Biochemistry-Feast Starve Cycle Flashcards
In the intestine, you are absorbing massive amounts of glucose. What prevents all of that glucose from being phosphorylated?
During glycolysis hexokinase in under feedback inhibition by glucose-6-P in all tissues but the liver. As more glucose gets phosphorylated, hexokinase gets inhibited.
How does pyruvate go to alanine?
Note that it is a readily reversible reaction.
What is normal glucose level after an overnight fast? After a meal? With diabetic dehydration?
5 mM. 8 mM after meal. 10 mM with diabetic dehydration.
Where does blood glucose come as you fast?
1-4 hours: exogenous. 3-24 hours: liver glycogen begins to break down. 8 hours on: gluconeogenesis enzymes induced in liver as glycogen stores wane.
How does muscle help you get to the starting point for gluconeogenesis?
Muscle protein is broken down to amino acids and pyruvate. Pyruvate is converted to Ala via transamination and sent to the liver for nitrogen metabolism. Another transamination reaction creates pyruvate from alanine and pyruvate enters gluconeogenesis and the free NH3 enters the urea cycle.
What organ provides all essential amino acids to the tissues?
Muscle
What cells die in patients with type I diabetes?
Beta cells in the pancreas
What are the effects of insulin secretion during the well-fed state?
Increased glucose transport into adipose and muscle. Glycogen synthesis in liver and muscle, inhibition of glycogen breakdown. De novo triglyceride synthesis in liver and fat deposition, inhibition of triglyceride breakdown. Protein synthesis, inhibition of protein breakdown.
What are the effects of glucagon secretion during the fasting state?
Glycogenolysis in the liver, lipolysis in fat and gluconeogenesis in the liver.
What cells release glucagon during the fasting state?
Alpha cells in the pancreas.
What happens in the intestine, liver, brain, RBCs, muscle and adipose during the fed state?
INTESTINE: carbohydrate digested to glucose, fat digested to TGs and packed into chylomicrons that go into the lymph, protein digested to AA. Blood glucose levels rise, bind to beta cells in pancreas, insulin levels rise. LIVER: receives glucose and AAs via portal circulation from intestine. Liver glycolysis, glycogen synthesis and de novo fat synthesis are switched on by insulin. BRAIN: receives glucose, astrocytes send lactate to neurons. RBC: glucose goes in to produce ATP and lactate. MUSCLE: GLUT-4 allows glucose in and glycogen stores are replenished and glucose is used for energy. ADIPOSE: chylomicrons reach LPL at the adipose surface, they are broken down to fatty acids and transported into adipose tissue and they are reassembled into triglycerides. ALL TISSUES: amino acids are used to resynthesize proteins.
What are the insulin sensitive tissues?
Liver, muscle and adipose tissue all have insulin receptors. Binding to this receptor affects metabolic pathways.
What molecules are responsible for carrying fat away from the liver?
VLDL
What component of our body is the major contributor of lactate to the blood? Why do you get lactic acidosis in people with liver disease?
RBCs contribute lactate because they do not have mitochondria and can only gain ATP by taking glucose to lactate. The liver takes lactate and converts it to pyruvate and sends pyruvate through gluconeogenesis. This is why you get lactic acidosis with liver disease.
What is the insulin-sensitive glucose transporter found in adipose tissue and muscle?
GLUT-4.
What happens in the liver, brain, RBCs, kidney, muscle and adipose during the fed state?
Low blood glucose cause secretion of glucagon by the alpha cells in the pancreas. LIVER: glucagon stimulates glycogenolysis, glucose is released into the blood. Converts excess fatty acids to ketone bodies. Performs gluconeogenesis and gets rid of nitrogen by urea cycle. Receives glycerol from fatty acid breakdown and routes it to gluconeogenesis. BRAIN & RBCs: receive glucose and ketone bodies (brain) from liver. ADIPOSE: glucagon stimulates breakdown of triglycerides to fatty acids, fatty acids are distributed to all tissues. MUSCLE: receives ketone bodies. Protein is broken down to Ala, Ala is sent to liver for gluconeogenesis. KIDNEY: secretes urea.
What are the ketone bodies?
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When do ketone bodies become useful as an alternative fuel for the brain?
They rise to an appropriate level after a few days of starvation. The brain will outcompete other tissues for ketone bodies because it induces ketone body receptor expression. At this point, gluconeogenesis becomes less important and muscle will be spared.
How does insulin affect each of these processes?
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How does glucagon affect each of these processes?
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