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39 Cards in this Set
- Front
- Back
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Fed
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glucose from dietary carbs
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Fasting
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glucose from glycogen stores (primary source)
glucose from new synths (secondary source) |
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Starving
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glucose from new synths
glucose is scarce |
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What is the ideal amount of daily glucose?
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70 - 100 mg/dL for RBC and brain
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Hyperglycemia
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macrovascular complications:retinopathy, neuropathy, nephropathy
microvascular:stroke, cardiovascular disease to much glucose |
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Hypoglycemia
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CNS symptoms:headache, confusion, slurred speech, seizures, coma, death
too low blood glucose levels |
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Fatty acids are broken down into?
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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
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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
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synthesis of glucagon in the alpha cells of the pancreas
tells organs that low levels of glucose are circulating |
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Glycolysis
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oxidation of glucose
results in ATP |
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Lipolysis
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degradation of fat stores (triacylglycerols)
release fatty acids |
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Glycogenolysis
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degradation of glycogen stores
release glucose |
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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 |
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Glycogenesis
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synthesis of glycogen stores
stores glucose |
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Lipogenesis
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synthesis of fat stores
stores fatty acids |
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Gluconeogenesis
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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 |
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Insulin in the liver
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stimulates: glycolysis, fatty acid synthesis, glycogenesis
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Insulin in muscle
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glucose xport into cells, glycogenesis, protein synths, amino acid xport into cells
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Insulin in adipose
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glucose xport into cells, lipogenesis
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Insulin in brain/RBCs
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NO EFFECT!!
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Active pathways in Brain during fed state
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glycolysis (ATP from glucose)
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Active pathways in RBCs during fed state
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glycolysis (ATP from glucose)
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Active pathways in Liver during fed state
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glycolysis, glycogenesis (storage of gluc), fatty acid synths
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Active pathways in Adipose during fed state
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glycolysis, lipogenesis (storage of fatty acids from the liver VLDLs & dietary chylomicrons)
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Active pathways in muscle during fed state
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glycolysis, glycogenesis, prot synths
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Active pathways in Brain during fasting state
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glycolysis
ketolysis (ATP from ketone bodies) glucagon has no effect on brain |
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Active pathways in RBCs during fasting state
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glycolysis
glucagon has no effect on RBCs |
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Active pathways in Liver during fasting state
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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
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energy from fatty acids & ketone bodies
B-oxidation, ketolysis, prot degradation glucagon has NO EFFECT on muscle |
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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 |
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Fasting
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equal level of ketone bodies and fatty acids
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Starvation
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more ketone bodies used than fatty acids
muscle switches to fatty acids for fuel |
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Diabetes Mellitus
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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 |
