GLYCOGEN PATHWAYS
Glycogenolysis =
Glycogenolysis = breakdown of glycogen into glucose monomer
Glycogenesis
= glycogen synthesis = addition of glucose monomers to form polymer
Glycogenolysis 2
Glycogenesis 2
= glycogen synthesis = addition of glucose monomers to form polymer
• Glucose converted to glucose-6-phosphate
Hormonal regulation of glycogen pathways
1.
Hormonal regulation of glycogen pathways
For fight-or-flight:
Gluconeogenesis
USED TO RAISE BLOOD SUGAR***
Not all cells do this, happens mostly in the liver. Happens at the same time probably as break down of glycogen* when haven’t eaten in a while, definitely breaking down glycogen, our next move would be to do gluconeogenesis
Gluconeogenesis Steps
Many steps are same as in glycolysis but reverse direction=
Three steps are not simply the reverse of glycolysis:
Pyruvate → PEP
Fructose 1,6 – bisphosphate → fructose 6-phosphate
Glucose 6-phosphate → glucose
Pentose Phosphate Pathway
Alternative pathway for glucose metabolism
G6P is not broken down to produce ATP
Pathway is primarily anabolic, not catabolic
Occurs in cytoplasm, especially in liver and adrenal cortex
Pentose Phosphate Pathway 2
Cells do this pathway for two main reasons:
Protein Metabolism
Proteins can hydrolyzed into amino acids and then deaminated
Deamination = amino group removal
Deaminated amino acids can feed into glycolysis as pyruvate
Deaminated amino acids can feed acetyl CoA formation
Deaminated amino acids can feed into TCA as α-ketoglutarate or oxaloacetate
Amino groups from amino acids are incorporated into urea for excretion
Deamination means=
Deamination = amino group removal
Lipids
Lipids = a non-polymer class of macromolecule
Examples include fatty acids, mono-, di-, and triacylglyerols (triglycerides)
Triglycerides can be metabolized into glycerol and fatty acids
Glycerol enters glycolysis
β-oxidation breaks fatty acids into 2C pieces, then converted to acetyl CoA → TCA
Other examples of lipids: sterols and sterol esters (e.g., cholesterol); waxes; tocopherols (Vitamin E)
Fatty acid catabolism
Fatty acids are prepared for beta-oxidation in the mitochondrial matrix
In order to enter the matrix, most fatty acids require the carnitine shuttle
Carnitine shuttle
The carnitine shuttle consists of three steps:

Beta-oxidation 1
Beta-oxidation = breakdown of fatty acids
** beta odication puts carbonyl group on beta carbon, that is the same thing as 3-hydroxyacly-CoA, so beta-hydroxy aclycoa and 3-hydroxylacl-coa are the same thign!

Beta-oxidation 2
Beta-oxidation of saturated, even-chain fatty acids (as acyl-CoA’s) proceeds in 4 steps:
• Yield: 1 NADH

Odd Chain fatty acids
Odd-chain fatty acids are broken down to acetyl-CoA molecules and propionyl-CoA

Ketone Bodies
An alternate energy source
Can be especially important for the brain
Produced under conditions of low caloric intake or carbohydrate restriction
Produced in the liver, in the mitochondria
Produced from acetyl coA
Excess acetyl coA cannot be used directly in Krebs because there’s not enough oxaloacetate to react with it
High levels of circulating ketone bodies make blood more acidic
Ketone bodies enter the Krebs cycle as acetyl-CoA
Where are ketone bodies produced?
Produced in the liver, in the mitochondria
Produced from acetyl coA
Excess acetyl coA cannot be used directly in Krebs because there’s not enough oxaloacetate to react with it
ketone bodies are used directly by the brain. if really really in a pinch brain has a way to use ketone bodies, prefers glucose but it can use ketone bodies plan B. CANNOT use fatty acids*** so have to have fatty acids broken down into acetyl-coa, aceyl-co gets turned into ketone bodies and that in turns supplies hte brain
Why does the body turn acetyl-CoA into ketone bodies when glucose-starved?
Acetyl CoA can’t be circulated for two reasons: it’s a high energy compound and it’s labile. So it’s not a stable form for circulation to tissues. Also acetyl coA cannot cross cell membrane.
Ketone bodies are an alternate fuel source. More importantly, they are water soluble analogs of fatty acids. This is important since, during starvation there is fat breakdown and excess fatty acids circulate in blood. However, fatty acids cannot be used by brain as fuel since, they cannot cross the blood brain barrier. Liver by producing ketone bodies helps brain cells during starvation.
Also, these ketone bodies, as such, can be used by other tissues as well. There by other tissues refrain from using glucose. Hence, ketone bodies have a glucose-sparing effect. This glucose will be available for tissues like brain and red cells for use.
ketoacidosis
Extreme form → ketoacidosis (also called ketosis)
Seen in uncontrolled diabetes
Identifiable as the smell of acetone on the breath
three kinds of ketones bodies are:
acetoacetate, beta-hydroxybutyrate, and acetone
= made from acetyl coa, issue say someone eats a very high fat diet, ton of acetyl coa waiting to get into krebs cycle, but not a lot of acetyl coa can enter krebs cycle immediately, each acetyl coa needs an oxoloactate! So oxoloactate is limiting, so only so much acetyl coa waiting in line to enter krebs cycle, huge traffic jam and then coenzyme A, big molecule not good to have a lot of that soaked up acetyl coa sitting there twiddling thumbs to get into krebs cycle, so from that body makes ketone bodies instead*
acetone
