Integration of metabolism
17 important questions on Integration of metabolism
What does cholecystokinin (CCK) do?
What does glucagon-like peptide 1 (GLP-1) do?
What is the key regulator of leptin and adiponectin?
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What is type 1 diabetes mellitus?
* Insulin-dependent diabetes
What is type 2 diabetes mellitus?
Which pathways contribute to insulin resistance?
Mitochondria are not capable of processing all of the fatty acids by B oxidation; fatty acids accumulate in the mitochondria and eventually spill over into the cytoplasm. They reincorporate into triacylglycerols.
How does ATP depended insulin release work?
What is the molecular mechanism behind type 1 diabetes?
Insulin is deficient, so the entry of glucose in adipose and muscle cells is impaired.
The liver becomes stuck in a gluconeogenic and ketogenic state.
The excessive level of glucagon relative to that of insulin leads to a decrease in the amount of fructose 2,6-bisphosphate, which stimulates glycolysis and inhibits gluconeogenesis.
An excessive amount of glucose is produced by the liver and released into the blood.
Water accompanies the excreted glucose (through urine) so the patient is hungry and thirsty. Because of the ketone body production, the pH also drops.
Why is there ketone production in diabetes?
Large amounts of acetyl CoA are then produced by B oxidation. However, much of acetyl CoA cannot enter the citric acid cycle because there is insufficient oxaloacetate for the condensation step. So the cells generate ketone bodies.
How does muscular activity help to prevent diabetes?
The increase in fatty acid oxidizing capability and additional mitochondria allow for the efficient metabolism of fatty acids. Because an excess of fatty acids results in insulin resistance, efficient metabolism of fatty acids results in an increase in insulin sensitivity.
How is an optimal mix of fuels achieved during a marathon?
- Fatty acids enter muscle, where they are degraded by B oxidation to acetyl CoA and then to CO2.
- The elevated acetyl CoA level decreases the activity of pyruvate dehydrogenase complex to block the conversion of pyruvate into acetyl CoA.
- Fatty acid oxidation decreases the funneling of glucose into the citric acid cycle and oxidative phosphorylation.
- Glucose is spared so that just enough remains available at the end of the marathon.
How is the blood-glucose concentration kept at or above 4.4 mM during fasting?
2. The release of fatty acids by adipose tissue
3. The shift in the fuel used from glucose to fatty acids by muscle
Describe what happens in the refed state
- The liver does not initially absorb glucose from the blood, but leaves it to other tissues instead. The liver even remains in a gluconeogenic mode. The newly synthesized glucose is used to replenish the liver's glycogen stores. As the blood-glucose concentration continues to rise, the liver completes the replenishment of its glycogen stores and begins to process the remaining glucose for fatty acid synthesis.
What are the dominant metabolic processes during starvation?
- Gluconeogenesis by the liver
How do organs yield energy from ketone bodies?
What happens after the depletion of the triacylglycerol stores?
Describe the metabolism of ethanol and what happens to the body after excessive drinking.
Ethanol + NAD+ --> Acetaldehyde + NADH + H+
2. Aldehyde adehydrogenase
Acetaldehyde + NAD+ + H2O --> Acetate + NADH + H+
Ethanol consumption leads to an accumulation of NADH.
- High concentration of NADH inhibits gluconeogenesis by preventing the oxidation of lactate to pyruvate > lactate accumulates > hypoglycemia and lactic acidosis.
- High concentration of NADH inhibits fatty acid oxidation. The excess of NADH signals that conditions are right for fatty acid synthesis > triacyglycerols accumulate in liver > fatty live
- NADH inhibits citric acid regulatory enzymes > accumulation Acetyl CoA > prododuction ketone bodies > acidosis. Buildup acetaldehyde (insufficient processing)
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