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39 Cards in this Set
- Front
- Back
Fed
|
glucose from dietary carbs
|
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Fasting
|
glucose from glycogen stores (primary source)
glucose from new synths (secondary source) |
|
Starving
|
glucose from new synths
glucose is scarce |
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What is the ideal amount of daily glucose?
|
70 - 100 mg/dL for RBC and brain
|
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Hyperglycemia
|
macrovascular complications:retinopathy, neuropathy, nephropathy
microvascular:stroke, cardiovascular disease to much glucose |
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Hypoglycemia
|
CNS symptoms:headache, confusion, slurred speech, seizures, coma, death
too low blood glucose levels |
|
Fatty acids are broken down into?
|
ketone bodies in the liver
|
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Glucose, fatty acids, and ketone bodies are oxized to produce?
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ATP
|
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What signals metabolic states?
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glucose
|
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How is glucose availability communicated?
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via the synthesis of hormones
|
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Fed state signal
|
synthesis of insulin in the beta cells of the pancreas
tells organs that high levels of glucose are in circulation |
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Fasting state/starvation signal
|
synthesis of glucagon in the alpha cells of the pancreas
tells organs that low levels of glucose are circulating |
|
Glycolysis
|
oxidation of glucose
results in ATP |
|
Lipolysis
|
degradation of fat stores (triacylglycerols)
release fatty acids |
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Glycogenolysis
|
degradation of glycogen stores
release glucose |
|
Ketolysis
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oxidation of ketone bodies
results in ATP |
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B-oxidation
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oxidation of fatty acids
results in ATP |
|
Glycogenesis
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synthesis of glycogen stores
stores glucose |
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Lipogenesis
|
synthesis of fat stores
stores fatty acids |
|
Gluconeogenesis
|
new synthesis of glucose from nonsugars
produce glucose |
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Ketogenesis
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synthesis of ketone bodies from fatty acids
produce ketone bodies |
|
Insulin in the liver
|
stimulates: glycolysis, fatty acid synthesis, glycogenesis
|
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Insulin in muscle
|
glucose xport into cells, glycogenesis, protein synths, amino acid xport into cells
|
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Insulin in adipose
|
glucose xport into cells, lipogenesis
|
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Insulin in brain/RBCs
|
NO EFFECT!!
|
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Active pathways in Brain during fed state
|
glycolysis (ATP from glucose)
|
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Active pathways in RBCs during fed state
|
glycolysis (ATP from glucose)
|
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Active pathways in Liver during fed state
|
glycolysis, glycogenesis (storage of gluc), fatty acid synths
|
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Active pathways in Adipose during fed state
|
glycolysis, lipogenesis (storage of fatty acids from the liver VLDLs & dietary chylomicrons)
|
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Active pathways in muscle during fed state
|
glycolysis, glycogenesis, prot synths
|
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Active pathways in Brain during fasting state
|
glycolysis
ketolysis (ATP from ketone bodies) glucagon has no effect on brain |
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Active pathways in RBCs during fasting state
|
glycolysis
glucagon has no effect on RBCs |
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Active pathways in Liver during fasting state
|
energy ATP from fatty acids
ketogenesis, gluconeogenesis, glycogenolysis, B-oxidation glucagon causes gluconeog, glycogenoly |
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Active pathways in Adipose during fasting state
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ATP from fatty acids
lipolysis, B-oxidation glucagon causes lipolysis |
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Active pathways in Muscle during fasting state
|
energy from fatty acids & ketone bodies
B-oxidation, ketolysis, prot degradation glucagon has NO EFFECT on muscle |
|
What is the bodies source of glucose during starvation?
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glycogen stores are depleted
gluconeogenesis only source of blood glucose brain uses ketones for glucose during starvation |
|
Fasting
|
equal level of ketone bodies and fatty acids
|
|
Starvation
|
more ketone bodies used than fatty acids
muscle switches to fatty acids for fuel |
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Diabetes Mellitus
|
high blood glucose is interpreted as low blood glucose
Fed state is interpreted as fasting/starvation absence of endogenous insulin or absence of insulin response Hyperglycemia |