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M103 T3 > M103 T3 L5 > Flashcards

M103 T3 L5 Flashcards

1
Q

What is the role of steroids and FAs?

A

regulatory roles as hormones, vitamins and bile acids

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2
Q

In what form is E stored in for short term?

A

Redox agents (NADH, FADH2)
Ionic transmembrane gradients
ATP (phosphate bonds)

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3
Q

How are carbohydrates handled by the body from the point of entry?

A

Starch is digested into sugars (glucose) in gut
Sugars are absorbed from gut into blood stream
Sugars are absorbed into the liver via the hepatic portal vein where they are stored as glycogen

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4
Q

Is glycogen stored in the brain and why?

A

no bc there is nearly no glycogen in brain
the brain needs either glucose directly, at the very moment that it’s consuming energy, or ketone bodies from plasma constantly

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5
Q

What happens in the citric acid cycle?

A

starts with a (4C) OAA inside the cell
OAA + 2C (from acetyl co-A) = 6C citric acid
citric acid + o2 = OAA (+co2 + ATP + NADH + FADH)

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6
Q

What is the equation for FA synthesis?

A

acetyl CoA + ATP + E- = FA + CoA + CO2

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7
Q

What happens in beta oxidation?

A

a long FA uses E to break it down into acetyl CoA + e- + ATP

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8
Q

In humans how long are most FAs? What percentage of them have double bonds?

A

mostly 16-20 carbons long

50% have double bonds

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9
Q

What are the two ways cholesterol comes to be in the body?

A

made by the liver

received from diet

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10
Q

Why and how does the body recycle cholesterol?

A

it takes lots of E to generate

recycles it from the bile salts

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11
Q

What is the main form of cholesterol in the body? How is it used?

A

esterified cholesterol - 75%

lipase breaks it down into FAs and free cholesterol

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12
Q

How is vitamin D is produced by the skin?

A

by the action of light on a cholesterol derivative

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13
Q

What chemical is made from acetyle co-A during fasting and how is it useful?

A

ketone bodies from the liver

can be used as E if in the blood esp by the brain and heart

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14
Q

How long do ketone bodies last?

A

short lived in the blood - only lasts 5 hours

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15
Q

What are the features of unsaturated FAs?

A

have a lower mp - more liquid at body temperature, results in increased fluidity of the cell membranes

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16
Q

What are the most naturally occurring unsaturated FAs?

A

nearly all are cis - they have an even number of carbons from 14 to 22

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17
Q

Why are saturated fats are popular with manufacturers of processed foods?

A

they are less vulnerable to rancidity and are, in general, more solid at room temperature than unsaturated (plant) fats

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18
Q

What are the degree angles for cis and trans?

A

cis - 123

trans - 132

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19
Q

What types of fats are bad?

A

Saturated fats - bad bc they increase LDL

Trans unsaturated fats - bad (processed food)

20
Q

Are cis unsaturated fats bad and if so, why?

A

they are not as risky as saturated fats and trans fats
They have a lower mp bc of kinks - less likely to solidify into fat
However, high melting temperature is bad for unsaturated fats - solid & unmobilisable - will become solid lump of fat that can’t easily be broken down

21
Q

What are the four different pathways for lipid transport?

A

exogenous & endogenous pathways
reverse cholesterol pathway
bile production

22
Q

What happens in the exogenous pathway?

A

lipids from the diet in the gut are packaged by the SI into chylomicrons
these are taken from the blood vessels of the GI tract toward where they have to be stored - liver

23
Q

What happens in the endogenous pathway?

A

lipids are made by the body (the liver releases stored or generated) fats
packaged into LDL
takes lipids from the liver to the periphery

24
Q

What happens in the reverse cholesterol pathway?

A

the pathway takes lipids from the periphery to the liver
occurs when lipid supplies in liver are being exhausted
e.g. exercise or starving
serves as a sign of reduced body lipid
HDL in blood indicates that there is activity in the reverse path activity

25
Q

What happens in the pathway of bile production?

A

the pathway takes lipids from the liver to the digestive tract
cholesterol is made into bile by the liver
on eating a fatty meal, the liver releases bile salts into cystic duct leading to the gall bladder and emulsifies fats
most bile acids are reabsorbed by gut
they are returned to the liver and recycled until they are excreted in stool

26
Q

What do lipoprotein lipases do?

A

they are a cell surface-linked enzyme in capillary walls
they can’t metabolise triglyceride bc won’t fit through membrane so breaks it down into FAs and glycerol
IOT remove triglycerides from VLDL and to move the TG across the capillary membrane, TG must first be metabolised via lipoprotein lipase

27
Q

What are lipoprotein particles made up of?

A

apolipoproteins & lipids

28
Q

What are the densities of triglycerides and cholesterol like?

A

Triglycerides are very low density

Cholesterol is mid-way between TGs and proteins

29
Q

What is the most dangerous lipoprotein type and why?

A

LDLs bc a high presence in the blood is a sign of risk for CAD
Excess LDL accumulates in atheromas

30
Q

Is HDL a bad or good lipoprotein and why?

A

not as bad as LDL
increased HDL = lower CV risk
HDL leads to lipid transport from the fat cells to the liver - reverse cholesterol transport
usually appears when cholesterol is being used up

31
Q

What do high levels of VLDLs signify?

A

an increase risk of atheroma

32
Q

What are the functions of chylomicrons?

A

Not usually associated with CV risk - is normally high after fat-containing meals
Carries exogenous lipids from the gut to the periphery for storage

33
Q

Which cells in the pancreas release what two hormones?

A

β-cells release insulin

α-cells release glucagon

34
Q

What are features of Type II Diabetes Mellitus?

A

High blood glucose
Insulin resistance
Relative Insulin Deficiency

35
Q

What are the two causes of Type II Diabetes Mellitus?

A

obesity

genetic predisposition

36
Q

What are the two causes of Hypercholesterolaemia?

A

a combination of environmental and genetic factors

37
Q

What do statins block?

A

endogenous cholesterol synthesis
HMG-CoA Reductase
the entry step into cholesterol synthesis

38
Q

What are the main causes of metabolic syndrome?

A

Insulin resistance
Central obesity, waist circumference
high bp

39
Q

How many amacs long is a long FA?

A

between 16-20 amacs long

40
Q

How does the size of TGCs and cholesterol correspond with density?

A

Bigger lipoprotein particles usually are carrying a lot of lipids - thus lower in density

41
Q

What is the role of VLDL?

A

to transport endogenous cholesterol and TGCs from the liver to the peripheries

42
Q

What is a consequence of the fact that VLDL being launched from the liver has fat inside it?

A

the more VLDL present in the blood, the more fat and tryglycerides are being thrown out of the liver

43
Q

What happens after the VLDL gets to the periphery?

A

the TGC is removed from the periphery
VLDL is turned into IDL
IDL will become LDL

44
Q

What is the difference between VLDL and IDL?

A

VLDL is the same molecule but has a lower density

45
Q

What is the relationship between LDL and VLDL?

A

LDL is eventually “left-over” after periphery absorbs endogenous TG from VLDL from liver

46
Q

What are the products of fat mobilization?

A

ATP + Acetyl-CoA

47
Q

By what vessel are sugars absorbed into the liver?

A

the hepatic portal vein

M103 T3 (21 decks)

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