Lipids: Biosynthesis of Fatty Acids Flashcards

1
Q

HCl

A

secreted by parietal cells to help digest protein in stomach.

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2
Q

Chief cells

A

secrete pepsinogen, which is activated by HCl to pepsin. Breaks down protein to peptides

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3
Q

Trypsinogen

A

in the intestines, converts to trypsin which is the active form by enteropeptidase.

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4
Q

trypsin

A

activates trypsinogen, chymotrypsinogen, proelastase, and procarboxypeptidase A and B. Peptides break down into tri and di and amino acids

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5
Q

Intestinal lumen

A

absorbs di and tri peptides and amino acids through Na+ dependent secondary active transport

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6
Q

a-amylase

A

secreted by salivary when starch, lactose, or sucrose enter the mouth

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7
Q

HCl from cheif cells

A

stop the salivry amylase

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8
Q

Pancreas

A

secretes a-amylase to help break down the carbs that go into the intestines and tri and oligosaccharides, maltose and isomaltose

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9
Q

Carbs absorbed

A

ONLY monosaccharides, these are transported from the cell to the blood by facilitated diffusion

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10
Q

Glucose, fructose and galactose

A

used by cell for energy
stored as glycogen
enter portal circulation and go to the liver to be converted to fat.

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11
Q

Duodenum

A

where most fat digestion occurs.

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12
Q

Fat globule

A

bound by bile salts from the liver and a phospholipid which causes emulsification. This increases the surface area of the hydrophobic lipid.

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13
Q

Jejunum

A

free fatty acids, cholesterol, and 2-monoacylglycerol are primary products of dietary lipid degradation here. They mix with bile salts to form micelles.

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14
Q

Micelles

A

disk shaped clusters of amphipathic lipids. Mixed micelles are soluble in aqueous solution of the intestinal lumen. Their hydrophilic suface helps facilitate transport of hydrophic lipids

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15
Q

Enterocytes

A

primary site of particle absorption at the brush border membrane

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16
Q

Which FA are directly absorbed into bloodstream?

A

short and medium chain. Do not require mixed micelles. This makes them an effective way to give people energy

17
Q

mono and diacylglycerolacyltransferase

A

converts 2-monoacylglycerols to triacylglycerols. occurs within the cell

18
Q

Chylomicrons

A

Triacylglycerols and cholesteryl esters and incorporated into them. released by exocytosis from enterocytes into the lacteals. They travel through lymph, enter blood. Go to peripherals.

19
Q

Lacteals

A

lymphatic vessels. Basically the immune system and waste disposal

20
Q

Fatty Acids

A
low levels are in all tissues. Found in fatty acyl esters in more complex molecules. 90% contained in lipoprotein particles. HDL and LDL. 
Large amounts in plasma during fasting 
Transported in blood by albumin
Precursors to hormones
Stored in adipose 
Major energy reserve
21
Q

Structure of FA

A

Hydrophobic hydrocarbon chain
terminal carboxyl group - high water affinity, amphipathic (hydrophobic compound with a hydrophilic end)
Long chain FA hydrophobic portions predominate

22
Q

Saturated FA

A

No double bonds
longer FA, higher meling point
solid at room temp
butter

23
Q

Unsaturated FA

A
Double bonds - create a kink 
Lower melting point
Cis config - Trans is synthetic
Liquid at room temp
Oil
They produce less energy, are less highly reduce, and less products are produced
24
Q

Cis config

A

loose pliable membranes,

25
Q

Trans config

A

still membranes –> CV disease

hydrogen gas is pushed through an unsaturated FA. Converts to saturated. Some double bonds reform, but it is different

26
Q

Linoleic acid (w-6)

A

can metabolize into arachidonic acid
Key part in Dihomogamma linolenic acid
potentially produces PGE1 prostaglandins non-inflamatory
anti-spasmotic
can potentially product PGE2 - inflammatory prostaglandins

27
Q

Linolenic acid (w-3)

A

Metabolized into PGE3 - non inflammatory
inhibits AA production
deficiency results in decreased vision and altered behavior.

28
Q

VLDL

A

assembled in liver from cholesterol and apolipoproteins.
Convertd to LDL in bloodstream
Transport endogenous products (chylomicrons exogenous)
associated with small dense LDL and TG - marker of metabolic syndrome, particularily atherogenic

29
Q

De Novo Synthesis of FA

A

supplied by diet as carbs, proteins and other molecules in excess
Stored as triacylglycerols
Synthesis occurs primarily in the liver and lactating mammary glands - some in adipose
uses Acetyl CoA from glycolysis and kreb cycle

30
Q

Fatty Acid Synthase

A

mnomer is multicatalystic polypeptide with seven different enzymatic activities plus domain
Domain covalently binds to 4’phosphopanteheine - is a derivative of pantothenic acid and an enzyme component of vitamin A

31
Q

Storage

A

mono, di, and tri cylglycerols consist of one, two, or three molecules of faty acid esterified to a molecule of glycerol.

32
Q

Triacylglycerol structure

A

3 FA esterified to a glycerol molecule. Not typically same
C1 FA saturated
C2 FA unsaturated - decrease melting temp
C3 FA either

33
Q

Glycerol Phosphate

A

initial acceptor of FA during TAG synthesis
made in liver and adipose. Adipocytes can take up glucose only in presence of insulin. Low plasma glucose and insulin limit capacity to synthesize glycerol phosphate.
2 pathways - 1st from glucose using reactions from glycolysis produced by dihyroxyacetone phosphate
Reduced by glycerol phosphate dehydrogenase
2nd only in lvier uses glycerol kinase

34
Q

FA to active form

A

must be converted to active form (have a CoA attached) before it can TAG synthesis

35
Q

Fates of TAG

A

Adipose - stored in cytosol of cells. anyhydrous
“Depot Fat” - available to mobilize when fuels needed
Liver - very little
exported, packaged with cholesteryl esters, cholesterol, phospholipid and protein to form lipoprotein particles VLDL
VLDL secreted into blood
Mature and function to deliver endogenously derived lipids to peripheral tissues

36
Q

Release FA from TAG

A

mobilization requires hydrolytic release of FA and glycerol
Initiated by hormone sensitive lipase - which removes FA from C1 and or C3
Additional lipases specific for di and mono acylglycerols remove the remaining FA

37
Q

Glycerol

A

released during TAG degradation.
Cannot be metabolized by adipocytes
lacks glycerol kinase
Transported to liver - phosphorylated - used to form TAG in liver or converted to DHAP

38
Q

Hormone-Sensitive Lipase

A

activated by phosphorylated by 3’ 5’ cyclic AMP dependent protein kinase. Produced in adipocyte. Binds to receptors on the cell membrane. Activated adenylate cyclase.