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This document was created by Alex Yartsev ([email protected]); if I have used your data or images and forgot to reference you, please email me. Carbohydrates The variety of saccharides - MONOSACCHARIDES: simple sugars, single molecules o PENTOSES eg. ribose, with 5 carbons o HEXOSES eg. glucose, with 6 carbons DISACCHARIDES – 2 molecules o Eg. Sucrose POLYSACCHARIDES – polymers of sugar o Eg. glycogen MOST DIETARY SUGARS ARE HEXOSE POLYMERS MOST CIRCULATING SUGARS ARE DEXTRO-ISOMERS - Hexokinase is inhibited by its product, G6P. Insulin Hepatocyte Glucokinase Unlike hexokinase, glucokinase activity is increased by insulin and decreased by diabetes and starvation. CIRCULATING GLUCOSE WHAT THE HELL IS THE POINT OF ALL THIS Turning glucose into something else causes the concentration in the cell to drop, thus making it easier to suck glucose into the cell via a concentration gradient Adding a phosphate group to glucose causes it to become more polar, thus making it difficult to negotiate the lipid cell wall and escape. Glucose-6-phosphate Any cell Hexokinase Unlike hexokinase, glucokinase cativity is increased by insulin and decreased by diabetes and starvation Glycolysis Glycogenesis: Catabolism of glucose-6-phosphate into pyruvate or lactate Polymerization of glucose-6-phosphate into glycogen molecules for storage Glycolysis proceeds along 2 major paths Catabolism to PYRUVATE via fructose and the trioses: Embden-Meyerhof pathway Pyruvate is then converted to Acetyl-CoA CONVERSION OF PYRUVATE TO Acetyl-CoA IS IRREVERSIBLE - unlike most steps in the glycolysis pathway Catabolism via 6-phosphogluconate and the pentoses: Direct oxidative pathway (hexose monophosphate shunt) This is actually an anabolic pathway; it results in ribose. It just happens to catabolise glucose as well. There is an interconnection between fat, protein and carbohydrate, which hinges around glucose metabolism. For example, amino acids can get deaminated into intermediates in the Krebs cycle or the Embden-Meyerhof pathway Glycerol, made from fats, can be made into dihydroacetone phosphate, and plug into Embden-Meyerhof pathway. In this way, and by means of converting lactate to glucose, other molecules can be turned into glucose – this is gluconeogenesis This document was created by Alex Yartsev ([email protected]); if I have used your data or images and forgot to reference you, please email me. Citric acid cycle, otherwise known as Krebs Cycle - the whole point is to convert Acetyl-CoA to CO2 and hydrogen. Acetyl-CoA is the major entry point, but amino acids when deaminated can enter at various points along the cycle This cycle requires O2 and does not function under anaerobic conditions ENERGY PRODUCTION - HOW MUCH ENERGY YOU MAKE DEPENDS ON WHICH PATHWAY OF GLYCOLYSIS YOU TAKE: whether you go down the Embden-Meyerhof pathway or the hexose monophosphate shunt pathway. o Embden-Meyerhof pathway produces 4 mol of ATP per mol of glucose, and uses up 1 mol. The end product is phosphoglyceraldehyde o This is an ANAEROBIC process o Thus, there is a net gain of 3 mol of ATP o However, when the glucose enters the cell, phosphorylating it takes 1 mol of ATP o Thus, for BLOOD GLUCOSE, there is a net gain of only 2 mol of ATP NAD+ is required to convert phosphoglyceradehyde to phosphoglycerate. In absence of oxygen, you would think that you would rapidly run out of NAD+ (because it all gets turned to NADH) However, pyruvate can accept a hydrogen atom from NADH, making more NAD+ (and in the process pyruvate is converted into lactate). THUS, GLYCOLYSTIC ENERGEY PRODUCTION CAN CONTINUE WHILE THERE IS NO OXYGEN. The lactate thus produced can be turned back into pyruvate once oxygen supply is restored END POINT: anaerobic metabolism converts 1 molecule of glucose into 2 molecules of ATP Aerobic metabolism is much more efficient: - 6 ATP is produced when 2 mol phosphoglyceraldehyde is converted into phosphoglycerate 6 ATP is produced when 2 mol of pyruvate is converted to Acetyl-CoA 24 ATP is produced during the subsequent 2 turns of the Krebs cycle This adds up with the 2 you alredy get from the Embden-Meyerhof pathway END POINT: aerobic metabolism converts 1 molecule of glucose into 38 molecules of ATP Glycogen synthesis and breakdown - Glycogen synthase catalyses the final steps of the pathway, which starts on the protein glycogenin Glycogen breakdown is catalyzed by PHOSPHORYLASE Blood Glucose levels - 5% of ingested glucose is converted into glycogen by the liver straight away 30-40% is converted to fat The remainder is metabolized in other tissues During fasting, the liver adds glucose to the bloodstream by breaking down glycogen During even longer fasting, once you run out of glycogen, the liver catabolises fats and amino acids, via GLUCONEOGENESIS METABOLISM OF HEXOSES OTHER THAN SUGAR - APART FROM THE GLUCOSE, YOU ALSO ABSORB FRUCTOSE AND GALACTOSE Galactose gets phosphorylated like glucose, and its uptake is also insulin-dependent o It reacts with uridine diphosphoglucose to form uridine diphosphogalactose. o If you are defif\cient in the catalyzing enzyme, the galactose accumulates in the bloodstream and causes GALACTOSEMIA which produces serious developmental disturbances This document was created by Alex Yartsev ([email protected]); if I have used your data or images and forgot to reference you, please email me. - FRUCTOSE is converted to fructose-6-phosphate, analogous process to the phosphorylation of glucose; its even mediated by the same enzyme (hexokinase). The reaction of fructose phosphorylation can occur in the ABSENCE of insulin; but most of this occurs in the intestine, so it is not especially great in treating a hypoglycemic attack in a diabetic. Fructose can be phosphorylated again in the 1 position (in absence of insulin as above) or in the 2 position, which produces fructose 2,6-diphosphate. This substance is a regulator of hepatic gluconeogenesis. If there is a lot of fructose 2,6-diphosphate, breakdown of glucose to pyruvate is increased. If the level of fructose 2,6-diphosphate is low, there is increased gluconeogenesis. References: Ganong's Review of Medical Physiology, Chapter 1 http://themedicalbiochemistrypage.org/glycolysis.html