Lipids Flashcards

1
Q

Functions of lipids

A

Phospholipids & cholesterol - cell membranes

TG = key energy store

Steroids and fatty acids play regulatory roles as hormones, vitamins and bile acids

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2
Q

Cellular energy - short-term storage

A
ATP (and other phosphate bonds)
Redox agents (NADH, FADH2)
Ionic transmembrane gradients
H+ across mito memb, Na+ across Plasma Membrane
All of the above are labile
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3
Q

Limit on ATP stored

A

Some energy is stored intracell as creatine phosphate

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4
Q

Carbohydrate as energy

A

Sugars are absorbed from gut into blood stream

Sugars absorbed by liver and stored as glycogen
Via hepatic portal vein

Also sugars stored throughout body as glycogen:
Glucose spike leads to insulin

Glycogen is broken down into glucose when more is needed

No glycogen in brain: it needs glucose or ketone bodies from plasma constantly

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5
Q

Citric acid cycle

A

A-CoA + Oxalo-acetic acid -> Citric acid (6C)

Citric acid + O2 -> Oxalo-acetic acid + CO2 + ATP

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6
Q

Fatty Acid Synthesis

A

Acetyl-CoA + ATP + e- (ATP) -> fatty acid + CO2 + CoA

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7
Q

Fatty Acids

A

Simple straight C chain + COOH 16-20Cs

50% have double bonds

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8
Q

Cholesterol

A

Essential component of cell membranes
precursor of bile acids, steroid hormones and vitamin D

Sources: from diet OR made in liver
A major emphasis on recycling
Bile salts
Endogenous pathway

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9
Q

Cholesterol esters

A

75% of plasma cholesterol is esterified

Broken down by lipase to free cholesterol & FA

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10
Q

Acetyl-Coenzyme A

A

Main energy production precursor

Cannot be transported in plasma

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11
Q

Ketone

A

“Ketone bodies” are 3 soluble chemicals

Made from acetyl-CoA during fasting
By liver
Last for only 5 hours

During fasting, major energy source

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12
Q

Acetoacetic acid & beta-hydroxybutyric acid

A

Acetone is a waste product
Made spontaneously by decarboxylation
eliminated by kidney

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13
Q

Kink(veg)

A

Lowers melting temperature

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14
Q

Fats

A

Saturated fats are bad
- Increase LDL

Trans unsaturated fats are bad

Cis unsaturated fats are either
Monounsaturated
Polyunsaturated
Health information on these changes but they are probably good for you
Lower melting temperature b/c of kink
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15
Q

Exogenous Pathway

A

From gut to liver (and to periphery)

Diet and packaged into chylomicrons in small intestine

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16
Q

Endogenous Pathway

A

From liver to periphery
Peripheral lipids stored in adipose & muscle

Endogenous = made by the body

Lipid from liver packaged into VLDL

17
Q

Reverse Cholesterol Transport

A

From periphery to liver

Occurs when lipid supplies in liver are being exhausted

HDL in blood indicates reverse path activity

18
Q

Bile production

A

From liver into gut (and gall bladder)
- Bile released into cystic duct

Cholesterol converted into bile acids

  • Bile is necessary to digest fats in diet
  • Emulsifies fats

Most bile acids are reabsorbed by gut
- Returned to the liver and recycled

19
Q

Lipoprotein lipase

A

Metabolises TG -> fatty acids + glycerol
Because TG cannot go through cell membrane
Cell surface-linked enzyme in capillary walls
In order to remove triglycerides from VLDL and to move the TG across the capillary membrane, TG must first be metabolised via lipoprotein lipase

20
Q

Lipoprotein particles

A

In plasma

Soluble and carry lipids

21
Q

Apolipoproteins

A

Proteins in LP particles that can hold lipids

22
Q

Lipid identified by density

A

Lipid is much less dense than protein
TG are very low density
Cholesterol is midway between TG and protein

23
Q

LDL

A

LDL contents get incorporated into atheromas
LDL in blood may be “storage” for cholesterol that “cannot be stored elsewhere”
Excess LDL accumulates in atheromas

Left over LDL absorbs endogenous TG from VLDL from liver

24
Q

HDL

A

Increased HDL -> lower CV risk

lipid transport from fat cells to liver

25
Q

VLDL

A

Signifies risk of atheroma
Used to transport endogenous cholesterol and TG from Liver to adipose and muscle

After TG is removed by periphery from VLDL, leaves over IDL

26
Q

IDL

A

Results from VLDL losing TG to periphery

IDL will become LDL

27
Q

Chylomicrons

A

Not usually associated with CV risk
Normally high after fat-containing meals

Carries lipids from gut to periphery
For exogenous lipids

28
Q

Hypercholesterolaemia

A

High fasting levels of plasma cholesterol

Increased risk of arteriosclerosis
HDL reduces risks

Due to a combination of environmental and genetic factors

29
Q

Statins

A

Drugs used to treat hypercholesterolaemia
Block endogenous cholesterol synthesis
By Blocking HMG-CoA Reductase
The entry step into cholesterol synthesis

30
Q

Metabolic syndrome

A

Group of risk factors that occur together, leading to increased risk for CAD, stroke, and type 2 diabetes

Main causes
Insulin resistance
Central obesity
Waist circumference

31
Q

Endothelial injury due to

A

raised LDL
‘toxins’ eg cigarette smoke
hypertension
haemodynamic stress

32
Q

Endothelial injury causes

A

platelet adhesion, PDGF release, VSMC proliferation and migration
insudation of lipid, LDL oxidation, uptake of lipid by VSMC and macrophages
migration of monocytes into intima

Stimulated VSMC produce matrix material

Foam cells secrete cytokines causing
further VSMC stimulation
recruitment of other inflammatory cells