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pryuvate to acetyl co a and actyl coA is further oxidized to generate co2. and large amounts of ATP through oxidativ phorphoylation.

actyl co a u break down carbohydrates to generate actyl coA. u also begin making larer moclules like faty acids, choelstrol, from acetyl coA. and how does the cell know where to shung these intermediates, so the enzymes and their activites can be regualted by energy charge of the cell. what is it? it is nothing but atp to adp ration in the cell. soif the cell is low. in ernegy charge whcih meeans that apt levels are lower than what are requied compared to adp levels, u start to metablize carbohydrates and other moclules so the catbolic pathway can replish atp. if the ernegy charge of the clel is high we are now in a good postition to do biosyntheies and make new molcules and store them for later use.

Glucose is not only a excellend fuel but also a versatile precurosr for many intermeditas. that can be used in various biosynthetic reactions. for example it can be used in the syntehtis of complex polysachs, it can be polymerized as sotred as as glycogen in animals and plants starch, when the enrgy demansds increas ehte lgucose. can be released form polymers and then it can be oxidized via glycolysis to generate pyrutvate and then lead. to productions of ATP. glucose can also be oxidizzed through a different pathway called pentose phosphate pathway . and the prupsoe of pentos phosphate pathway it o make NADPH and that is used for reductive biosynthesis(remember NADPH is for catabolism) when u oxidize glycose thourgh petnose phosphate pathways what u generate this 5-carbon sugar called ribose 5-phosphate is the precuros for nucleic acid biosyntheis . so the major carbohydrates in our human diet are. starch lactose, fuctorse and glucose, starch is for plants is a long polymer of glucose linked by alpha 1-4 glycosidic bonds. and some occasional alpah 1-6 breanches. difference between starch and glycogen is that. glyocgen is more branched than starch. starch is more or less linear with occasional alpha 1-6 barnching and glycogen is more branched than starch.

looking at carbon c1 is the anomeric carbon. what happens. as soon as we eat the enzyme salivary amtlase at the back of our tonegue,it starts to breath downt he starch by hyhdrolysing the alpha 1-4 glycodisid ebonds. so this salivary amylase is going to start to hydrolyase the alpha 1-4 bond and start to break down this complex startch into more managable sort of di’s and trisachrides as we are eating we swallow the food quickly. so its not the salivary alpha amylase that does the job it is the pancreatic amylase that really sort of break it down into di and tri saccharides. this is how u depolymerize starch into di and tri saccharides. withing these di saccharides were intersted in a few of them like sucrose is a dissachride of glucose that is linkd to a fructose through alpha 1-2 linakge lgycosid bond, this is further broek downinto indival units by glycosidase enzyme into glucose and fructose which is called sucrose isomaltase complex. its a bunch of protiens that come together and its called sucrase isomaltase complex. which also breaks down isomaltase,

now the sucraose isomaltase complex deficency so there are indivuals who have deficenty so there are indivals who ahve defincty in sucrose isomaltase enzyme complex and that results in in intolerance for ingested sucros so u wont be able to break down sucrose. that particular deficenty is highly prevelants in the inuit people. so the treament is bascially u try to avoid sucros in ur diet and u restrict dietary sucrose and thers also now enzymes avaiable that u can eat before u eat anything that has sucros os that sucrose.

now lactose - lactos is a disachride with a beta 1-4 linakge and this is one between galactose and glucose ,lactose on the brush border surface of our intestinal eptuhail cells. if u think about this as ur intestine the cells that are linking the intesine these are the brush border cells. a lot of the enzymes are localized here . so the lactase activity is very high in infacnts bc infants drink milk, and the enzyme activity and expression changes drastically as we age, adults have 10% of the lactase actiivty compared to when we were infants, if u dont hav e a working lactase enzyme u cant break down lactose and that is called lactose intolerance. ¾ of adult pop are lactose intolerant, how to treat that u can lower the ocnsuption of dairy products in the diet and u hav emilk like lactase treated with lactase and lactase pills.

we have igested carbohydates and broken them down using salivary and pancreatic alpha amylase so what we’ve got in our gut right now is these disaccharides and trisaccharides and then we use enzymes like sucrase and lactase to further break them down and now we have glucose single units in our intestiesn and now we need to abrob that glucose, so what happens is the sugars like glucose are going to be transported across these intestinal epithelial cells into the bloodstream so that we can distrubute that glucose ot the rest of our tissues.

so if we consider these brush border cellsthat are shown in the middle, the apical side here is going to face the lumen or the gut and the basolaterla side is going to face the capillaries or the blood ciruclation , so the absortpion of the glucos eform the intestinal lumen inot the brush border cell is going to occur through a tranpsoter called soidum glucose linked transporter 1 abbreviated as SGLT1 which is a symporter. it transports glucose or galactose against the ocnetrion gradent that is provide by the electrochemcial gradient of sodium.

now u may recall that the sodium con inside the cell bc of hte sodium potassium atpase pump is continnously pumping sodium out and bringin potassium in. so now theres a concentraiton gradient, so sodium wants to go in, and along with the sodium comes in glucose so this is a symport. if u hav sglt1 deficnety that resutls in glucose and galctos malabsoprtion so u wont be able to abrob form ur gut glucose or galactose. what happens to glucose once its itside this intestinal epithelic cell is that u want to push it now towards the basolateral side. u use tranporter called GLUT2 which is going to move glucose n from inside of the cell to the basolaterla side down its conc gradient. so glut 2 tranporter in additon to being on the basolater side of the. intestinal epithali cells as we shall see is also the main trnaporter pesent on our liver cells the heptaocytes.

also present on our beta cells on our pancrease, cells that make insulin. GLUT2 is a high capcity but low affintity transporter for glucose. GLUT5 is another trnaporter that is not shown. here. its also present on the apical site and this one brings in furctose to the inside of the cell, so GLUT 5 is the fructose trnaporter and ther eis also GLUT5 deficency and if someone is deficent in GLUT 5. theyre going to suffer from fructose malabosprtion or dietary fructose intoelrance. and in fructose metaolism we will learn that having

LGUT5 deficnty is much better than having a decifney downstream in a enzyme called frutokinase bc this one u can treat by avoiding fructose in ur diet , but if somebody has dieficnety in frutokinase that can be deadly.

Glucose tranport into cells, on the left iw the depicitn of ur portal vien, this big red tube and this is going to bring in nutrients from the intesinte to the portal blood and then to the liver first and also the pacnreaseand now this is how we take care of carbohydate rich diets bceuase hte liver cells , have glut2 tranport and gluten trnaprot is high cpacity and bring in large amounts of glucose into the liver clels. if u think abou the concentraion of glucose in our body in our blood stream the peripheral whichis the systemic circualtion, the coneitonr of glucose is ebtween 4 to 5 millimolar, 5 milimolar in fat state and 4 milimolar in the fasted state. so u can see that it does not fluctate a lot if u think abot. portable blood the conetirno of glucose cna be anywhere from 5 to 20 milimolar. that is because when we eat carbohdyrate rich dieta ll of the glucose that is aborbed first goes ot hte protal blood so the concentiron can rise really quickly but what we dont watn is shock our systmeic ciruclation by putting odlet glucose directly from portal blood into the peripheral ciruclation so tahts why this si imponrtant. this GLUT2 trnaproter which is present on the liver is going to start aborbing excess glucose that came from the diet. so this is our first to pass to take care of the excess glucose so GLUT2 is going to bring in that excess gluose and if u think about. GLut2 the km for glucos is 15 milimolar so its a low affinity but high cpacit and i told u that in addition to the liver and pancreati silets or the beta cells are going to have this GLUT2tranporter . so now u have taken care of excess glucose . teh portal blood also the pancrease and the liver are strategically placed so that the protal blodo both of these tissues are sort of exposed ot th eportal blood. the beta calels have the GLUT2 transporter so glucose levels rise and some of that glucose gets in to the pancreatic beta clels and that their sensory mecahnism that ‘we have a psike in glucose we should realse some insulinso beta cells are going to start to secrete insuling in reposne to this increase in gucose now wha thappens is when insuling is realsed in our blood stream we hav ea seperate trnaproter called