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Biochemistry 2 > Lecture (7) Lipid METABOLISM (part 1) > Flashcards

Lecture (7) Lipid METABOLISM (part 1) Flashcards

1
Q

what is the Importance of lipids in diet?

A

1) Lipids are one of the main sources of energy in the body.
2) Lipids supply the body with essential fatty acids.
3) Lipids supply the body with fat-soluble vitamins.
4) Lipids make the diet palatable.

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2
Q

Lipids are one of the 1st sources of energy in the body.

T or F?

A

F, carbohydrates

Lipids are one of the MAIN sources of energy in the body.

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3
Q

Lipid digestion begins in the mouth.

T or F?

A

F, in the stomach.

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4
Q

…………. is secreted from Ebner’s glands of the tongue

A

Lingual lipase

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5
Q

Lingual lipase secreted from…………. of the tongue

A

Ebner’s glands

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6
Q

give a reason, Lingual lipase and gastric lipase are very important in lipid digestion in neonates?

A

because the mother milk contains mainly triglyceride with a short chain of FA, Lingual lipase and gastric lipase act on this type of FA.

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7
Q

mixing of lipids occurs due to…………….

A

peristalsis.

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8
Q

Emulsification (solubilization) of dietary lipids occurs in………..

A

small intestine (duodenum)

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9
Q

Emulsification (solubilization) of dietary lipids in the small intestine (duodenum) by………..

A

by bile salts

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10
Q

Degradation of dietary lipids occurs by………….

A

Pancreatic enzymes (Pancreatic lipase, Phospholipase and Cholesteryl esterase).

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11
Q

the resynthesis of TAG & cholesterol esters occur in………

A

intestinal mucosal cells (enterocytes)

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12
Q

The newly resynthesized TAGs and cholesteryl esters are very hydrophobic. Therefore, they are packaged as particles of lipid droplets surrounded by a thin layer composed of phospholipids, unesterified cholesterol, and a molecule of the protein (apolipoprotein) forming……………….

A

chylomicron.

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13
Q

…………. is the absorbed form of lipid from the small intestine.

A

Chylomicron.

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14
Q

………….is milky appearance after a lipid-rich meal

A

Lipemia.

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15
Q

what is the mechanism of action of Orlistat?

A

is an anti-obesity drug, inhibits gastric and pancreatic lipases, thereby decreasing fat absorption, resulting in weight loss.

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16
Q

what is the Steatorrhea?

A

Fat content of the stool is abnormally increased (normally < 5 gm/day).
It is caused by a defect in lipid digestion or absorption. • ↓ Pancreatic lipase (↓ fat digestion).
• ↓ Bile salts (↓ fat absorption).
• Defective Intestinal mucosa (↓ fat absorption).

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17
Q

TAG in chylomicrons is broken to….. & ……….by…………

A

to free fatty acids & glycerol by lipoprotein lipase

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18
Q

lipoprotein lipase present in……….

A

capillaries of adipocytes, muscle cells & peripheral tissues

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19
Q

the decrease in lipoprotein lipase causes……….

A

Type I hyperlipoproteinemia

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20
Q

Type I hyperlipoproteinemia is caused due to………

A

deficiency in lipoprotein lipase

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21
Q

what is the Fate of FFA?

A

transported in the blood in association with albumin to cells for energy production or stored as TAG in adipocytes.

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22
Q

what is the Fate of glycerol?

A

transported to the liver → glycerol-3-P by glycerol kinase (in liver only) → glycolysis or gluconeogenesis.

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23
Q

what are the Sources of fatty acids FA?

A

1) Diet.
2) Lipolysis of TAG in adipocytes.
3) De novo synthesis from precursors (Excess CHO and Proteins).

24
Q

FA oxidation takes place in…….

A

mitochondria.

25
Q

FA biosynthesis takes place in the……..

A

cytosol.

26
Q

FA oxidation is increased when other sources of energy such as blood glucose and liver glycogen are high.
T or F?

A

F, when other sources of energy such as blood glucose and liver glycogen are low.

27
Q

FA oxidation is decreased when other sources of energy such as blood glucose and liver glycogen are low.
T or F?

A

F, increased.

28
Q

FA are stored as………….. in………

A

FA are stored as triacylglycerol (fat) in adipose tissue

29
Q

DE NOVO SYNTHESIS OF FATTY ACIDS occurs in …………. and requires………

A

cytosol

a. Acetyl CoA
b. NADPH
c. CO2
d. ATP

30
Q

Cytosolic acetyl CoA is produced from……… by………..

A

citrate, by ATP-citrate lyase

31
Q

Carboxylation of acetyl CoA to………. by……….

A

malonyl CoA, by acetyl CoAcarboxylase.

32
Q

seven different enzymic activities plus a domain that covalently binds acetyl CoA called……….. that has SH group.

A

acyl carrier protein (ACP)

33
Q 
Palmitic acid (C16) synthesis needs........ and........... and..............
** 7 CO2 and 14 NADP are released.
A

1 acetyl CoA, 7 malonyl CoA and 14 NADPH.

34
Q

what is the Fate of Palmitate?

A
  1. Activation of palmitate by palmitoyl CoA synthetase to give palmitoyl CoA.
  2. Esterification of palmitoyl CoA (to form TAG and stored).
  3. Chain elongation.
  4. Desaturation.
35
Q

the Elongation of palmitate occurs in………

A

Smooth endoplasmic reticulum (SER).

36
Q

Humans have carbon …., ….., …….., and……desaturases.

A

4, 5, 6, and 9

37
Q

Linoleic acid is an essential fatty acid. Why?

A 
Because it has a double bond at carbon number 12 linoleic (18:2 Δ9, 12), Since there is no desaturation from carbon 10 in humans, so humans cannot desaturate from
carbon 10 (No Δ12 desaturase) so it must be taken in diet.
38
Q

lipogenesis means…….

A

(Synthesis of triacylglycerols)

39
Q

what is the Function of TAG?

A

TAG is a major energy store, stored in adipose cells.

40
Q

Lipogenesis occurs in……. and…….

A

Liver and adipose tissues.

41
Q

Lipogenesis needs……… and ……… and both must be activated.

A

glycerol and FA.

42
Q

Lipolysis means…………

A

the hydrolysis of TAGs into glycerol and free fatty acids.

43
Q

Lipolysis occurs in……….

A

adipose tissues.

44
Q

what is Aim of the Lipolysis?

A

During fasting, provide the body with FFA which oxidized and give energy.

45
Q

Lipolysis needs 3 enzymes, mention them.

A

(by 3 lipases):
1- Hormone-sensitive lipase (HSL)
2- Diacylglycerol lipase
3- Monoacylglycerol lipase

46
Q

what is the Fate of glycerol?

A

The fate of glycerol: Glycerol cannot be metabolized by adipocytes because they lack glycerol kinase.
It goes to the liver to be activated to glycerol-3-P which is then converted to DHAP (that can participate in glycolysis or gluconeogenesis).

47
Q

what is the Fate of FAs?

A

FAs binds to albumin to be taken up by tissues for energy production.

48
Q

Brain prefer fatty acid oxidation to provide energy, T or F?

A

F, Brain does not favour fatty acids oxidation to provide energy.

49
Q

Glucagon inhebits HSL. It causes phosphorylation to HSL. T or F?

A

F, Glucagon stimulate HSL. It causes phosphorylation to HSL

50
Q

the phosphorylated form of HSL is the inactive form.

T or F?

A

F, (the phosphorylated form is the active one)

51
Q

Only glycogen phosphorylase and HSL are active in dephosphorylated form.
T or F?

A

F, in phosphorylated form.

52
Q

In the Fasting State Inhibition of lipolysis occur.

T or F?

A

F, Activation of Lipolysis.

53
Q

In the Fed State Activation of Lipolysis occur.

T or F?

A

F, Inhibition of lipolysis.

54
Q

In the presence of high plasma levels of insulin, HSL is dephosphorylated and activated.
T or F?

A

F, inactivated

55
Q

Only……… and……….. are active in phosphorylated form.

A

glycogen phosphorylase and HSL.

Biochemistry 2 (7 decks)

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