HLSC 2110U Lecture 5: Study Notes - Lecture 5
2 Feb 2019
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Glucose comes from:
1. Diet
2. Glycogen (liver and muscle)
3. Gluconeogenesis (glucose made from amino acids and fatty acids)
- If glucose is not available in the diet then glycogen is used, if glucose is not available from diet and
glycogen then gluconeogenesis happens
Summary of Glycolysis
- Glucose molecule is split into 2 pyruvate molecules
- Pyruvate is the precursor of acetyl-CoA that starts the CAC
- C6H12O6 + 6O2 → 6CO2 + 6H2O + energy
Intro to Glycolysis
- Catabolism of various compounds including lipids, CHOs, and proteins, includes the breakdown
of each and ends with a molecule integrating itself into the central metabolic cycle (TCA) which
is linked to the electron transport chain
Transport of Glucose into Cells
- Glucose cannot move into cells alone
- Sodium-independent facilitated diffusion transport system (mediated by family of 14
glucose transporters in cell membranes)
- Follows a concentration gradient
Tissue-specific GLUT Isoforms
- GLUT-1 → abundant in RBCs and brain, low in adult muscle
- GLUT-3 → primary glucose transporter in neurons
- GLUT-4 → abundant in adipose tissue and skeletal muscle, insulin increases its expression
- GLUT-2 → found in liver, kidney, and pancreas; either transport glucose into cells or out of cells
depending on glucose concentration
- GLUT-5 → transporter of fructose in SI and testes
- GLUT-7 → expressed in liver and other gluconeogenic tissues, mediated glucose flux across ER
membrane
Glycolysis
- First step in the breakdown of glucose
- Takes place in the cytoplasm of prokaryotes and eukaryotes
- 2 distinct phases
- 1. uses ATP to split glucose into 2 G-3-P molecules
- 2. G-3-P molecules are converted into pyruvate and ATP and NADH are produced
- If cell cannot catabolize pyruvate further, then only 2 ATP molecules will be had from 1 glucose
- This happens in RBCs
- Pivotal to carb metabolism because all sugars can be converted to glucose
- In cells with mitochondria and adequate oxygen, pyruvate is the end product of aerobic
glycolysis
- Oxygen is need to re-oxidize NADH in the oxidation of G-3-P
If Oxygen is Present
- Ends with oxidative decarboxylation of pyruvate to acetyl CoA
If Oxygen is Absent
- Pyruvate is reduced to lactate as NADH is oxidized to NAD+
- Called anaerobic glycolysis which allows ATP production in cells without mitochondria (RBCs) or
when oxygen level is insufficient
Reactions of Glycolysis
- Phosphorylation of glucose into G-6-P
- 1st irreversible step
Glucokinase D
- a.k.a. hexokinase D or type IV
- In liver parenchymal cells and islet cells of pancreas
- Responsible for phosphorylation of glucose
- In beta cells of pancreas, functions as glucose sense that determines threshold for
insulin secretion
- In liver, facilitates glucose phosphorylation during hyperglycemia
Overview of Glycolysis
- Isomerization of G-6-P to F-6-P
- Phosphorylation of F-6-P to F 1,6-bisphosphate (2nd irreversible reaction catalyzed by PFK-1;
most important control point, rate-limiting step, and commits to the process of glycolysis)
- Cleavage of F 1,6-bisphosphate by dihydroxyacetone phosphate and G-3-P
Document Summary
Glucose comes from: diet, glycogen (liver and muscle, gluconeogenesis (glucose made from amino acids and fatty acids) If glucose is not available in the diet then glycogen is used, if glucose is not available from diet and glycogen then gluconeogenesis happens. Glucose molecule is split into 2 pyruvate molecules. Pyruvate is the precursor of acetyl-coa that starts the cac. C6h12o6 + 6o2 6co2 + 6h2o + energy. Catabolism of various compounds including lipids, chos, and proteins, includes the breakdown of each and ends with a molecule integrating itself into the central metabolic cycle (tca) which is linked to the electron transport chain. Sodium-independent facilitated diffusion transport system (mediated by family of 14 glucose transporters in cell membranes) Glut-1 abundant in rbcs and brain, low in adult muscle. Glut-3 primary glucose transporter in neurons. Glut-4 abundant in adipose tissue and skeletal muscle, insulin increases its expression.
