Quiz 3: Metabolism

• Insulin in a fed state pathway one:

  1. GI tract distention
  2. stretch receptors
  3. increased sensory neural input
  4. CNS
  5. increased parasympathetic output
  6. B-cells in pancreas stimulated
• Insulin in a fed state pathway 2:

  1. GI lumen carbs
  2. endocrine cells in small intestine
  3. GLP1 and GIP
  4. B-cells in pancreas stimulated
• Insulin in a fed state pathway three:

  1. nutrient digestion
  2. increased amino acids and glucose
  3. amino acids stimulate B-cells in pancreas
  4. glucose stimulates a-cells in pancreas
• Insulin secretion could be increased by:

  • increased plasma glucose
  • parasympathetic activation
  • increased plasma amino acids
  • peptides secreted by the small intestine
• Rapid insulin functions in fed state take seconds and increase transport of glucose, amino acids, and potassium into insulin-sensitive cells
• Intermediate insulin functions in fed state takes minutes and works to:

  • stimulate protein synthesis
  • inhibit protein degradation
  • activate glycolytic enzymes and synthase
  • inhibit phosphorylase and gluconeogenesis enzymes
• Delayed insulin functions in fed state takes hours and increases mRNAs for lipogenic and other enzymes
• Liver insulin handles glycolysis, glycogenesis, lipogenesis, and protein synthesis
• Muscle and fat insulin handle glucose transport
• In adipose and resting skeletal muscle, without insulin glucose cannot enter the cell, while with insulin:

  • lipogenesis in adipose is stimulated by G3P
  • hormone-sensitive lipase is inhibited
  • insulin binds > signal transduction cascade > exocytosis (GLUT4) > glucose enters cell
• In hepatocytes (liver) GLUT2 works indirectly with insulin

  • fed state: insulin activates hexokinase to maintain the glucose gradient, which results in glucose trapping
  • fasted state: glucose gradient favors glucose to leave the cell
• type 1 diabetes is when the pancreas stops producing insulin

  • if carbs are ingested, protein degradation and gluconeogenesis increases
  • pancreatic B-cell destruction
  • concordance rate = 33%
  • genetic defect in major histocompatibility complex on chromosome 6
• type 2 diabetes is a resistance to insulin

  • cells cannot respond to insulin
  • concordance rate = 90%
  • genetic defects in glucokinase, insulin molecule, insulin receptor, and GLUT4
• type 1 diabetes causes:

  • increased hyperglycemia
  • increased gluconeogenesis
  • lipolysis and ketogenesis
  • protein breakdown
  • decreased blood pressure
  • circulatory failure
• Primarily on liver, glucagon promotes glycogenolysis, gluconeogenesis, ketogenesis, and lipolysis, while muscle cells lack glucagon receptors