Diet & Metabolism Flashcards

1
Q

Define nutrition.

A

Processes regarding growth, maintenance & repair of the living body

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2
Q

Define nutrients.

A

Components of food which have recognisable functions in body

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3
Q

x2 types of nutrients?

A

-Essential nutrients
-Conditionally essential nutrients

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4
Q

Define essential nutrients.

A

Cannot be made by the body (e.g., water!!)

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5
Q

Define conditionally essential nutrients.

A

Body is unable to synthesise enough to meet normal metabolic demand (e.g., disease-induced deficiency)

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6
Q

What is glycaemic index (GI)?

A

How quickly a carbohydrate containing food causes an increase in blood glucose
–> higher value = the food breaks down more quickly (not last as long) & causes increase in blood glucose

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7
Q

Give the malnutrition & ill health spiral.

A
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8
Q

Define catabolism & anabolism.

A

-Catabolism - produces energy
-Anabolism - uses energy

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9
Q

Give the 3 metabolic fates of glucose?

A
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10
Q

Describe basics of carbohydrate metabolism in the liver?

A

**Glycogenesis
-Glucose enters liver
-Generate glucose-6-phosphate by phosphorylation of glucose by glucokinase (uses x1 ATP)
*G6P = intermediate of glycogen
-Then from G6P - glycogen is eventually made

**Glycogenolysis
-Glycogen broken down to glucose = inc. blood glucose (for transport & use elsewhere)

**Glycolysis
-Glucose enters liver
-Converted to G6P (by glucokinase) = intermediate
-Then eventually form pyruvate (x2 per glucose)
-Pyruvate -> converted to Acetyl-CoA
-Acetyl-CoA -> converted to cholesterol
-Acetyl-CoA is a precursor to -> fatty acids (= alternative energgy supply for mitochondria)
==> so trigylcerides & phospholipids can be synthesised (= fat) -> used for storage
-Acetyl-CoA enters citric acid cycle = energy production

**Pentose phosphate pathway
-Glucose enters liver
-Converted to G6P (by glucokinase) = intermediate
-Eventually ribose-5-phosphate is made
-R5P -> converted to nucleotides (RNA/DNA/ATP)

**Lactate = also a carb
-Lactate converted to -> pyruvate then to -> glucose (via cori cycle)

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11
Q

Summarise the uses of carbohydrate metabolism in liver - basics?

A
  1. Released as blood glucose for transport & use elsewhere
  2. Storage (glycogen)
  3. Energy production (citric acid cycle)
  4. Conversion to something else -> pyruvate & Acetyl-CoA
    -Cholesterol (steroid hormones, bile, fat soluble vitamins)
    -Free fatty acids (alternative energy supply for mitochondria)
    -Triacylglycerol & Phospholipids (fat = energy storage)
  5. Conversion to something else – via Ribose-5-Phosphate
    -Nucleotides - RNA/DNA/ATP (energy packages)
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12
Q

Categorise adrenaline/glucagon & insulin - as catabolic or anabolic.

A

-Adrenaline/glucagon = catabolic hormones = produces energy
-Insulin = anabolic hormone = uses energy

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13
Q

When is glucagon/adrenaline released -> link to catabolic role?

A

When blood glucose is low
–> catabolism produces energy - produces glucose = increases blood glucose

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14
Q

When is insulin released -> link to anabolic role?

A

When blood glucose is high
–> anabolism uses energy - uses/converts glucose = decreases blood glucose

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15
Q

What processes do glucagon/adrenaline promote?

A

-Glycogenolysis (glycogen -> glucose)
-Gluconeogenesis (AA/glycerol/FAs -> glucose)

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16
Q

What processes does insulin promote?

A

*Glycogenesis (glucose -> glycogen)
*Glucose metabolism (using up glucose)
-Energy production
-Conversion to something else: pyruvate (glycogen), ribose-5-phosphate (-> to nucleotides), Acetyl-CoA -> cholesterol & FAs & triglycerides & phospholipids (tri & ph - for storage)
*Storage of FAs in adipose tissue (adipogenesis)

17
Q

What processes does insulin inhibit?

A

-Glycogenolysis (glycogen -> glucose)
-Gluconeogenesis (AA/FAs/glycerol -> glucose)

18
Q

What transporter protein facilitates glucose uptake by liver?

A

GLUT 2

19
Q

Describe what happens to glucose metabolism after an overnight FAST?

A

-Blood glucose = low
-Low insulin:glucagon (glucagon released by pancreas)
-Anabolism = OFF
-Catabolism = ON (produce energy)

-Liver releases glucose:
–> via glycogenolysis (glycogen -> glucose) & gluconeogenesis (alanine/lactate/glycerol -> glucose)
-Gluconeogenesis = promoted by high glucagon levels
-Kidney also contributes to gluconeogenesis

–> once glucose is made:
-Glucose is mainly utilised by brain (limited capacity to use alternative energy sources)
-Muscles & adipose tissue can switch to alternative fuel sources to preserve glucose for brain–> they switch to FAs & ketones (due to LOW INSULIN)

(alanine = from muscles)
(lactate = from blood cells)
(glycerol = from adipose tissue)

20
Q

Describe what happens to glucose metabolism in the FED state?

A

-Blood glucose = high
-High insulin:glucagon (insulin released by pancreas)
-Anabolism = ON (use energy)
-Catabolism = OFF

-Brain was already metabolising glucose
-But now other tissues switch to metabolise glucose too - & storage of glucose

-Muscle = glucose metabolism + glycogen storage
-Adipose = glucose take up & stored as fat
-Liver = glycogen storage promoted & gluconeogenesis suppressed

21
Q

Describe fat metabolism in liver - basics?

A

FROM LIVER:

-Stored in adipose issue (transport here as VLDL)
-Used for energy production
= FAs undergo B oxidation -> forms Acetyl-CoA -> undergoes citric acid cycle = energy!
-Forming ketone bodies
= FAs undergo B oxidation -> forms Acetyl-CoA -> then converted to ketone bodies in blood
-Cholesterol formation
= FAs undergo B oxidation -> forms Acetyl-CoA -> then converted cholesterol -> then converted to bile salts/steroid hormones
-Conversion to lipoproteins (VLDL)
-Released as free FAs in blood (alternative energy supply for mitochondria)

22
Q

How does cholesterol travel through blood?

A

On lipoproteins
–> is insoluble in blood so attaches to these

23
Q

What are the x2 main sources of cholesterol?

A

-Made by body & used to make hormones & digest fatty foods
-In foods – egg yolks, fatty meats & “regular” cheese

24
Q

Risk of excess cholesterol?

A

-Build up on walls of blood vs - deposits = called plaques
-Over time plaque narrows blood vs = less blood flow
-Less blood to heart & other organs
-When plaque fully occludes coronary artery carrying blood to heart - causes heart attack
–> or if partially occluded coronary artery = angina (reduced blood flow to heart -> chest pain)
-OR -> plaque deposit can rupture/burst - releases clot in coronary artery

25
Q

What are the x2 types of lipoproteins which ‘carry’ cholesterol in blood?

A

-HDL - high density lipoprotein = good!
-LDL - low density lipoprotein = bad!

26
Q

Describe HDL - why is it good?

A

-HDL held tightly to cholesterol it carries
-So cholesterol cannot become loose to attach to arterial walls
-Keeps cholesterol in solution & moves it safely throughout the body
-Can even snatch up additional cholesterol already stuck to artery wall -> reducing size of deposits

27
Q

Describe LDL - why is it bad?

A

-It deposits its cholesterol on walls of arteries
-Also is the type of cholesterol that becomes oxidized & damages lining of arteries -> enabling mineral & fat deposits

28
Q

Why are triglycerides often grouped together with cholesterol?

A

= a type of blood lipid
–> its strategies for reducing triglyceride levels are same as those for lowering cholesterol

29
Q

Describe fat metabolism in FASTING state?

A

-Blood glucose = low
-Low insulin:glucagon (glucagon released by pancreas)
-Anabolism = OFF
-Catabolism = ON (produce energy) -> LIPOLYSIS!!!!!

**Lipolysis = promoted by low insulin / high glucagon

-NEFA (non-essential FAs) = a type of FA generated via lipolysis of TAG in adipose tissue-> used/metabolised by muscle, liver & kidneys
-NEFA used by liver to form ketone bodies & TAG (i.e., some FA converted back to triglyceride)

-Glycerol = from lipolysis of TAG in adipose tissue -> metabolised by liver (glycolysis, gluconeogenesis) & TAG production!

TAG = triglycerides (in adipose tissue here!!!)

30
Q

Describe fat metabolism in FED state?

A

-Blood glucose = high
-High insulin:glucagon (insulin released by pancreas)
-Anabolism = ON (use energy)
-Catabolism = OFF

Insulin = activates lipoprotein lipase (LPL)

-Fat absorbed from SI -> packaged into chylomicrons -> transported to lymphatics

-LPL is activated by insulin in adipose tissue & muscle -> releases free FAs -> can be taken up & stored as TAG
==> LPL + insulin -> free FAs -> TAG

31
Q

Describe protein metabolism?

A

Proteins = made of many constituent elements (S,N,O,H,C) -> & prots are broken down into their constituent AAs during digestion

Uses of liver AAs:
1. Synthesis of Liver / plasma prots (albumin, globulins, coagulation)
2. Released via blood for tissue prot synthesis
3. Conversion to something else (Nucleotides, Hormones, Porphyrins)
4. Catabolism via Urea/Ornithine Cycle – generates urea & ammonia
-> Pyruvate & Acetyl-CoA as intermediate steps for:
-Gluconeogenesis & glycogen storage
-Energy production
-FA synthesis
5. Alanine from muscle converted into Pyruvate and used for energy via the Citric acid cycle or used for gluconeogenesis

Pyruvate - formed from AAs
-> converted back to glucose (gluconeogenesis) -> to glycogen (glycogenesis)

Pyruvate - formed from AAs
-> converted to Acetyl-CoA -> into citric acid cycle = ENERGY production
-This Acetyl-CoA - also used to form FAs -> to form lipids

To form pyruvate ammonia is made -> which is converted to urea

AAs converted to ‘something else’
-Nucleotides
-Hormones
-Polymorphins

32
Q

Give name of process of pyruvate to glucose?

A

Gluconeogenesis

33
Q
A