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Nutrition and Metabolism Unit 1 Exam Study Guide: Regulation of Carbohydrates and Lipids

by: Victoria Hills

Nutrition and Metabolism Unit 1 Exam Study Guide: Regulation of Carbohydrates and Lipids NUTR 4550

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Here is a study guide for the carbohydrate regulation PowerPoints 1 and 2 (1/8 and 1/11) and the lipid regulation PowerPoint (1/13).
Nutrition and Metabolism
Dr. Elliot Jesch
Study Guide
nutrition, metabolism, Jesch, regulation, lipid, Carbohydrate, Clemson, 4550
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This 16 page Study Guide was uploaded by Victoria Hills on Tuesday February 2, 2016. The Study Guide belongs to NUTR 4550 at Clemson University taught by Dr. Elliot Jesch in Spring 2016. Since its upload, it has received 94 views. For similar materials see Nutrition and Metabolism in Nutrition and Food Sciences at Clemson University.

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Date Created: 02/02/16
Clemson  University   Spring  2016     Nutrition  and  Metabolism  (NUTR  4550)  Unit  1  Regulation  Exam  Study  Guide     I. Glycolysis   • Figure  12.8  is  showing  glycolysis  on  the  left  side  and   gluconeogenesis  on  the  right  side  +  their  corresponding  regulatory   factors     • First  regulated  step  in  glycolysis:   -­‐ Glucose  à  Glucose-­‐6-­‐Phosphate  via   glucokinase/hexokinase     -­‐ Points  of  regulation:     a) Insulin:     o Up  regulates  glucokinase/hexokinase   o Increases  the  concentration  (number)  of   glucokinases/hexokinases  in  order  for  glucose  to  be   phosphorylated  to  be  glucose-­‐6-­‐phosphate   o When  carbohydrates  (Such  as  glucose  or  fructose)  are   more  quickly  phosphorylated,  more  uptake  of  the   carbohydrates  is  able  to  enter  the  cell     b) Fructose-­‐1-­‐Phosphate:   o Up  regulates  glucokinase/hexokinase  via  increasing  its   activity     o Fructose-­‐1-­‐phosphate  comes  from  fructose  and  is  one  of   the  pathways  that  fructose  is  able  to  enter  glycolysis     c) Fructose-­‐6-­‐Phosphate:     o Down  regulates  (Inhibits)  glucokinase/hexokinase   when  large  amounts  of  fructose-­‐6-­‐phosphate  are   present  from  the  step  where  glucose-­‐6-­‐phosphate  à   fructose-­‐6-­‐phosphate   o Down  regulates  glucokinase/hexokinase  in  preparation   rd for  the  next  (3 )  step  in  glycolysis  where  fructose-­‐6-­‐ phosphate  à  fructose-­‐1,6-­‐bisphosphate  via  P6FK1   because  fructose-­‐6-­‐phosphate  is  acting  at  this  point  as  a   precursor  to  this  reaction  (fructose-­‐6-­‐phosphate  à   fructose-­‐1,6-­‐bisphosphate)    for  regulation  in  order  not   to  overwhelm  the  rest  of  glycolysis  (This  is  known  as   feed  back  regulation)   o Feed  back  regulation:  Where  a  product  of  a  reaction  will   feed  back  to  the  previous  reaction  à  Here:  A  lot  of   fructose-­‐6-­‐phosphate  will  down  regulate   glucokinase/hexokinase  activity     • Second  regulated  step  in  glycolysis:   -­‐ Fructose-­‐6-­‐Phosphate  à  Fructose-­‐1,6-­‐Bisphosphate  via   P6FK1  (Phosphofructokinase)   -­‐ Points  of  regulation:   a) ATP:   o Down  regulates  PFK     o Down  regulates  PFK  because  the  cell  has  enough  ATP  so   it  is  unnecessary  to  continue  shuttling  glucose/other   monosaccharides  in  to  produce  more  ATP   o Key  to  note  that  ATP  will  not  shut  down  this  pathway   but  instead  the  monosaccharides  will  continue  to  go   through  glycolysis  à  Pyruvate  à  Acetyl  CoA  in  order  to   enter  fatty  acid  synthesis  instead  of  continuing  through   the  TCA  cycle  and  electron  transport  chain     o In  general,  ATP    production  is  slowed  down  by  heavy   ATP  presence  in  the  cell     b) Hydrogen  (Protons):   o Down  regulates  glucokinase/hexokinase     o The  protons  are  being  referred  to  their  place  in  the   electron  transport  chain  when  they  are  being  pumped   into  the  inner  mitochondrial  space  that  creates  the   chemiosmotic  gradient  used  to  make  ATP  with  ATP   synthase     o If  the  concentration  of  protons  is  sustained  though,  this   means  that  the  cell  is  signaling  that  there  are  enough   reducing  equivalents  providing  the  protons  so  that  the   TCA  cycle  and  glycolysis  should  slow  down  as  a  result     c) AMP/Pi  (Inorganic  phosphate):   o Up  regulate  PFK   o When  there  is  increased  AMP  and  Pi  present  in  the  cell,   the  cell  is  sensing  that  it  is  currently  using  energy  (ATP)   o Therefore,  it  is  necessary  to  continue  having  more  of  a   flow  of  glucose  into  the  cell  through  the  glycolytic   pathway     d) Citrate  (Indirectly):   o Down  regulates  (slows  down)  PFK     o Citrate  is  a  TCA  cycle  intermediate  that  is  formed  when   oxaloacetate  and  acetyl  CoA  are  combined     o As  citrate  circles  back  around  to  oxaloacetate  in  the  full   TCA  cycle,  therea  re  4  dehydrogenase  enzymes  that  are   producing  reducing  equivalents  that  will  be  shuttled  to   the  electron  transport  chain  to  donate  their  electrons   for  the  chemiosmotic  gradient  and  ultimately  ATP   production  through  ATP  synthase     o A  buildup  of  citrate  is  indicating  that  the  electron   transport  chain  has  enough  protons  and  therefore  ATP   in  the  cell  (Citrate  is  the  stopping  point  as  a  result)     o Further,  a  buildup  of  citrate  tells  glycolysis  in  the   cytoplasm  that  glucose  and  other  monosaccharides  do   not  need  to  be  broken  down  at  this  point   e) Insulin:   o Up  regulates  6PFK1   o Increases  fructose-­‐2,6-­‐bisphosphate  (Metabolite)  and   its  enzyme  =  6PF2K  (This  enzyme  phosphorylates  the   second  carbon  of  fructose-­‐6-­‐phosphate)  à  This  is  a   shunt  pathway  in  glycolysis     o Fructose-­‐2,6-­‐bisphosphate  is  an  allosteric  regulator  of   6PFK1   o Allosteric  regulator  definition:  A  metabolite  that  binds   to  a  protein  and  modifies  that  protein  to  increase  or   decrease  its  activity   o The  cell  sense  the  presence  of  insulin  so  that  the   enzyme  for  fructose-­‐2,6-­‐bisphosphate  increases  which   tells  the  cell  to  produce  more  6PF1K  to  allow  more   glucose  to  flow  through  the  glycolytic  pathway  and  have   more  of  rapid  conversion  from  fructose-­‐6-­‐phosphate  à   fructose-­‐1,6-­‐bisphosphate   o Overall:  Fructose-­‐2,6-­‐Bisphosphate  acts  upon  6PF1K  as   a  result    (An  allosteric  regulator  of  6PF1K)  so  molecule   will  bind  or  interact  with  6PF1K  to  increase  its  activity   (NOT  concentration)  so  allows  for  more  rapid   conversion  from  F6P  to  F-­‐1,6-­‐BisP   • Third  regulated  step  in  glycolysis:     -­‐ PEP  (Phosphoenolpyruvate)  à  Pyruvate  via  pyruvate   kinase   -­‐ Points  of  regulation:     a) ATP:   o Down  regulates  pyruvate  kinase  activity     o Sensing  that  the  cell  has  enough  energy  at  this  point   b) Alanine:   o Down  regulates  pyruvate  kinase     o Pyruvate  is  the  alpha  keto  acid  of  alanine  (Alanine  is   deaminated  or  transaminated  with  the  removal  of  NH   3 to  produce  pyruvate)   o Therefore,  a  lot  of  glucose  is  not  needed  when  there  is  a   lot  of  alanine  around   o Alanine  is  abundant  when  eating  protein  sources     o Glucose-­‐Alanine  Cycle:  Occurs  when  there  is  an  attempt   to  make  glucose  from  peripheral  tissues  so  that   pyruvate  à  alanine  à  liver  à  gluconeogenesis,  which   slows  down  the  glycolytic  pathway  (Alanine  up   regulates  gluconeogenesis)   c) Glucagon:   o Down  regulates  pyruvate  kinase   o Signals  for  the  release  of  glucose  into  the  blood  stream     o Signals  for  the  breakdown  of  glycogen  and  up  regulates   gluconeogenesis     o Inhibits  pyruvate  kinase   o Insulin  levels  are  low  when  glucagon  is  present,   therefore  it  is  not  necessary  to  have  more  products   going  through  the  glycolytic  pathway  when  glucose  is   needed  in  the  blood     o When  the  liver  senses  glucagon,  it  will  start  breaking   down  glycogen  (Muscle  and  liver)  and  initiating   gluconeogenesis  (Liver  and  little  occurs  in  the  kidneys)   to  breakdown  to  get  free  glucose     d) Epinephrine:   o Down  regulates  pyruvate  kinase   o Fight  or  flight  hormone     o Inhibits  pyruvate  kinase     o Increases  FA  catabolism     e) Fructose-­‐1,6-­‐bisphosphate:   o Up  regulates  pyruvate  kinase   o Product  of  PFK1  so  signals  the  up  regulation  of  pyruvate   kinase  because  if  the  cell  is  signaling  for  more  PFK1   enzymes  to  be  produced,  it  wouldn’t  make  sense  to   down  regulate  its  follow  up  metabolism  later  in  the   glycolytic  pathway     o This  is  known  as  feed  forward  regulation—Here  it’s   necessary  to  up  regulate  pyruvate  kinase  to  ensure  that   fructose-­‐1,6-­‐bisphosphate  ends  up  at  the  end  of  the   metabolic  pathway   o Feed  forward  regulation:  When  a  compound  regulates   another  reaction  further  down  a  pathway     f) Insulin:   o Up  regulates  pyruvate  kinase   o Facilitates  post-­‐translational  modifications  where   enzymes  will  be  phosphorylated  or  de  phosphorylated   to  either  increase  or  reduce  the  activity  of  that  enzyme     o With  pyruvate  kinase,  insulin  increases  it  via  de-­‐ phosphorylation     • The  prime  difference  between  glycolysis  and  gluconeogenesis  are   the  enzymes  for  the  regulated  steps  à  Even  though  most  of   gluconeogenesis  is  the  reverse  of  glycolysis,  it’s  important  for   there  to  be  different  enzymes  so  that  there  won’t  be  a  flow  of   molecules  going  through  one  of  the  pathways  at  the  same  time  as   the  flow  of  molecules  going  through  the  other  pathway   (Inefficient)     II. Gluconeogenesis     • First  regulated  step  in  gluconeogenesis:   -­‐ Pyruvate  à  oxaloacetate  via  pyruvate  carboxylase   -­‐ Points  of  Regulation:   a) Acetyl  CoA:   o Up  regulates  pyruvate  carboxylase   o When  one  is  consuming  and  using  FA  as  an  energy   source,  beta  oxidation  must  occur  which  produces  much   acetyl  CoA   o In  order  to  use  acetyl  CoA,  oxaloacetate  must  be  used  to   combine  with  acetyl  CoA  to  form  citrate  in  the  TCA  cycle   o Running  out  of  oxaloacetate  is  a  concern  since  there  is   so  much  acetyl  CoA  production  from  beta  oxidation   because  then  the  TCA  cycle  won’t  continue  to  run   o Ovearall:  Pyruvate  à  oxaloacetate  via  pyruvate   carboxylase  partly  for  TCA  cycle  in  the  production  of   energy  and  in  gluconeogenesis  to  make  glucose  since   pyruvate  is  unable  to  go  back  to  PEP  (Oxaloacetate  is   able  to  be  converted  to  PEP)   • Second  regulated  step  in  gluconeogenesis:   -­‐ Oxaloacetate  à  PEP  via  PEP  carboxykinase   -­‐ Points  of  Regulation:   a) Insulin:     o Down  regulates  PEP  carboxykinase     o When  the  liver  or  kidney  senses  insulin,  there  is  a   decrease  in  the  concentration  of  PEP  carboxykinase   o The  ubiquitin  proteosomal  pathway  is  used  to   decrease  the  number  of  PEP  carboxykinases  by   degrading  the  enzymes  and  returning  their  AA  parts  to   the  AA  pool     • Third  regulated  step  in  gluconeogenesis:   -­‐ Fructose-­‐1,6-­‐bisphosphate  à  Fructose-­‐6-­‐Phosphate  via   fructose-­‐1,6-­‐bisphosphatase   -­‐ Points  of  Regulation:   a) Fructose-­‐2,6-­‐bisphosphate:   o Down  regulates  fructose-­‐1,6-­‐bisphosphatase  because   ample  product  is  flowing  through  glycolysis     b) AMP:     o Down  regulates  fructose-­‐1,6-­‐bisphosphatase  because  it   is  signaling  for  an  increase  in  PFK  in  glycolysis  since  the   cell  needs  energy     • Fourth  regulated  step  in  gluconeogenesis:     -­‐ Glucose-­‐6-­‐Phosphate  à  Glucose  via  glucose-­‐6-­‐ phosphatase     -­‐ Occurs  in  the  liver  and  kidney  only   -­‐ Points  of  Regulation:   a) Insulin:   o Down  regulates  glucose-­‐6-­‐phosphatase     • Liver  specifics:     -­‐ Glucose  is  taken  up  by  the  liver  through  GLUT  2  and  uses  purely   facilitated  diffusion  à  free  glucose/fructose  in  the  cell     -­‐ As  free  glucose  comes  into  the  cell,  it’s  important  to  phosphorylate   glucose  because  a  high  concentration  of  free  glucose  will  slow  down  the   glucose  uptake     -­‐ So  phosphorylating  glucose  (or  any  other  carbohydrate)  will  increase  the   amount  of  glucose  taken  up  by  the  cell     -­‐ Fructose  is  able  to  enter  as  fructose-­‐1-­‐phosphate  or  predominantly  as   fructose-­‐6-­‐phosphate  via  glucokinase   -­‐ Liver  wants  to  take  up  as  much  carbohydrate  as  possible  because  it’s   going  to  break  it  down  to  pyruvate  for  ATP  production  (First)  or  it  is   going  to  store  the  glucose  as  glycogen  or  FA/triglyceride  (Not  all  tissues   are  able  to  do  this)  à  This  all  occurs  (especially  in  the  liver)  to  make  the   body  as  efficient  as  possible     *Extra  elaboration  on  the  following  slides  in  PPT  2-­‐  1/11/16  *     Figure  12.9   • In  the  top  left  of  the  figure:  Shows  how  glucose  is  entering  the  liver  cell   through  GLUT  2  and  how  glucokinase  is  phosphorylating  glucose  à  glucose-­‐ 6-­‐phosphate,  which  occurs  primarily  in  the  fed  state   • In  the  top  right  of  the  figure:  Shows  how  in  the  endoplasmic  reticulum  (ER),   there  is  an  inorganic  phosphate  transporter,  glucose-­‐6-­‐phosphatase,  and  a   different  glucose  transporter  for  the  ER  facilitating  the  reverse  process  of   reproducing  glucose  from  glucose-­‐6-­‐phosphate   -­‐  The  reverse  process  of  producing  glucose  from  glucose-­‐6-­‐phosphate  in  the   cell  occurs  during  times  in  the  fasted  state     • Fasted  State:     -­‐ Glycogen  is  broken  down  to  glucose-­‐6-­‐phosphate  à  glucose   o Glucose-­‐6-­‐phosphate  that  is  produced  in  the  cytoplasm  from  the   breakdown  of  glycogen  à  ER  where  glucose  phosphatase  converts   glucose-­‐6-­‐phosphate  à  glucose  +  inorganic  phosphate     -­‐ Lactate  à  glucose-­‐6-­‐phosphate  via  gluconeogenesis  process  that  must  go   through  the  ER  as  well     o Other  tissues  and  red  blood  cells  generate  lactate  mainly  because   NAD+  must  be  regenerated  as  an  electron  acceptor  in  glycolysis   involving  the  step  from  glyceraldehyde-­‐3-­‐phosphate  à  1,3-­‐ bisphosphoglycerate   o Skeletal  muscle  generates  lactate  because  of  the  lack  of  oxygen  in   high  intensity  movement;  The  lactate  is  transported  back  to  the   liver  to  go  through  gluconeogenesis   • After  glucose  has  been  regenerated  from  glucose-­‐6-­‐phosphate  in  the  ER,  the   glucose  transporter  T  t3kes  the  free  glucose  to  the  membrane  of  the  ER   where  GLUT  2  picks  the  glucose  up  and  takes  it  to  the  cellular  membrane  to   be  released  back  into  the  blood  stream  to  maintain  blood  glucose   concentrations   • Inorganic  phosphate  also  has  its  own  transporter  in  the  ER  so  it  can  be   reused  for  phosphorylation  of  other  incoming  glucose  in  fed  state  times   Figure  12.10  (Slight  review  of  previously  discussed  concepts)   • Top  portion  of  the  figure  (A):  Insulin  is  present   -­‐ Fed  state   -­‐ Insulin  signals  cell  to  take  up  glucose  à  glycolysis     -­‐ Specially  showing  the  point  where  glucose  àà  fructose-­‐6-­‐phosphate  à   Fructose-­‐1,6-­‐bisphophate  via  6PFK1  (Step  3)  –  Insulin  up  regulates  this   enzyme   -­‐ Serine  residue  of  6PF2K  and  insulin  à  Shunted  Pathway:   o Within  6PF2K,  there  is  a  specific  serine  residue  that  is  de-­‐ phosphorylated  when  insulin  is  secreted,  which  leads  to  the  active   form  of  6PF2K  that  generates  fructose-­‐2,6-­‐bisphophate  from   fructose-­‐6-­‐phosphate  that  up  regulates  6PF1K  so  more  glucose  à   pyruvate     • Bottom  portion  of  the  figure  (B):  Glucagon  and  epinephrine  are  present   -­‐ Fasted  state   -­‐ Pancreas  has  secreted  glucagon  to  signal  cells  to  break  down  glucose  for   energy   -­‐ Figure  shows  how  pyruvate  à  oxaloacetate  à  PEP  à  fructose-­‐1,6-­‐ bisphosphate  à  fructose-­‐6-­‐phosphate  via  fructose-­‐1,6-­‐bisphosphatase   (Part  of  the  steps  for  gluconeogenesis  discussed  here)   -­‐ Serine  residue  of  6PF2K  and  glucagon:   o Fructose-­‐2,6-­‐bisphophate  is  decreased  in  amount  being  produced   because  the  serine  residue  of  6PF2K  is  phosphorylated  à  down   regulation  of  6PF1K  and  up  regulation  of  fructose-­‐2,6-­‐phosphatase   à  fructose-­‐6-­‐phosphate     -­‐ Therefore,  overall  gluconeogenesis  is  up  regulated  +  eventually  get  back   to  free  glucose  that  can  be  used  by  tissues  in  the  body  (Especially  red   blood  cells  and  the  brain  first)     III. Glycogenesis     • Glycogen  synthase:  Enzyme  that  creates  glycogen  from  glucose   à  glucose-­‐6-­‐phoshpate  (And  other  carbohydrate  sources)   • Glycogen  synthase  A:  Activated  version  and  is  not   phosphorylated   • Glycogen  synthase  B:  Less-­‐active  version  and  is  phosphorylated     • Points  of  Regulation:   a) Insulin:   -­‐ Up  regulates  glycogen  synthase  A   -­‐ Insulin  is  secreted  by  the  pancreas  in  the  fed  state  after  the   consumption  of  a  meal  with  carbohydrate,  and  insulin   signals  PIK3/Akt  to  down  regulate  glycogen  synthase   kinase  3  so  that  glycogen  synthase  A  is  not  phosphorylated   to  produce  glycogen  synthase  B     -­‐ Big  picture:  Insulin  is  an  anabolic  hormone  that  promotes   glycogen  synthesis  so  it  is  important  for  glycogen  synthase   A  to  be  less  active  at  this  point   b) Glucagon  and  epinephrine:   -­‐ Up  regulates  glycogen  synthase  B   -­‐ Secreted  during  the  fasted  state  or  due  to  a  stress  stimulus       -­‐ Requires  the  cAMP  mechanism     -­‐ cAMP  activates  protein  kinase  A  and  phosphorylase   kinase  which  causes  the  phosphorylation  of  glycogen   synthase  A  à  glycogen  synthase  B  (Less-­‐active  version)   -­‐ Big  picture:  Glucose  is  needed  in  the  blood  and  for  energy   when  glucagon  and  epinephrine  are  present  so  glycogen   stores  are  going  to  need  to  be  broken  down  for  the  release   of  glucose     c) Epinephrine:   -­‐ Up  regulates  glycogen  synthase  B   -­‐ Able  to  use  PIP-­‐Calcium  mechanism  as  well     -­‐ Signals  the  phosphorylation  of  glycogen  synthase  à  B   version     d) Other  ways  to  inhibit  the  conversion  of  glycogen  synthase  B  to   glycogen  synthase  A  when  glucagon  and  epinephrine  are   present  (Referring  to  bottom  half  of  figure  12.15)   -­‐ Inhibitor  1A  (Phosphorylated)—Less  active  version   -­‐ Inhibitor  1B  (De-­‐phosphorylated)—Active  version   -­‐ Focus  on  top  half  of  figure  12.15  though   e) Depolarization  of  muscle  cells:   -­‐ For  muscle  movement  and  contraction  to  occur  energy  in   the  form  of  ATP  is  needed     -­‐ ATP  signals  another  kinase  enzyme  to  phosphorylated   glycogen  synthase  A  à  B     -­‐ Up  regulation  of  glycogen  synthase  B  is  necessary  so   glycogen  won’t  be  shuttled  into  storage  but  instead,  the   glucose  can  be  used  for  ATP  so  the  muscle  can  contract     IV. Glycogenolysis   • Glycogen  phosphorylase:  Enzyme  that  breaks  down  glycogen  à   glucose-­‐6-­‐phosphate  à  glucose     • Glycogen  phosphorylase  B:  Less  active  and  de-­‐phosphorylated   • Glycogen  phopshorylase  A:  Active  and  phosphorylated     • Points  of  Regulation:   a) Glucagon  and  Epinephrine:   -­‐ Up  regulates  glycogen  phosphorylase  A   -­‐ Use  cAMP  mechanism   -­‐ Glucagon  presence  in  the  blood  activates  protein  kinase  A,   which  phosphorylates  phosphorylase  kinase  A  that   phosphorylates  glycogen  phosphorylase  B  (To  give  glycogen   phosphorylase  A  =  active)   -­‐ Review:  Glucagon  and  epinephrine  also  signal  for  the   phosphorylation  of  glycogen  synthase  A  (Active)  à  B  (Less   active-­‐  Makes  glycogenesis  less  active  and  glycogenolysis  more   active)   b) AMP:   -­‐  Up  regulates  glycogen  phosphorylase  B  (Increases  the   activity  of  the  enzyme)   c) ATP:   -­‐  Down  regulates  glycogen  phosphorylase  B  (Decreases  the   activity  of  the  enzyme)   d) Glucose:   -­‐ Down  regulates  glycogen  phosphorylase  A  (Decreases  the   activity  of  the  enzyme)   -­‐ Meaning  that  the  breakdown  of  glycogen  to  glucose  is  not   necessary  since  there  is  an  influx  of  glucose     V. PDH  (Pyruvate  Dehydrogenase)  Complex   • PDH:  Enzyme  used  to  convert  pyruvate  (product  of  glycolysis)  à   Acetyl  CoA   • General  process:   -­‐ Pyruvate  transporters  transport  pyruvate  from  the  cytoplasm   into  the  mitochondria  where  PDH  is  located     -­‐ Pyruvate  à  Acetyl  CoA  so  acetyl  CoA  can  be  used  in  the  TCA   cycle  to  produce  ATP  from  the  reducing  equivalents  (3  NADH   and  1  FADH ) 2  à  electron  transport  chain  for  oxidative   phosphorylation     -­‐ 1  NADH  and  1  FADH 2are  also  produced  with  beta  oxidation   • Points  of  Regulation:   a) NADH  and  Acetyl  CoA  (Allosteric  regulators-­‐  Metabolite  that   interacts  with  an  enzyme  by  changing  its  confirmation  but   doesn’t  create  a  bond)   -­‐ Ratio  of  NADH:NAD (Refer  to  top  right  of  figure  12.18-­‐  In   terms  of  other  processes  such  as  beta  oxidation  producing   NADH  as  well)   -­‐ Increased  NADH  (More  than  NAD )  down  regulates  PDH   -­‐ Decreased  NADH  (Less  than  NAD )  up  regulates  PDH     -­‐ Middle  of  figure  12.18:  NAD  acts  as  a  substrate  for  pyruvate  à   acetyl  CoA  +  NADH  reaction     -­‐ NADH  and  acetyl  CoA  as  ample  products  of  the  reaction  down   regulate  PDH   -­‐ Example:  Fasted  state  or  ketogenic  diet  à   -­‐ Beta  oxidation  of  FA  is  occurring  at  these  points  and  are   producing  ample  acetyl  CoA  as  a  result  that  is  going  through   the  TCA  cycle  and  electron  transport  chain  for  energy   production;  Ample  NADH  is  produced  as  a  result  of  the  TCA   cycle   -­‐ Ample  acetyl  CoA  and  NADH  from  beta  oxidation  cause  a   buildup  so  these  2  products  are  not  necessary  to  be  produced   by  PDH  through  the  conversion  of  pyruvate   -­‐ Concern  about  reduction  in  oxaloacetate  that  is  necessary  for   the  TCA  cycle  to  keep  working:   § Because  of  the  massive  influx  of  acetyl  CoA   produced  with  beta  oxidation,  it  is  important   for  there  to  be  enough  oxaloacetate  present     § Carbohydrate  Solution:  Pyruvate  is  used   instead  to  be  converted  à  oxaloacetate  via   pyruvate  carboxylase    (Anaplerotic  reaction-­‐  A   reaction  that  refills  an  intermediate  of  another   pathway)   § AA  Solution:  If  no  pyruvate  is  available,  can   deaminate  AA  and  produce  oxaloacetate   directly  (Acts  as  alpha-­‐ketogenic  acid)   • Middle  of  figure  12.18:     -­‐ Active  PDH  is  de-­‐phosphorylated   -­‐ Less  active  form  of  PDH  is  phosphorylated     • PDK  (Pyruvate  Dehydrogenase  Kinase):   -­‐ Phosphorylates  PDH  to  make  it  inactive  (Indirectly  regulates   PDH)   -­‐ Different  forms  of  PDK:  1,  2,  3,  4  (Be  aware)   -­‐ Points  of  Regulation:   a) Pyruvate:   o Down  regulates  PDK   o PDH  will  be  up  regulated  and  in  the  active  state  as  a   result   b) Acetyl  CoA:COA:   o Up  regulates  PDK  if  there  is  an  increased   concenrration  of  acetyl  CoA  in  the  mitochodnria   o PDH  will  be  down  regulated  (via  being   phosphorylated  by  PDK)  to  less  active  version   c) NADH:NAD :   + o Up  regulates  PDK  if  there  is  an  increased   concentration  of  NADH  in  the  mitochondria   o PDH  will  be  down  regulated     • PDP  (Pyruvate  Dehydrogenase  Phosphate)-­‐  PDP  1  and  2   -­‐ Another  enzyme  used  to  indirectly  regulate  PDH   -­‐ Points  of  Regulation:   a) Calcium:   o Up  regulates  PDP  to  up  regulate  PDH   o Secreted  in  muscle  tissue  during  contraction  which   signals  the  cell  that  there  is  a  demand  of  energy   o Pyruvate  à  acetyl  CoA  reaction  by  PDH  is  up   regulated  as  a  result  so  acetyl  CoA  à  TCA  cycle   b) Insulin:   o Up  regulates  PDP  to  up  regulate  PDH   o Although  insulin  is  seen  as  an  anabolic  hormone,   upon  initial  consumption  of  a  meal,  some  ATP  will   be  made  for  the  immediate  needs  of  that  cell     o Also,  insulin  promotes  FAS  with  excess  after  the   needs  of  the  cell  are  met  and  acetyl  CoA  is  necessary   as  a  precursor  for  the  creation  of  a  FA     VI. Lipid  Metabolism  (Review  of  general  processes  on  the  focus  on  TAG  and   FA)   • Fed  State:   -­‐ Consumption  of  mixed  meal  with  lipid  à  digestion   -­‐ Lingual  lipase:  Digests  TAG  minimally  in  the  mouth;   st rd Hydrolyze  FA  at  the  1  and  3  carbon     -­‐ Gastric  lipase:  Digests  TAG  minimally  in  the  stomach  à  TAG,   DAG,  and  MAG;  Hydrolyze  FA  at  the  1  and  3  carbon   -­‐ Pancreatic  lipase  and  colipase:  Secreted  by  the  pancreas     -­‐ For  pancreatic  lipase  and  colipase  to  function,  it  is  necessary   for  bile  to  be  released  from  the  gallbladder  into  the  proximal   portion  of  the  small  intestine  to  help  emulsify  lipids   -­‐ Bile:  Composed  of  emulsifiers  =  Cholesterol,  phospholipids,   and  bile  acids     -­‐ With  mostly  TAG  +  also  some  DAG  and  MAG  coming  from  the   stomach  +  bile  à  Micelle  production  where  the  outer  surface  is   composed  of  phospholipids,  bile  acids,  some  cholesterol  and   the  core  =  DAG,  MAG,  TAG   -­‐ Effectively  malese  lipids  soluble  in  water  as  a  result  by  bile   -­‐ Process:  Colipase:  Binds  to  the  surface  of  micelle  onto  the  bile   acids,  which  allows  for  the  binding  of  pancreatic  lipase-­‐ Functions  to  hydrolyze  FA  from  DAG  and  TAG  that  are  attached  to   micelle   -­‐ The  products  of  pancreatic  lipase  (Which  are  then  officially  put   into  the  micelle)  =  2  Free  FA  +  MAG  à  The  micelle  is  then  able  to   be  taken  up  by  the  enterocyte   -­‐ So  the  enterocyte  has  taken  up  2  MAG  and  2  free  FA  where  the   next  step  is  to  re-­‐esterify  the  2  FA  on  MAG  to  TAG  again  à   Formation  of  chylomicron   -­‐ Chylomicron:  A  lipoprotein  (Used  for  the  transport  of  lipids  in   the  blood—because  it’s  in  a  water/aqueous  environment);   Formed  in  the  small  intestine  and  their  specific  function  is  to   transport  TAG  from  the  diet  (Exogenous)  to  tissues  first  via  the   lympathic  system—by  passes  the  liver   -­‐ After  the  chylomicron  delivers  the  TAG  to  the  necessary  tissues,   the  chylomicron  remnant  then  goes  back  to  the  liver  to  be  broken   down  in  order  to  use  its  components  for  VLDL  synthesis  or   energy  metabolism   -­‐ Liver:  Makes  FA  and  TAG  à  VLDL  formed  for  the  transport  of   endogenous  TAG  (TAG  that  is  contained  in  body)   -­‐ As  mentioned  before,  esterification  of  FA  onto  glycerol   produces  TAG   -­‐ VLDL  synthesis  of  TAG  and  secretion  in  the  blood   -­‐ In  the  blood,  have  lipoproteins  that  are  carrying  TAG  to  be   deposited  in  skeletal  muscle,  adipose  tissue  à  In  times  of  energy   need,  can  take  to  muscles  or  other  tissues  that  need  ATP  and  if   fulfill  need,  can  take  to  adipose  tissue  to  be  stored  for  a  later  time   -­‐ Enzyme  responsible  for  breakdown  of  TAG  (Endogenous)   contained  within  lipoproteins  =  Lipoprotein  lipase  (LPL)— Hydrolyzes  FA  from  TAG  so  the  FA  are  transported  across   membrane  into  the  cell  where  they  can  be  used  for  ATP  or   storage  (Depends  on  state  of  cell—but  for  the  fed  state,  they  will   be  stored)   • Fasted  State:   -­‐ No  digestion  occurs  because  not  consuming  a  meal  here     -­‐ Right  side  of  figure  16.1  in  adipose  tissue:     o Store  lipids  as  TAG   o Need  to  break  down  TAG  into  FA  and  glycerol  so  it  can  be   transported  across  the  plasma  membrane  and  be  carried   into  the  blood  to  be  carried  to  tissues  to  be  used  for  energy   production   -­‐ Enzyme  to  breakdown  TAG  in  adipose  tissue:  Hormone   Sensitive  Lipase  à  AKA:  Adipose  Tissue  TAG  Lipase;  Essentially   know  that  there  is  a  lipase  in  adipose  tissue  that  is  responsible  for   breaking  down  TAG  into  free  FA  and  glycerol  so  these  can  be   transported  across  membrane     -­‐ Glycerol  is  freely  soluble  and  be  carried  in  the  blood  as  is   -­‐ FA  must  be  carried  in  the  blood  by  albumin  to  whatever  tissue   needs  the  FA   -­‐ Skeletal  muscle:   o Will  be  using  lipids  in  two  different  manners   o There  is  some  storage  of  TAG  in  some  muscle   (Intramuscular  TAG)  à  Can  be  used  for  ATP     o Can  take  up  FA  from  the  blood  and  use  for  ATP  production   as  well  (Ketone  bodies  apply  here  too)   o Largely  going  to  be  a  user  of  FA   -­‐ Liver:   o Central  processing  organ  that  will  sense  how  much  energy  is   in  the  body  and  what  we  need  to  do  to  survive     o Fasted  State  means  that  the  body  as  a  whole  needs  energy   o Liver  will  secrete  glucose  from  glycogenolysis  first  to  fulfill   energy  needs  and  maintain  blood  glucose  concentrations   o Continue  in  progression:  HSL  of  adipose  tissue  breaks  down   TAG  and  secretes  3  free  FA  and  glycerol  into  the  blood,  it   will  take  a  while  for  these  products  to  get  back  to  the  liver   o Glycerol  goes  back  to  the  liver  where  it  will  be  used  in   gluconeogenesis  to  secrete  glucose  into  the  blood  to   maintain  blood  glucose  concentrations   o IDL  and  LDL  come  back  to  liver  with  other  types  of  lipids   (Not  focusing  on  these  though)     o 3  free  FA  (Focus)  coming  back  to  liver  through  albumin:   Depending  on  the  state  and  how  long  have  been  fasting,  FA   will  go  back  into  VLDL  synthesis  (Re-­‐esterified  onto  glycerol   à  make  VLDL)  to  be  secreted  back  into  the  blood   o Any  tissues  with  mitochondria  can  use  FA   o Depending  on  how  long  been  fasting,  get  into  ketone   synthesis  à  When  carbohydrate  supply  is  low   o The  brain  is  a  primary  user  of  ketones   o Glucose  starts  running  low,  the  liver  is  signaled  by  the  body   that  it  still  need  energy  so  the  cells  that  can’t  use  FA  as  an   energy  source,  ketone  bodies  are  produced  in  the  liver  that   are  secreted  into  the  blood  to  tissues  with  mitochondria     o Ketone  Bodies:  Acetone,  Beta  hydroxybutyrate,   Acetoacetate     o Beta  hydroxybutyrate  and  acetoacetate  are  used  for  energy   production;  Used  interchangeably  as  ketone  bodies   (Interconverted)  à  The  concentration  of  either  is   dependent  on  the  NADH  concentration  in  the  mitochondria     o Acetone  is  aspired  off  in  the  lungs  (Not  used  for  energy   production)   o Ketone  bodies:  Think  acetoacetate  and  beta   hydroxybutyrate  (Don’t  think  it’s  one  or  the  other  because  it   depends  on  the  mitochondria  state)   o FA  à  Ketone  Body  via  beta  oxidation  (Acetyl  CoA  is   produced  as  the  precursor  for  FAS)   o FA  that  come  into  the  liver  in  fasted  state,  will  go  through   beta  oxidation  for  energy  production  and  if  the  liver  has  met   its  energy  demands,  there  is  a  build  up  of  acetyl  CoA     o Acetyl  CoA  will  be  used  to  make  acetoacetate  and  beta   hydroxybutyrate  to  be  secreted  in  the  blood  to  the   appropriate  tissues  that  will  convert  the  ketone  bodies  back   to  acetyl  CoA  to  be  used  in  the  TCA  cycle   -­‐ Heart:   o Excellent  oxidizer  of  lipids   o Uses  lipids  as  a  primary  energy  source  (Whether  it’s  FA  or   ketone  bodies)  because  it’s  a  highly  aerobic  tissue     VII. Lipid  Regulation  (Factors  into  carbohydrate  regulation)   • Fed  State:  Insulin  regulation   -­‐ Points  of  Regulation:   a) Lipoprotein  lipase  (LPL)-­‐  Used  to  hydrolyze  FA  from  TAG  to   be  taken  into  the  corresponding  cell:   o Insulin  up  regulates  LPL   o LPL  breaks  down  TAG  in  both  chylomicrons  and  VLDL   (Clears  lipid  from  the  blood  so  it  can  be  stored  or  used)   o Enzyme  relates  to  fed  state   b) Pyruvate  (FAS  relation):   o Insulin  increases  glucokinase/hexokinase,  PFK,  and   pyruvate  kinase  in  glycolysis  that  all  contribute  to   producing  pyruvate     o Insulin  signals  glycogenesis     o Pyruvate  à  acetyl  CoA  via  PDH,  which  is  used  in  FAS   o Insulin  therefore  up  regulates  FAS  à  palmitic  acid   o Key  because  a  build  up  of  FA  in  the  liver  is  toxic  so   progressive  storage  of  FA  is  necessary   c) Making  TAG  and  secreting  VLDL:  Once  again,  related  to  LPL   • Fasted  State:  Glucagon  and  Epinephrine  regulation     -­‐ Points  of  Regulation:   a) HSL  (Hormone  Sensitive  Lipase)     o Glucagon  and  epinephrine  up  regulate  HSL   o Occurs  in  a  time  of  energy  need  (Fasted  state)   • Regulation  of  FAS:   -­‐ Basics  of  FAS:   o Pyruvate  à  Acetyl  CoA  à  Citrate  (In  mitochondria)  à  Back   to  cytoplasm  à  Re-­‐converted  to  acetyl  CoA  à  Malonyl  CoA   à  FA  (2  Carbons  are  added  on  at  a  time  to  initially  produce   palmitic  acid  16:0)   o Acetyl  CoA  Carboxylase:  One  of  the  enzymes  contained   within  the  FA  synthase  enzyme  complex  that  is  important   for  the  initiation  of  FAS   o Phosphorylated  Acetyl  CoA  Carboxylase:  Less  active   version—Occurs  because  of  AMP-­‐activated  protein  kinase   o De-­‐Phosphorylated  Acetyl  CoA  Carboxylase:  Active   version  –  Occurs  because  of  protein  phosphatase  2A   -­‐ Points  of  Regulation:  Acetyl  CoA  Carboxylase   a) Insulin:   o Up  regulates  protein  phosphatase  2A  that  up   regulates  acetyl  CoA  carboxylase   o Up  regulates  protein  phosphatase  2C  that  prompts   the  conversion  of  AMP-­‐activated  protein  kinase  (high   activity)  to  the  low  activity  version  so  that  acetyl  CoA   carboxylase  is  able  to  be  more  active  in  initiating  FA   synthesis     b) Citrate:  Allosteric  regulator     o Up  regulates  de-­‐phosphorylated  active  acetyl  CoA   carboxylase   o TCA  cycle  intermediate  that  also  is  a  precursor  for  FAS   (When  citrate  is  converted  back  to  acetyl  CoA  à   cytoplasm)   o Occurs  because  citrate  favors  à  FA  when  there  is  a   buildup  of  citrate  and  reducing  equivalents  in  the  TCA   cycle   o Review:  Citrate  buildup  also  indicates  signaling  in   slowing  down  glycolysis     c) Fatty  Acyl-­‐CoA:  Allosteric  regulator   o Down  regulates  acetyl  CoA  carboxylase  à   phosphorylated  less  active  version   o The  bond  between  fatty  acyl  and  CoA  is  a  high  energy   bond  (An  activated  FA—energy  was  required  to   activate  it)   o Fatty  acyl-­‐CoA  is  also  a  precursor  for  other  lipid  classes   o Focus  on  fatty  acyl-­‐CoA  à  TAG  in  this  case   o A  buildup  of  FA-­‐CoA  down  regulates  acetyl  CoA   carboxylase ?


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All subscriptions to StudySoup are paid in full at the time of subscribing. To change your credit card information or to cancel your subscription, go to "Edit Settings". All credit card information will be available there. If you should decide to cancel your subscription, it will continue to be valid until the next payment period, as all payments for the current period were made in advance. For special circumstances, please email


StudySoup has more than 1 million course-specific study resources to help students study smarter. If you’re having trouble finding what you’re looking for, our customer support team can help you find what you need! Feel free to contact them here:

Recurring Subscriptions: If you have canceled your recurring subscription on the day of renewal and have not downloaded any documents, you may request a refund by submitting an email to

Satisfaction Guarantee: If you’re not satisfied with your subscription, you can contact us for further help. Contact must be made within 3 business days of your subscription purchase and your refund request will be subject for review.

Please Note: Refunds can never be provided more than 30 days after the initial purchase date regardless of your activity on the site.