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BIOL 204 > Lecture 22 -- review questions > Flashcards

Lecture 22 -- review questions Flashcards

1
Q

what is bile?

A

fluid made and released by liver, stored in gallbladder

helps with digestion by breaking down fats into fatty acids

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2
Q

what is bile made of?

A

1) bile salts (which are made by bile acids)

2) proteins

3) bilirubin

4) cholesterol

5) lecithin (phospholipid)

“boys poop brown colored liquid”

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3
Q

what are the main components of bile?

A

bile acids (make up bile salts)

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4
Q

what are bile salts made of?

A

bile acids that are often bonded to glycine or taurine to increase water solubility (=conjugated bile acids)

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5
Q

what is the role of bile salts in the digestive process?

A

break down fat

large fat globules –> smaller fat droplets

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6
Q

where is bile produced? from which molecule?

A

liver

cholesterol

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7
Q

what are conjugated bile salts?

A

made up of bile acids that are bonded to glycine or taurine to increase water solubility

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8
Q

what is the only way for the body to get rid of cholesterol?

A

bile salts are produced from cholesterol in the liver

liver synthesizes bile salts from cholesterol to replace the bile lost in feces

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9
Q

what percentage of bile salts are lost in the feces?

A

20%

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10
Q

in what part of the intestine are bile salts recycled (= taken back to the liver)?

A

ileum

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11
Q

what is the role of emulsification?

A

bile salts in duodenum break large fat globules into smaller fat droplets

–> increase surface area available to lipase enzymes

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12
Q

what are micelles?

A

aggregates of bile salt that forms a polar outer shell and a hydrophobic inner core

long chain FAs, cholesterol, and other hydrophobic molecules dissolve in the core

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13
Q

what are triglycerides composed of?

A

1 triglyceride = 1 glycerol molecule + 3 fatty acids

3 fatty acid chains linked by a glycerol

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14
Q

which enzyme is mainly responsible for digesting triglycerides in the small intestine?

A

pancreatic lipases

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15
Q

what is the function of micelles in the absorption of lipids?

A

micelles incorporate the lipid digestion products and enable these lipid digestion products to be transported to the small intestinal surface (plasma membrane of enterocytes) for absorption

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16
Q

why do the lipids need to be transported in the core of the micelles to the enterocytes?

A

lipids are hydrophobic —> must be kept in the core of a hydrophilic bile salt shell of the micelle in order to diffuse across the water layer adjacent to the enterocyte surface in order to reach the surface of the enterocyte

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17
Q

what happens to the fatty acids and monoglycerides once inside of the enterocyte?

A

FAs and monoglycerides pass by simple diffusion into the enterocyte (intestinal epithelial cell)

within the cell, FAs and monoglycerides are converted to TGs

proteins coat the TGs and other fatty substances to form chylomicrons

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18
Q

which lipoprotein does it form inside of enterocyte?

A

chylomicrons

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19
Q

are lipids absorbed into the blood or lymph? Through which structure?

A

chylomicrons are too large to penetrate endothelium of capillary

lymph

lacteals

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20
Q

what is chyle?

A

fatty, milk-white intestinal lymph

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21
Q

will chylomicrons always be in the lymphatic system (until degradation), or will they be transferred to the blood circulation at one point?

A

will be transferred to blood circulation at one point

carried thru lymphatic system to general circulation

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22
Q

where is fat absorbed? (organ of the alimentary canal)

A

small intestine

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23
Q

what are lipoproteins?

A

tiny droplets w/ a core of cholesterol and TGs and a coating of proteins (apolipoproteins) and phospholipids

coating has 2 purposes:
- enables lipids to remain suspended in the blood
- recognition marker for cells that absorb them

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24
Q

what molecules can you find at the core and the surface of lipoproteins?

A

core:
- cholesterol
- TGs

coating:
- proteins (apolipoproteins)
- phospholipids

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25
Q

what is the classification of lipoprotein based on? (ie which characteristic?)

A

density

4 major categories

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26
Q

what do VLDL, LDL, and HDL stand for?

A

VLDL – very low density lipoprotein

LDL – low density lipoprotein

HDL – high density lipoprotein

27
Q

what is the most abundant component of chylomicrons?

A

triglycerides

28
Q

what is the most abundant component of VLDL?

A

triglycerides

29
Q

what is the most abundant component of LDL?

A

cholesterol

30
Q

what is the most abundant component of HDL?

A

protein

31
Q

which lipoprotein contains the most cholesterol?

A

LDL

32
Q

which lipoproteins contain the most triglycerides: HDL, LDL, or VLDL?

A

VLDL

33
Q

what is apolipoprotein, and where can you find it?

A

a protein that coats lipoproteins

surface of lipoproteins

34
Q

what is the function of lipoprotein lipase, and where is it found?

A

removes TGs from lipoproteins
breaks down TGs into fatty acids and glycerol

found in surface of endothelial cells

35
Q

the removal of TGs from chylomicrons by lipoprotein lipase on the vascular endothelial surface results in which molecule?

A

fatty acids

glycerol

36
Q

where do chylmicron remnants go?

A

liver for disassembly

37
Q

where is VLDL produced?

A

liver

38
Q

what is the function of VLDL?
Does VLDL carry fat synthesized by the liver?
where?

A

bring more TGs to the body’s cells (including adipose tissue for storage)

yes; VLDLs do carry fats synthesized by the liver

carry them to the body’s cells

39
Q

what converts VLDL to LDL?

(tip: which molecules are removed from VLDL thru their journey in the circulation?)

A

lipoprotein lipase removes TGs from VLDL and converts them to FAs and glycerol

40
Q

what is the function of LDL?

A

deliver cholesterol to the body’s cells

41
Q

what is the function of HDL?

A

pick up excess cholesterol from tissues and deliver to the liver for use or disposal

42
Q

what is lipolysis?

A

breakdown of fats by hydrolysis to release FAs

43
Q

what happens to the glycerol and fatty acid products obtained upon the action of lipase in the adipose tissue? (metabolic pathways)

A

glycerol is converted to a glycolysis intermediate

FAs undergo beta-oxidation to generate acetyl-CoA

44
Q

which part of TG molecules enters glycolysis?

A

glycerol

45
Q

what is beta oxidation?

A

process that converts FAs to generate acetyl-CoA to use for the citric acid cycle to generate ATP and NADH and FADH2 which are used for the electron transport chain

46
Q

why do fats have glucose-sparing and protein-sparing effects?

A

as long as enough fat is available to meet the energy needs of the tissues, protein isn’t catabolized for fuel and glucose is spared for consumption by cells that can’t use fat (e.g. neurons)

47
Q

how is glycolysis related to lipid metabolism?

A

TG –> broken down by lipoprotein lipase into glycerol

glycerol –> converted to a glycolysis intermediate –> degraded to pyruvate

pyruvate gets converted to acetyl-CoA for the citric cid cycle –> help synthesize ATP

48
Q

what causes ketone bodies to form?

A

when body is rapidly oxidizing fats, excess ketone bodies accumulate –> pH imbalance (ketoacidosis)

ketosis can be a serious risk in extreme low-carb diets

49
Q

what does Acetyl-CoA stand for?

A

acetyl coenzyme A

50
Q

what is lipogenesis?

A

synthesis of triglycerides from excess carbs and amino acids

51
Q

can our body synthesize triglycerides from glucose?

A

yes;

excessive amounts of carbs and amino acids are converted to TGs by lipogenesis and stored

diets that are high in carbs generate excess acetyl-CoA that can be converted into fatty acids

glucose –> glycerol –> TGs

glucose –> pyruvic acid –> acetyl-CoA –> fatty acids –> TGs

52
Q

is Acetyl-CoA converted to glycerol or fatty acids?

A

fatty acids

diets that are high in carbs generate excess acetyl-CoA that can be converted into fatty acids

53
Q

what 4 hormones influence the short-term regulation of feeding behavior?

do they regulate satiety or hunger?

A

ghrelin –> hunger

amylin –> satiety
CKK (cholecystokinin) –> satiety
peptide YY (PYY) –> satiety

54
Q

where and when is ghrelin released?

A

secreted when stomach is empty

signal to being a meal

causes hypothalamus to secrete GH-RH (to take advantage of nutrients about to be absorbed)

also stimulated party by gastric peristalsis

55
Q

where is peptide YY secreted?

A

enteroendocrine cells in ileum and colon

sense that food has arrived

56
Q

where is amylin synthesized?

A

B-cells in the pancreas

57
Q

what is the most important long-term regulator of feeding behavior and appetite?

A

leptin

insulin

58
Q

what 2 hormones tell your brain how much fatty tissue the body has, contributing to maintaining energy balance?

A

leptin and insulin

59
Q

does leptin inhibit or promote appetite?

A

inhibit

fat cells empty –> no leptin signal –> we eat

fat cells full –> leptin signal –> we stop eating

60
Q

when the adipocytes are full of stored lipids, do they inhibit or stimulate leptin release?

when the adipocytes are lacking lipid stores, do they inhibit or stimulate leptin release?

A

leptin makes you stop eating

full –> leptin release –> stop eating

empty –> no leptin release –> start eating

61
Q

what is leptin insensitivity?

A

receptor defect where the body doesn’t respond to leptin

leptin signals when fat cells are full –> you’re supposed to stop eating

if body doesn’t respond to leptin, will keep eating, even when fat cells are full –> this causes obesity

a common factor in obesity

62
Q

how does leptin stimulate lipolysis?

A

leptin stimulates sympathetic nerve fibers in adipose tissue to secrete Noradrenaline
–> stimulates lipolysis

63
Q

what hypothalamic nucleus receives input from hormones regulating the feeding behavior?

A

arcuate nucleus of the hypothalamus

64
Q

in the arcuate nucleus, there are 2 sets of neurons that, when stimulated, have different outcomes:

which hormones stimulate or inhibit each of these set of neurons and what are the outcomes related to the feeding behavior (hunger, satiety)?

which neurotransmitters are released in these neurons (at the arcuate nucleus level)?

A

Neuropeptide Y-secreting neurons –> promotes hunger and food intake –> releases Neuropeptide Y (NPY) neurotransmitters (this is a potent appetite stimulant)
- stimulated by: ghrelin
- inhibited by: PYY, CCK, insulin

melanocortin-secreting neurons –> satiety and inhibits eating –> releases melanocortin neurotransmitter (inhibits eating)
- stimulated by leptin

BIOL 204 (35 decks)

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