Lecture 22 -- review questions Flashcards

(64 cards)

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
what is the classification of lipoprotein based on? (ie which characteristic?)
density 4 major categories
26
what do VLDL, LDL, and HDL stand for?
VLDL -- very low density lipoprotein LDL -- low density lipoprotein HDL -- high density lipoprotein
27
what is the most abundant component of chylomicrons?
triglycerides
28
what is the most abundant component of VLDL?
triglycerides
29
what is the most abundant component of LDL?
cholesterol
30
what is the most abundant component of HDL?
protein
31
which lipoprotein contains the most cholesterol?
LDL
32
which lipoproteins contain the most triglycerides: HDL, LDL, or VLDL?
VLDL
33
what is apolipoprotein, and where can you find it?
a protein that coats lipoproteins surface of lipoproteins
34
what is the function of lipoprotein lipase, and where is it found?
removes TGs from lipoproteins breaks down TGs into fatty acids and glycerol found in surface of endothelial cells
35
the removal of TGs from chylomicrons by lipoprotein lipase on the vascular endothelial surface results in which molecule?
fatty acids glycerol
36
where do chylmicron remnants go?
liver for disassembly
37
where is VLDL produced?
liver
38
what is the function of VLDL? Does VLDL carry fat synthesized by the liver? where?
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
what converts VLDL to LDL? (tip: which molecules are removed from VLDL thru their journey in the circulation?)
lipoprotein lipase removes TGs from VLDL and converts them to FAs and glycerol
40
what is the function of LDL?
deliver cholesterol to the body's cells
41
what is the function of HDL?
pick up excess cholesterol from tissues and deliver to the liver for use or disposal
42
what is lipolysis?
breakdown of fats by hydrolysis to release FAs
43
what happens to the glycerol and fatty acid products obtained upon the action of lipase in the adipose tissue? (metabolic pathways)
glycerol is converted to a glycolysis intermediate FAs undergo beta-oxidation to generate acetyl-CoA
44
which part of TG molecules enters glycolysis?
glycerol
45
what is beta oxidation?
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
why do fats have glucose-sparing and protein-sparing effects?
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
how is glycolysis related to lipid metabolism?
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
what causes ketone bodies to form?
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
what does Acetyl-CoA stand for?
acetyl coenzyme A
50
what is lipogenesis?
synthesis of triglycerides from excess carbs and amino acids
51
can our body synthesize triglycerides from glucose?
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
is Acetyl-CoA converted to glycerol or fatty acids?
fatty acids diets that are high in carbs generate excess acetyl-CoA that can be converted into fatty acids
53
what 4 hormones influence the short-term regulation of feeding behavior? do they regulate satiety or hunger?
ghrelin --> hunger amylin --> satiety CKK (cholecystokinin) --> satiety peptide YY (PYY) --> satiety
54
where and when is ghrelin released?
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
where is peptide YY secreted?
enteroendocrine cells in ileum and colon sense that food has arrived
56
where is amylin synthesized?
B-cells in the pancreas
57
what is the most important long-term regulator of feeding behavior and appetite?
leptin insulin
58
what 2 hormones tell your brain how much fatty tissue the body has, contributing to maintaining energy balance?
leptin and insulin
59
does leptin inhibit or promote appetite?
inhibit fat cells empty --> no leptin signal --> we eat fat cells full --> leptin signal --> we stop eating
60
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?
leptin makes you stop eating full --> leptin release --> stop eating empty --> no leptin release --> start eating
61
what is leptin insensitivity?
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
how does leptin stimulate lipolysis?
leptin stimulates sympathetic nerve fibers in adipose tissue to secrete Noradrenaline --> stimulates lipolysis
63
what hypothalamic nucleus receives input from hormones regulating the feeding behavior?
arcuate nucleus of the hypothalamus
64
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)?
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