Cell Metabolism 2 Flashcards

1
Q

5 main classes of lipids

A

Free fatty acids, steroids, triacylglycerides, phospholipids, glycolipids

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2
Q

Why are fatty acids a useful storage molecule

A

It is reduces and anhydrous

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3
Q

What are the three main sources from which fat is derived from

A

Diet, lipogenesis ( from scratch) and storage depots in adipose tissue

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4
Q

Where are bike salts made and stored

A

Made in liver and stored in gall bladder

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5
Q

Where are bile salts generated from

A

Cholesterol. During digestion they move from bile duct into small intestine

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6
Q

What do bile salts do

A

Emulsify fats in the intestine, aiding the digestion and absorption of fat soluble vitamins A, D,E and K

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7
Q

What does a lack of bile salts result in

A

Lack of bile salts results in the majority of fats passing through the gut undigested and unabsorbed resulting in fatty stool ( steatorrhea)

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8
Q

What is orlistat( aka tetrahydrolipstatin)

A

Potent inhibitor of gastric and pancreatic lipases. It therefore reduces fat absorption and can be used to treat obesity

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9
Q

What are the main side effects of orlistat

A

Abdominal pain, increased flats, steatorrhea and urgency to defecate

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10
Q

What is the role of chylomicrons

A

Dietary fat transport

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11
Q

What is the role of very low density lipoproteins

A

Endogenous fat transport

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12
Q

What is the role of immediate density lipoproteins

A

LDL precursor

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13
Q

What is the function of low density lipoproteins

A

Cholesterol transport

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14
Q

What is the role of high density lipoproteins

A

Reverse cholesterol transport

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15
Q

What happens before the triglycerides are incorporated into chylomicrons

A

Digested dietary products are absorbed by the enterocytes that line the brush border of the small intestine. Triglycerides are resynthesized under the control of several enzymes prior to the incorporation into chylomicrons

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16
Q

What happens to the chylomicrons

A

They are transported via the lymphatic system and into the blood stream. They acquire apoproteins from HDL following release into blood stream. Lipoprotein lipase is located one the capillary endothelial cells lining tissues including adipose, heart and skeletal muscle. Fatty acid undergoes beta oxidation. Glycerol is returned to liver for use in gluconeogenesis

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17
Q

What is the anatomy of lipoproteins

A

Phospholipid monolayer containing cholesterol and apoproteins. This surrounds a core of cholesterol esters and triacylglycerols

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18
Q

How are cholesterol esters synthesised

A

In the plasma from cholesterol and the acyl chain of phosphatidylcholine ( lecithin) via a reaction catalysed by lecithin cholesterol actltransferase( LCAT)

19
Q

What is the role of HDL

A

Good cholesterol as it takes cholesterol from the peripheral tissues back to the liver for use or disposal ( reverse cholesterol transport). They help to lower total serum cholesterol

20
Q

What is the role of LDL

A

LDL’s is bad cholesterol as the elevation of LDL

levels lead to atherosclerosis( hardening of arteries)

21
Q

Where does beta oxidation occur and what is the end product produced

A

Beta oxidation occurs in the mitochondria and ultimately results in the production of acetyl CoA

22
Q

Describe the beta oxidation of fatty acids

A

Fatty aids are converted into an acetyl CoA species. During this process ATP-> AMP so 2 HIGH ENERGY BONDS ARE USED. This occurs on the outer mitochondrial membrane. To transport the species into the matrix, it is coupled to the molecule carnitine to form acyl carnitine; moved to and from matrix by translocase (shuttle mechanism ).

23
Q

What happens during primary carnitine deficiency

A

Mutations in genes encoding carnitine transporter results in a reduced ability of cells to take up carnitine needed for beta oxidation of fatty vides. If there isn’t enough fatty acids inside mitochondrial you will feel tired. Carnitor is used as a supplement / treatment

24
Q

Describe the process of the beta oxidation cycle

A

The acyl CoA undergoes a series of oxidation, hydration, oxidation and thiolysis reactions which are collectively known as beta oxidation. This results in the production of one molecule of acetyl CoA and 1 acyl CoA species which is 2 C shorter than the original. On the final cycle ( 4 acyl CoA intermediate, two acetyl CoA molecules are formed ).

25
Q

What is continuously removed from the beta oxidation cycle

A

2 carbons from the acyl CoA to produce acetyl CoA

26
Q

Overall reaction of beta oxidation of palmitic acid

A

Palmitoyl CoA + 7 FAD + 7 NAD+ + 7 H20 + 7 CoA -> 8 acetyl CoA + 7FADH2 + 7 NADH

During each cycle, one molecule of FADH2 and NADH are produced.

27
Q

What is ketone body formation

A

For acetyl coA to enter the Krebs Cycle, carbohydrate metabolism needs to have occurred as oxaloacetate is needed. But when fasting, glucose and therefore oxaloacetate production is low and acetyl coA cannot enter TCA cycle and so forms ketone bodies instead. Ketone bodies include acetoacetate, D-3-hydroxybutyrate and acetone

28
Q

Do you get more ATP when you oxidise fatty acids as opposed to glucose

A

Yes

29
Q

What occurs during fatty acid biosynthesis/ lipogensis

A

Fatty acids are formed sequentially by decarboxylative condensation involving acetyl CoA and malonyl CoA. Following each round of elongation, the fatty acid undergoes reduction and dehydration by sequential action of ketoreductase, dehydrated and Enol reductase.

30
Q

What are the 2 enzymes involved fatty acid synthesis

A

Acetyl CoA carboxylase and fatty acid synthase

31
Q

Difference in carriers in fatty acid synthesis and degredation

A

Synthesis; ACP

Degredation : CoA

32
Q

Reducing power in fatty acid synthesis and degredation

A

Synthesis : NADPH

Degredation : FAD/NAD+

33
Q

Locations of fatty acid synthesis and degredation

A

Synthesis : cytoplasm

Degredation ; mitochondrial matrix

34
Q

Overall reaction of fatty acid synthesis

A

Acetyl CoA + 7 Malonyl CoA (C3) + 14 NADPH + 14 H+-> palmitate (16C) + 7 CO2 +6H2O +8COA-SH +14NaDP+

35
Q

What enzyme carries out the desaturation of fatty acids

A

Fatty acyl-CoA desaturases

36
Q

Where does de novo FA biosynthesis occur in adults

A

Liver, adipose tissue and lactating breast

37
Q

Can we selectively target FA synthetase (FASN) in cancer?

A

Inhibition if FASN by celurelin ( an antifungal antibiotic) is shown to reduce tumour growth of ovarian cancer cells

38
Q

Short chain acyl-CoA-dehydrogenase

A

<6C

39
Q

Medium chain acyl CoA enzyme A dehydrogenase

A

6-12 C

40
Q

Long chain 3-hydroxacyl CoA enzyme A dehydrogenase

A

C13-C21

41
Q

Very Long chain acyl CoA enzyme A dehydrogenase

A

> 22

42
Q

Medium chain acyl coenzyme A dehydrogenase deficiency

A

Autosomal recessive and if diagnosed patients should not go more than 10-12 hrs no food as they are not very good at breaking down fatty acids to release energy. Patients with more illness resulting in loss of appetite or severe vomiting may bee IV glucose to make sure that the body is not dependent on fatty acids for energy

43
Q

What are the cotransporters in maltate aspartate shuttle and glycerol-phosphate shuttle

A

Maltate aspartate : NADH

Glycerol phosphate shuttle:NADH in cytoplasm and FADH in mitochondria