5 Metabolism Flashcards

1
Q

Oxidative phosphorylation

A

Stage 1: Energy of electron transport is used to pump protons across membrane.

Stage 2: Energy in the proton gradient is harnessed by ATP synthase to make ATP.

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2
Q

Glukogenes

A

Bildandet av lagringsformen glykogen från glukos.

Kräver energi.

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3
Q

Glykogenolys

A

Glykogen nedbrytning till glukos.

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4
Q

Pentosfosfathunten

A

Substrat: Glukos -6- fosfat.

Produkt:
•NADPH; Ges av irreversibla reaktioner. Behövs för anabola reaktioner i cellen.
•och Ribos-5- fosfat; Ges av reversibla reaktioner. Behövs till nukleotidsyntes.

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5
Q

Biological oxidation

A

1) Pyruvate dehydrogenase
2) TCA/ Citric acid cycle
3) Electron transport chain
4) Oxidative phosphorylation

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6
Q

Regulation of PDH and TCA

A

a) Energy state of the cell; High energy state: PDH & TCA slow down. Low energy state: PDH & TCA speed up.
b) Allosteric regulation by TCA intermediates
c) Ca2+ stimulate

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7
Q

Catabolism of AAs

A

1 Transaminate

2 Deaminate glutamate: remove N -> ammonia

3 Urea cycle: make urea from the ammonia -> excrete

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8
Q

Fate of the carbon skeleton

A

A) Glucogenic AAs: can give glucose

B) Ketogenic AAs: can give ketones & FAs: Leu, Lys

C) Glucogenic & ketogenic AAs: can give both (4 AAs)

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9
Q

Fate of nitrogen

A

1 Transamination gives glutamate

2 Deamination of glutamate = NH4+

3 Production of urea in the urea cycle;
•NH4+ bound as carbamoyl phosphate in the mitochondria

•NH3 = group from aspartate

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10
Q

Glykolysen

A

Glukos till energi

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11
Q

Netto från 1 glukos molekyl

A

2 NADH
2 ATP
2 Pyruvat

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12
Q

Netto (anaeroba förhållanden)

A

2 ATP
2 Laktat
2 NADH oxideras till 2 NAD+ (kan köra mer glykolys)

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13
Q

Glykolysens tre reglerande steg

A

Steg 1: Hexokinas

Steg 3: Fosfofruktokinas

Steg 10: Pyruvatkinas

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14
Q

Glukoneogenes

A

Glukos syntetiseras av laktat, glycerol, aminosyror.

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15
Q

Coricykeln

A

Lever: glukoneogenes (laktat -> glukos) via blodet till muskler

Muskel: glykolys (glukos -> laktat) via blodet till levern

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16
Q

Lipidomsättning

A

1) Release of FAs from TAGs in adipose
2) Activation of FAs to acetyl - CoA
3) Transport across mitochondrial IM; the carnitine shuttle
4) Beta - oxidation of FAs in the matrix (gives 9 acetyl- CoA to TCA + 8 NADH/FADH2)

17
Q

Ketonkroppar

A

Sker i leverns mitokondrier under svält.

Ketoner from överbliven Acetyl-CoA förser hjärnan och övriga vävnader = sparar på glukos och protein.

18
Q

Anabolism of FAs & triacylglycerols

A

1) Transport of acetyl- CoA to cytosol
2) The synthesis of malonyl - CoA
3) Build up of a FA hydrocarbon chain: FA synthesis
4) Storage of FAs as triacylglycerols

19
Q

Types of regulation

A

Allosteric regulation

Covalent modification

Regulation of gene expression

20
Q

Insulin

A
Released from: pancreatic β- cells 
Upon: high [glucose] 
Stimulates: decrease [glucose] 
By increasing: uptake & storage 
Target: most cells; especially liver, adipose & muscle
21
Q

Glucagon

A
Released from: pancreatic β- cells 
Upon: low [glucose] 
Stimulates: increase [glucose] 
By increasing: release from storage 
Target: mainly liver, no receptors in muscle
22
Q

Adrenalin

A
Released from: adrenal gland  
Upon: stress, exercise, low [glucose] 
Stimulates: increase [glucose] 
By increasing: release from storage 
Target: most cells; liver, adipose & muscle
23
Q

Cortisol

A
Released from: adrenal cortex 
Upon: prolonged stress/ starvation
Stimulates: gluconeogenesis/ lipolysis 
By increasing: release from storage 
Target: most cells; liver, adipose & muscle
24
Q

The process how insulin increases glucose uptake by muscle & adipose cells

A

1 Insulin binds to insulin receptor

2 Intracellular signalling cascade

3 More glucose transporters (GLUT-4) to cell membrane.

4 Increased uptake of glucose through GLUT-4

25
Q

De novo syntes

A

1 Aktivering av ribos-5-fosfat till fosforibosylpyrofosfat (PRPP)

2 Kvävebas (Purin/pyrimidin) på 1´ kolet istället för pyrofosfat.

26
Q

Nukleotidnedbrytning

A

1 Fosfataser och nukleotidaser tar bort fosfatgrupper —> nukleosider (P-P-P => OH)

2 Kvävebaser tas loss från nukleosid m.h.a fosforylys (Kvävebas => P)

3a Pyrimidiner: ring öppnas och bryts ned till lösliga ämnen.

3b Puriner: ring kvar men görs mer löslig i form av urinsyra

27
Q

Salvage syntes

A

Återanvändning av nukleotider, nukleosider och baser

  • Nukleosid —> Nukleotid (fosforylering)
  • Färdigs kvävebaser ex. A/G kan kopplas på PRPP av speciella salvage-enzym.