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Lipidnotater

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Cahpter 6 fatty acid synthesis

Først og fremst:

Forholdet mellom Karbohydrat og Lipid-syntese

Likheter mellom oksidasjon og syntese:

Oversikt

Bakgrunn: Substratet for Fettsyresyntese er Acetyl-CoA. Et produkt i sitronsyresyklus der glukose omdannes til energi. Dette kommer via citrat som passerer mitokondriemembranen. Citrat tar veien over til cytosol.

  • I simpleste form handler FAS om å kombinere Acetyl-CoA (2 C) til Palmitin-Syre (16 C) i en energikrevende sirkelreaksjon. ATP + H20 -> ADP + H+

Regnskapet for en hel runde fra Acetyl-CoA til palmitate blir da:

  • Palmitinsyre brukes videre som utgangspunkt for å lage lengre fettsyrer og for å legge til dobbeltbindinger.

Khan Academy on Syntese

Fatty acid synthesis starts with the carboxylation of acetyl CoA to malonyl CoA. This irreversible reaction is the committed step in fatty acid synthesis

  • The enzyme system that catalyzes the synthesis of saturated long-chain fatty acids from acetyl CoA, malonyl CoA, and NADPH is called the fatty acid synthase
  • Fatty acids are synthesized by the repetition of the following reaction sequence: condensation, reduction, dehydration, and reduction.
  • The growing fatty acid chain is elongated by the sequential addition of two-carbon units derived from acetyl CoA. The activated donor of twocarbon units in the elongation step is malonyl ACP.(Acyl carrier protein)
  • Fatty acids are synthesized in the cytosol, whereas acetyl CoA is formed from pyruvate in mitochondria. Hence, acetyl CoA must be transferred from mitochondria to the cytosol. The barrier to acetyl CoA is bypassed by citrate, which carries acetyl groups across the inner mitochondrial membrane
  • Elongation by the fatty acid synthase complex stops on formation of palmitate (C16). Further elongation and the insertion of double bonds are carried out by other enzyme systems.

Endelig skjebne Fettsyrene blir koblet på glycerol til triaceyl-glyserider og syntetisert til VLDL i leveren og transportert til resten av kroppen

Regulering

Acetyl-CoA karboksylase Rate limiting enzyme..

* Legger til karboksylgruppe til Acetyl-CoA --> Malonyl-CoA.

Pos regulering:

  • Alosterisk (molekyl fester seg på anne sted på enzymet) ved Citrat Regulerer oppover/fremover-
  • Hormonell: Insulin (Trenger fettsyresyntese etter høy glukose i blodet)

Neg Regulering:

  • Hormonell:Glukagon (Bryter ned fettsyrer for energi.)
  • Alosterisk: Langkjedede fettsyrer. (Neg tilbakekobling)

Chap 5. Oxidation of fatty acids in eukaryotes

Generell bakgrunn:

  • Fettsyrer trenger å transporteres fra cytosol til Mitokondriemembran.
  • Carnitine Acyl transferase I.
  1. Aktivere Fettsyren.
  • Legge til Carnitin
  1. Transport inn i mitokondriell matrix.
  2. Beta-oksidasjon
  • Lager NADH og FADH2 til elktrontransportkjeden og prod av ATP.

Beta oksydasjon

Hvert andre C fra karbonyl-ende av acyl-CoA bli oksydert til Acetyl CoA og prod Reduksjonsagenter for ATP-prod.

Regulering

Malonyl-CoA alosteriks hemmer av Carnitine Acyl transferase I

All produksjon av energi skjer i mitokondriet, både Oksidering samt celleånding. Krebs-syklus.

3.3 β-oxidation of unsaturated fatty acids

Legg til mer tekst.

Fettsyre: Karboksylsyre med lang karbonkjede. Karboksylsyre General Fatty Acid Formula

FA oxidation on Wikpedia In the words of Wikipedia:

"Beta-oxidation is the process by which fatty acid molecules are broken down in the mitochondria to generate acetyl-coA, which enters the citric acid cycle, and NADH and FADH2, which are used by the electron transport chain."

General chemical structure of an acyl-CoA, where R is a fatty acid side chain -->

NADH

In metabolism, NAD+ is involved in redox reactions, carrying electrons from one reaction to another.

FADH2

flavin adenine dinucleotide (FAD) is a redox cofactor involved in several important reactions in metabolism.

Chapter 7 Desaturation and chain elongation.

Elongering

Fettsyrer med 16C eller mer, blir modifisert i:

  1. ER
  2. Mitokondrier
  3. Perixosomer

"The major product of the fatty acid synthase is palmitate. In eukaryotes, longer fatty acids are formed by elongation reactions catalyzed by enzymes on the cytosolic face of the endoplasmic reticulum membrane. These reactions add two-carbon units sequentially to the carboxyl ends of both saturated and unsaturated fatty acyl CoA substrates. Malonyl CoA is the two-carbon donor in the elongation of fatty acyl CoAs. Again, condensation is driven by the decarboxylation of malonyl CoA."

"Uses acyl-CoAs, Malonyl-CoAs, and NADPH (Diagram 1, #2)"

  1. Kondensering mellom Malonyl-CoA og long kjedet fettsyre acyl-CoA-substrat.

Viktige enzymer

Elongation of very long chain fatty acids

  • Elovl 1-7
  • Elovl 1,3 og 6 (Elongering av SFA og MUFA. (C16 opp til c24)
  • Elovl 2 og 4 (PUFA synthetis)

Desaturering

Fatty acid desaturation system

  • DELTA-9 desauturase eller Steroyl-CoA desaturase som katalyserer mettede Acyl-Coa-fettsyrer til umettede fettsyrer. Most notably: 18-karbon-fettsyre (Acyl-CoA) 18:0 til oljesyre, 18:1. Lager en dobbeltbinding 9 karboner fra karboksyl-gruppen (COO-). Er under kopleks hormonell kontroll. *Desaturerer også :0 fettsyrer med C12-19 karboner

  • SCD1 og SDC5 mest studert. SCD5 mest aktiv i hjernen og pankreas og mutasjoner er forbundet med hareskår hos mennesker.

Andre desaturaser

FADS3 *

Esensielle fettsyrer Med dobbeltbindinger beyond DELTA-9 pos. Karbon nr. 9 etter kaboksylgruppen.

Linolenic acid is an unsaturated fatty acid that is an essential fatty acid in mammals because they cannot synthesize double bonds in fatty acids beyond position DELTA-9. This makes linoleic acid and linolenic acid essential in mammalian diets, since they have double bonds beyond position DELTA-9 (at positions 9,12 and at positions 9,12, and 15 for linoleic and linolenic acid, respectively).

Regulering

Lipoprotein Receptors

LDL receptors

Involvement of LDL receptors in cholesterol uptake and metabolism

Mutations

Phenotypes of the LDL receptor mutations in FH individuals are as follows:

  1. Reductions in amount of LDL receptor made;
  2. LDL receptor is made, but it fails to migrate to plasma membrane;
  3. LDL receptor is in plasma membrane, but it fails to bind LDL; and
  4. LDL receptor is in plasma membrane and binds LDL, but it fails to cluster in coated pits.
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