

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10
Q

What are the phases of insulin secretion?

A
  • BIPHASIC
    1. First phase: release of pre-packaged insulin
    2. Second phase: need to make and release more insulin
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11
Q

How does insulin stimulate GLUT-4 translocation?

A

Akt

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12
Q

How does insulin promote glycogenesis?

A
  • Allosteric activation
  • Protein dephosphorylation: synthase (more active) and phosphorylase (less active)
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13
Q

How does insulin reduce gluconeogenesis?

A
  • FBPase negatively regulated by F-2,6-BP
  • PEPCK and G6Pase (first two enzymes) inhibited by insulin:
    1. Allosterically
    2. Protein phosphorylation
    3. Transcriptionally repressed: Akt on FOXO (post-translational changes much faster than transcriptional ones)
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14
Q

How is glucagon released? What does it do?

A
  • Secreted from alpha-cells of pancreas
  • Released by low blood sugar levels
  • Acts primarily on LIVER, not muscle or fat
    1. Gluconeogenesis
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15
Q

What is the central transducer of glucagon signaling?

A

PKA: phosphorylates synthase (inactivating it) and phosphorylase kinase (which phosphorylates glycogen phosphorylase, activating it)

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16
Q

How does glucagon promote gluconeogenesis in the short-term?

A
  • Inactivation of phosphofructokinase-2, which normally generates the carbohydrate fructose-2,6,-bisphosphate, a positive regulator of glycolysis and a negative regulator of gluconeogenesis
    1. Remember: insulin INC F-2,6-BP
  • The alleviation of this inhibition allows for promotion of the gluconeogenic metabolism
17
Q

How does glucagon INC gluconeogenesis via transcription?

A
  • More G6Pase, FBPase, and PEPCK
18
Q

How are insulin and glucagon cleared by the body?

A
  • Short 1/2 lives: Insulin 5 min, Glucagon 5-10 min
  • Insulin degradation: 80% in liver, kidney, and the rest in other tissues (target and non-target tissues)
    1. Insulinase: insulin protease that may act when insulin-insulin receptor is internalized
    2. Possible site of drugs to prolong insulin life, and make limited supply last longer
  • Glucagon degradation: most in liver (peripheral concentrations are low)
19
Q

What does insulin do?

A
  • Blocks gluconeogenesis
  • Block glycogenolysis
  • Promotes glycogenesis
  • Enhances glucose uptake
  • Promotes lipid storage
20
Q

What does glucagon do?

A
  • Promotes gluconeogenesis
  • Promotes glycolysis
  • Promotes glycogenolysis
  • NOT really active in muscle and fat
21
Q

What happens to glucose/insulin/glucagon after a meal?

A
  • First: glucose goes up (food)
  • Insulin INC in response to glucose
  • Glucose levels drop
  • Glucagon levels DEC as glucose levels are high, then INC as normoglycemia returns
22
Q

How does the ANS regulate glucagon/insulin?

A
  • SYM: INC glucagon, DEC insulin
  • PARA: INC insulin, DEC glucagon
23
Q

What factors are involved in long-term glucoregulation (graph)?

A
  • As blood glucose drops, these changes are going to happen
  • GH and cortisol are adaptations to chronic hypoglycemia (starvation)
24
Q

What are the incretins? What do they do?

A
  • Enhancers of insulin release (this is why the red curve is so much higher than the blue curve in the graph on the left) -> GUT
  • Sensitize the beta cells to secrete more insulin
  • DPP-4 degrades GLP-1 and GIP
    1. What would it do to insulin and glucose? DEC insulin, INC glucose; also a drug target (e.g., Sitagliptin)

Endocrine (12 decks)

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