3 - Fate of major nutrient groups

Question 1

Where are the major nutrient groups absorbed and where are they transported to?

Answer 1

GI tract - small intestine

Dietary carbs and proteins - liver via hepatic portal vain

Dietary fats - packaged into chylomicrons and distributed via lymphatic system

Question 2

What are the 3 principle fates?

Answer 2

Energy production
Storage
Conversion

Question 3

How are carbs found (3 types)?

Answer 3

Simple monosaccharides
Di- and oligosaccharides
Complex carbohydrates

Question 4

In what form are carbs absorbed?

Answer 4

Glucose, fructose, galactose

Question 5

What are the 3 fates of carbs?

Answer 5

Storage - glycogen (in liver and skeletal muscles)
Energy - ATP
Conversion - fat storage, nucleotide precursor

Question 6

What is the main source of energy for the liver?

Answer 6

fat and amino acid oxidation

Question 7

What happens to most carbs in the liver?

Answer 7

Stored or converted

Question 8

Explain the importance of the GLUT2 transporter in the liver.

Answer 8

high Km -> low affinity and uptake
available for other tissues
high uptake in high glucose levels -> storage
Bonus question - why is GLUT2 important in pancreatic B cells?

Question 9

Why is glucose readily phosphorylated in the liver?

Answer 9

Can’t escape cell so no glucose equilibrium

Question 10

How does insulin and glucagon affect carbs in the liver?

Answer 10

Insulin: storage (glycogen) and conversion/storage (FFA synthesis)

Glucagon: breakdown (glycogen) and glucose release

Question 11

Define reciprocal control

Answer 11

one pathway/process is activated and other is inhibited

Question 12

Which glucose transporter do muscle cells have and what is its significance?

Answer 12

GLUT4

Question 13

What is allosteric regulation and how is this achieved with carbs in muscle cells?

Answer 13

Regulation of an enzyme by binding an effector molecule at a site other than the enzyme’s active site

ATP:AMP ratio, effect on phosphfructokinase

Question 14

What are the 3 fates of dietary fats?

Answer 14

Energy production - in liver and muscle
Storage - adipose tissues
Conversion - cholesterol, bile acids, steroids

Question 15

How long does it take for each dietary group to enter blood circulation and why does it take longer for fatty acids?

Answer 15

2-4 hours normal, fats 2-4 hours extra

Effect of insulin on adipose tissue more complex

Question 16

Describe the basic structure of triglycerides

Answer 16

Glycerol backbone

3 fatty acid chains

Question 17

How are fatty acids transported around the body?

Answer 17

Free fatty acids (FFA) are esterified into triglycerides (TAG)
transported around the body in lipoproteins

(some FFA transported boudnd to albumin)

Question 18

What are Chylomicrons and describe their structure

Answer 18

produced in intestines for dietary fat transport

phospholipid monolayer, surface proteins, what does it pack…

Question 19

Name 3 lipoproteins

Answer 19

Chylomicrons
LDL
HDL

Question 20

What are the principle roles of the liver in processing fats?

Answer 20

fatty acid synthesis (for storage in adipose)
oxidation (for energy)
ketogenesis (conversion) to provide ketones for the brain during ‘starved’ conditions

Question 21

Define allosteric regulation

Answer 21

allosteric regulation is the regulation of an enzyme by binding an effector molecule at a site other than the enzyme’s active site

Question 22

Which surface protein do chylomicrons acquire in circulation and why?

Answer 22

ApoCII (by transfer from HDL)

necessary cofactor for subsequent lipoprotein lipase activity, allowing delivering of contained TAG to tissues.
chylomicrons become smaller as a result, forming depleted remnant particles, where the ApoCII and ApoB48 are important in the activation of uptake of the particle by receptors, mainly in the liver.

Question 23

How is metabolism of fats in the liver regulated? +explain

Answer 23

Compartmentation (Acyl CoA and carnitine)
Insulin:glucagon
Allosteric regulation

Question 24

Why and how are fatty acids transported to the mitochondria?

Answer 24

For fatty acid oxidation
activated by attachment to coenzyme A
mitochondrial membrane is impermeable to CoA
switching the CoA for the alcohol carnitine
fatty acyl-carnitine is then transported to the mitochondria where is reattached to CoA

Question 25

How does Malonyl coA regulate fat metabolism in the liver?

Answer 25

regulates transport across mitochondrial membrane

blocks movement of acyl-CoA into mitochondria and therefore from oxidation

Question 26

When do skeletal muscles produce Malonyl coA and why?

Answer 26

produce malonyl coA (from glucose-derived acetyl CoA) when glucose is abundant
muscle fatty acid oxidation is slowed when glucose is plentiful -> fatty acid stores are more efficient

Question 27

Which pathway provides energy for the liver during lipogenesis?

Answer 27

amino acid oxidation

Question 28

How does insulin affect malonyl coA and how does this effect other pathways

Answer 28

Insulin promotes malonyl coA
without insulin the negative effect of malonyl- CoA on transport of acyl-CoA into mitochondria is lost and so is control of ketone body synthesis. This is the metabolic explanation for the high risk of ketoacidosis in uncontrolled diabetes due to absence of insulin (Type 1 Diabetes).

Question 29

How does insulin effect fat in adipose tissues (2 ways)?

Answer 29

Insulin activates/elevates an enzyme on the endothelial cell layer around adipose tissue involved in fat uptake -Lipoprotein Lipase (LPL)

• hydrolyses…
• GLUT?
• stored as…

Insulin suppresses an enzyme within adipose tissue involved in fat breakdown - Hormone-Sensitive Lipase (HSL)

• hydrolyses…
• Adrenaline…

Question 30

What are the fate of amino acids?

Answer 30

NO STORAGE
Conversion to substrate for fat synthesis or glycogen (indirect storage)
Energy in liver (especially during lipogenesis)

Question 31

What can amino acids be converted to?

Answer 31

• Protein synthesis/turnover
• Hormones, nucleotides, etc.
• Carbon ‘skeletons’ enter pathways of glucose and fat metabolism
• NH3 excreted