• Insulin stimulates glucose uptake by muscle and adipose tissue, where glucose is converted to G6P
• in liver it activates glycogen synthase and inactivates glycogen phosphorylase, so that much of the G6P is tacked onto glycogen
• in the liver it activates both the oxidation of G6P to pyruvate via glycolysis and oxidation of pyruvate to acetyl CoA
• acetyl coa can be used instead for fatty acid synthesis and sent to adipose tissue and converted to Triaglyserols when exported out of the liver
• ultimately, insulin favors the conversion of excess blood glucose to glycogen in liver and muscle, and triaglycerol in adipose tissue

•  glucose enters blood from the intestine after carb-rich meal, which increases insulin secreation and decreases glucagon secretion by the pancreas.
• release of insulin is essentially controlled by glucose levels
• glucose regulates insulin secretion in beta cells:
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• hours after carbohydrate intake, blood glucose levels fall because of oxidation of glucose and other tissues
• low glucose levels triggers secretion of glucagon and decreases insulin release
• it stimulates the breakdown of liver glycogen by activating glycogen phosphorylase and inactivating glycogen synthase; both of these are regulated by phosphorylation of enzymes which is controlled by cAMP
• inhibits glycolysis in liver and stimulates gluconeogenesis, both of which are stimulated by lowering [fructose 2,6-bisphosphate], an allosteric inhibitor of the gluconeogenic enzyme FBPase-1 and an activator of PFK-1. this is ultimately controlled by cAMP dependent phosphorylation
• glucagon inhibits glycolytic enz. pyruvate kinase (promotes its cAMP dependent phosphorylation), blocking conversion of PEP to pyruvte and preventing oxidation of pyruvate via TCA cycle
• accumulation of PEP favors gluconeogenesis. this is augmented by stimulation of the synthesis of gluconeogenic PEP carboxykinase
• glucagon ultimately helps liver export glucose to the blood and lets other tissues use glucose. all these are mediated by cAMP dependent protein phosphorylation

• four hours after meal, insulin secretion is slowed, glucagon goes up and triagycerols now become th primary fuels for the muscle and liver
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• acetyl coa regulates pyruvate; it allosterically inhibits pyruvate dehydrogenase and stimulates pyruvate carboxylase

• epinephrine and norepinephrine increase the flow of O2 to the tissues
• act mostly on the muscles, adipose, and liver tissues
• activates glycogen phosphorylase and inactivates glycogen synthase by cAMP dependent phosphorylation of the enzymes, converting liver glycogen to glucose...used for muscular work
• promotes anaerobic breakdown of muscle glycogen by lactic acid fermentation, forming ATP.
• glycolysis is stimulated by increasing [frucose 2,6 BP], an allosteric activator of PFK1
• also stimulates fat mobilization in adipose tissue, activating (by cAMP dependent protein phosphorylation) hormone sensitive lipase
• ultimately, epinephrine stimulates glucagon secretion and inhibits insulin secretion, reinforcing its effect of mobilizing fuels and inhibiting storage

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Plasma concentrations of ketone bodies and glucose during fasting

• glucose begins to diminish after 2 days of fasting.
  
• The level of ketone bodies rises dramatically after 2 to 4 days of fasting
  
• water-soluble ketones, acetoacetate and β-hydroxybutyrate, supplement glucose as an energy source during a long fast.
  
• Fatty acids cannot serve as a fuel for the brain; they do not cross the blood-brain barrier
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