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CPB 25: Dietary States and Metabolic Processes

Discuss organ inter-relationships in the fed and fasting states

  ‘Fed state’  –  ↑ Plasma glucose, amino acids, triglycerides

  Control: ↑ Insulin: secretion by the pancreas 

  Response: Anabolic (building of small to larger)

o  Liver: makes glycogen, proteins and triglycerides (VLDL)

  Carbohydrate: ↑Glycogen synthesis, glycolysis, hexose-monphos path 

  ↓Gluconeogenesis 

  Fat: ↑ Fatty acid and triglyceride synthesis 

  Amino-acid: ↑ Amino acid degradation and protein synthesis

o  Adipose: makes triglycerides

  Carbohydrate: ↑ Glycolysis, hexose-monophosphate path, glucose

transport to adipocytes

  Fat: ↑ Fatty acid and triglyceride synthesis o  Muscle:

  Carbohydrate: ↑ Glycogen synthesis and glucose transport

  Fat: FA’s are less important than glucose as fuel 

  Amino-acid metabolism: ↑ Protein synthesis and uptake of BCAA 

o  Brain 

  Carbohydrates: Brain uses only glucose as fuel (↓ glucose = problems) 

  Fats: Very little triglycerides in brain (FA cant cross blood-brain barrier)

  ‘Fasting state’  –  ↓ Plasma glucose, amino acids, triglycerides

  Control: ↓ Insulin: secretion by the pancreas 

  Response: Catabolic (breaking down of large to small)o  Liver 

  Carbohydrate: ↑Gluconeogenesis (creating glucose from pyru. lact, etc.) 

  ↑ Glycogenolysis (breakdown of glycogen) 

  Fat: ↑ β-oxidation of FA and ketogenesis

o  Adipose:

  Carbohydrate: Glucose uptake reduced, reducing FA/TG biosynthesis

  Fat: ↑ Triglyceride breakdown and FA release, ↓ uptake of FA 

o  Muscle:

  Carbohydrate: ↓ Glucose uptake (low insulin levels) 

  Fat: Week 1-2, FA and KB used as fuel, after 3rd

 only FAs  Amino-acid metabolism: Week 1: rapid proteolysis provides AA for

gluconeogenesis; reduces as brain begins to use KB as fuel.

o  Brain 

  First Days of fasting: Glucose as fuel, blood glucose maintained by

hepatic gluconeogenesis from AA precursors of muscle (Cori cycle)

  2-3 weeks of fasting: Plasma KB rise, brain begins to metabolize KB as

well as glucose. Reduces the need for muscle proteolysis.

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Describe hormonal participation in tissue /substrate integration

  Insulin: ↓ Glycogenolysis, gluconeogenesis, ketogenesis 

o  Activate another protein kinase which causes dephosphorylation 

  Glucagon and Epinephrine: ↑ Glycogenolysis, gluconeogenesis, ketogenesis 

o  Activate cAMP-dependant protein kinase A promoting phosphorylation 

Describe the nature of Type II Diabetes (pathophysiological example)

  Reduced insulin production and end organ resistance

  Onset in adulthood (obesity usually associated with it )

  Accounts for 90% of diagnosed diabetes cases

  Managed by diet, exercise, oral hypoglycaemic drugs (+/- insulin)

Untreated Type II Diabetes

1.  Hyperglycaemia  –  increased hepatic gluconeogenesis, decreased peripheral glucose use

**Ketosis is minimal/absent in type II because of low levels of insulin ↓ ketogenesis

2.  Hypertriglyceridaemia  –  The amount of Fas being released swamps the capacity of β-

oxidation and ketogenesis. Excess FAs converted to TGs which are packaged and

secreted as VLDL by the liver.

*Type I –  no insulin secretion at all (hyperglycaemia, ketosis, hypertriglyceridemia, diabetic

ketoacidosis)