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Unit 8 > Diet + Metabolism (not complete) > Flashcards

Diet + Metabolism (not complete) Flashcards

1
Q

Define:
Nutrients.
Essential nutrients cannot…
Conditionally essential nutrients..

A
  • Components of food which have recognisable functions in the body
  • … be made my the body
  • … when the body is unable to synthesis enough to meet normal metabolic demands
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2
Q

Define nutrition.

A
  • Scientific study of “the sum of the processes concerned with the growth, maintenance and repair of the living body”
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3
Q

What is Glycaemic Index?

A
  • How quickly a carbohydrate containing food causes an increase in blood glucose
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4
Q

1- Explain what happens to dietary carbohydrates and proteins?

2- Explain what happens to dietary fats?

3- What are the 3 principle fates of a nutrient?

A

1- Dietary carbohydrate and protein are absorbed in the GI tract and transported to the liver via the hepatic portal vein

2- Dietary fats are absorbed, packaged into chylomicrons and distributed via the lymphatic system

3-
Energy production
Storage
Conversion

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5
Q

What are the 4 types of carbohydrates?

A
  • Monosaccharides: 1 monomer such as glucose , galactose and fructose
  • Disaccharides: 2 monomers combines such as maltose, sucrose and lactose
  • Oligosaccharides: 3-9 monomers combined
  • Polysaccharides/Complex carbohydrates : 10+ monomers combined such as glycogen, starch and amylose.
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6
Q

What are the principle fate of carbohydrates? ( think E,S,C )

A
  • Energy (ATP),
  • Storage (glycogen)
  • Conversion (Fat storage, nucleotide precursors)
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7
Q

1- What happens to majority of glucose in the LIVER? Why?

2a- What facilitates glucose uptake in the LIVER?
2b- What chemical changes occurs to glucose in the LIVER readily?

3- Once glucose has been facilitated into the liver its fate depends largely on the overall metabolic profile. Describe the BASIC reactions that occur due to the following hormones: Insulin+ Glucagon.

A

1- Majority is either stored or converted > because main source of energy for liver is ß-oxidation of fats or amino acid oxidation

2a- GLUT 2 transporter > high Km > uptake even with high [glucose]
2b- Readily Phosphorylated to G-6-Phosphate

3-
Insulin: storage (glycogen) and conversion/storage (FFA synthesis)
Glucagon: breakdown (glycogen) and glucose release

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8
Q

Insulin/Glucagon+ Adrenaline have counter regulatory nature:

What reactions are stimulated by INSULIN? Starting with G6-P
What reactions are Stimulated by Glucagon/Adrenaline starting with G6-P?

A

INSULIN:
- Glycolysis (G6-P —> Pyruvate) - Substrate for biosynthesis NOT energy production
- Lipogenesis ( Acetyl CoA —> Fatty Acids)
- Glycogen Synthesis( G6-P —> Glycogen)
- Conversion of pyruvate to Acetyl CoA (Link reaction / Pyruvate oxidation)

GLUCAGON:
- Gluconeogenesis (Non-carbohydrate
precursors —> Glucose)
- Glycogen breakdown (Glycogen —> G6-P)

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9
Q

1- Glucose entry to muscle cells is tightly regulated by what transporter?

2- What happens to glucose in muscle cells?

3- What allosteric regulation is observed in muscle cells?

A

1- GLUT-4

2- Some storage as glycogen, regulated same as in liver by Insulin:Glucagon

3- glycolysis regulation via ATP:AMP ratio from contractile activity > Has an effect on phosphofructokinase.

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10
Q

What are the principle fate of fats? ( think E,S,C )

A
  • Energy production (liver and muscle)
  • Storage (adipose tissue)
  • Conversion (cholesterol, bile acids, steroids, ketone bodies in blood)
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11
Q

Compare the time taken for fatty acids from the diet to enter circulation to dietary glucose/ amino acids.

A
  • Several hours longer
    > Effect of insulin on adipose tissue more complex than dephosphorylation of target enzymes as for the regulation of glycogen storage.
    > May involve changes in gene expression
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12
Q

What happens to free fatty acids so they can be transported around the body?

A
  • Esterified into triglycerides and transported around the body in lipoproteins
    > Some free fatty acids transported in the blood bound to albumin
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13
Q

1- Where are chylomicrons produced? What do they transport?

2- What kind of catabolism do they undergo?

A

1- Intestines > transports dietary fat

2- Peripheral catabolism (lose TAG > FFAs for uptake in tissues)
> Chylomicron remnants (taken up by the liver)

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14
Q

1- What does VLDL do?
2- What kind of catabolism does it undergo?

A

1- Transports liver synthesised TAG (can include dietary fats or from de novo lipogenesis)

2- Peripheral catabolism (delivers TAG to peripheral tissues) to LDL particles, these are taken-up by tissues (mediated by LDL receptor)

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15
Q

1- How is the issue of lipids being insoluble or sparingly soluble in water and transportation solved?

2- What is the overall structure of lipoproteins?
> What dictates the ultimate fate of the lipoprotein. (Use chylomicrons as an example)

3- What do apolipoproteins do?

4- What do chylomicrons acquire in circulation?

A

1- Lipoproteins =. complex aggregates of lipids and protein (vary in size+density)

2-
- Monolayer of phospholipid enclosing hydrophobic material e.g. TAG
> Proteins bound to lipoprotein surface are known as apoproteins/apolipoproteins (ApoB-48)

3- Activate receptors for uptake or hydrolysis of stored TAG

4- Apo-CII

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16
Q

1- What happens to some fats in the liver when there is damage?

A

1- Stored especially when chronically elevated or following liver damage

17
Q

1- What is the principle role of the liver in processing fats? (ESC)

2- How are the fatty acid processed in the liver regulated?

A

1-
- E: Oxidation (for energy)
- S: Fatty acid synthesis (for storage in adipose)
- C: Ketogenesis (conversion) to provide ketones for the brain during ‘starved’ conditions

2-
- Compartmentation (synthesis in cytosol vs oxidation in mitochondria)
- Insulin:glucagon (fat synthesis vs. fat oxidation)
- Allosteric regulation (Malonyl coA regulates transport across mitochondrial membrane)

18
Q

During lipogenesis in the liver, when there is an excess of glucose, the liver’s energy demand is primarily met through…..

A
  • Oxidation of Amino Acids
19
Q

How does fatty acid oxidation (beta-oxidation) occur to produce Acetyl-Co A which can enter Krebbs cycle?

A

1- In Cytoplasm: Fatty acid couple with coenzyme A = fatty acyl-CoA

2- Transport into the mitochondria: Fatty acyl-CoA cannot directly cross the mitochondrial membrane.

3- Transported across the mitochondrial membrane as Acylcarnitine by the enzyme Carnitine acytransferase I

4- Inside mitochondria: Acylcarnitine is converted back to fatty acyl-CoA by Cartinine acyltransferase II

5- Beta-oxidation: The fatty acyl-CoA undergoes sequential rounds of beta-oxidation = One of the products is Acetyl-CoA entry into the citric acid cycle

20
Q

What are the key fatty acid metabolic reactions that occur in the liver?

A

1- Fatty acid synthesis/storage
2- Breakdown which leads to ketone bodies

21
Q

FAT METABOLISM IN THE LIVER:

What reactions are catalysed by the action of INSULIN?
> +ve stimulatory effect
> -ve inhibitory effect

A

> +ve stimulatory effect
1- Conversion of Acetyl-CoA to Malonyl-CoA - for fatty acid synthesis
2- Conversion of fatty acyl-CoA to triacylglyceride for storage

> -ve inhibitory effect
1- Upregulation of Malonyl-CoA > blocks movement of acyl-coA into mitochondria
thus OVERALL inhibiting fatty acid oxidation

22
Q

In type 1 diabetes there is absence of insulin due to autoimmune disease.

  • What happens as a result of this?
A
  • NO INSULIN = the negative effect of malonyl- CoA on transport of acyl-CoA into mitochondria is lost and so is control of ketone body synthesis. = KETOACIDOSIS
23
Q

FAT METABOLISM IN THE LIVER:
What reactions are catalysed by the action of GLUCAGON?

> +ve stimulatory effect

A

> +ve stimulatory effect
1- Stimulates fatty acid breakdown
Absence of Malonyl-CoA allows for the entry of fatty acids into the mitochondria matrix to undergo β-oxidation to be broken down

24
Q

FAT METABOLISM IN ADIPOSE:

A

Unit 8 (15 decks)

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