Metabolism Physiology

Question 1

What are the majority of ingested lipids?

Answer 1

90% triglycerides

Question 2

What are ingested lipids made of?

Answer 2

Essential (eg alpha-linolenic and linoleic acid) and non-essential fatty acids

Question 3

Where are ingested lipids broken down?

Answer 3

10-30% in stomach

Rest is broken down in duodenum and upper jejunum.

Bile salts are absorbed in the terminal ileum.

Question 4

Can ingested lipids be used as a source of ATP?

Answer 4

Yes they are energy dense, provide more than double the ATP than from glucose.

Question 5

What happens to the faeces if bile salts secretion is reduced?

Answer 5

Lipids in the faeces increases because bile salts are required to solubilize fats and aid their absorption.

Question 6

When can BMR be lower?

Answer 6

During sleep

Question 7

For every 1 degree C rise in body temp, what happens to the cerebral metabolic rate?

Answer 7

Increases by 8%

Question 8

What is BMR?

Answer 8

BMR is the energy output of an individual per unit time at rest, at room temperature

It must also be measured 12-14 hr after their last meal (a time when one is said to be thermoneutral).

Question 9

What can measure BMR?

Answer 9

A wet spirometer (measures indirectly)

Question 10

What does an ergometer measure?

Answer 10

Energy expenditure whilst active.

Question 11

What hormones antagonise insulin-induced hypoglycaemia?

Answer 11

• adrenaline
• noradrenaline
• glucagon
• GH
• cortisol

Question 12

What effect does insulin have on protein anabolism?

Answer 12

It facilitates it.

Insulin is the only major anabolic hormone and stimulates synthesis of proteins, fat and glycogen.

Question 13

What does insulin do to glycogen synthesis?

Answer 13

It promotes it

Question 14

In anaerobic metabolism, how much lactate is produced from one glucose?

Answer 14

Each glucose is converted to 2 pyruvate, therefore makes 2 molecules of lactate

Question 15

How do anaerobic and aerobic metabolism compare in speed of release of ATP?

Answer 15

Glucose metabolism to lactate releases ATP at least as TWICE as fast as mitochondrial metabolism and can optimally provide energy for 1.5 mins of maximal muscle activity.

Question 16

After exercise what happens to lactate?

Answer 16

80% is reconverted to glucose in the liver via the Cori cycle

Question 17

What happens to lactate in the kidney?

Answer 17

It is actively reabsorbed by the nephron to a transport max of 75mg/min

Question 18

Why can adrenaline cause hyperglycaemia?

Answer 18

It stimulates glucagon secretion and stimulates gluconeogenesis

Question 19

How can thyroid stimulating hormone cause hyperglycaemia?

Answer 19

Thyroid hormone stimultaes: increased glucose absorption from the gut, glycogenolysis and gluconeogenesis.

Question 20

What effect do thiazide diuretics have on blood glucose?

Answer 20

Hyperglycaemia.

Thiazide diuretics commonly precipitate Type 2 diabetes.

Question 21

What does administration of glucagon do to blood glucose?

Answer 21

Hyperglycaemia

Question 22

What do beta blockers do to blood glucose levels?

Answer 22

They can cause hypoglycaemia under GA

Question 23

What does glucagon do?

Answer 23

Stimulates gluconeogenesis, glycogenolysis and lipolysis.

Question 24

What receptor does glucagon act through?

Answer 24

Via G-protein linked receptors

Question 25

Where is glucagon made?

Answer 25

Pancreatic alpha cells

Question 26

How does glucagon affect growth hormone?

Answer 26

It stimulates secretion of GH

Question 27

What inhibits glucagon release?

Answer 27

• alpha stimulation
• insulin
• glucose
• ketones
• phenytoin
• somatostatin

Question 28

What stimulates glucagon release?

Answer 28

• cortisol
• infection
• theophylline
• other phosphodiesterase inhibitors

Question 29

What happens in starvation?

Answer 29

Glycogenolysis occurs and the liver begins to use fatty acids as a source of energy.

As glycogen is depleted, gluconeogenesis increases using amino acids from the breakdown of muscle protein. Glycogen is not replenished until return of nutrients, this restorative process is under control of cortisol.

The brain cannot survive without glucose but other tissues can adapt to using ketone bodies as a fuel.

Free fatty acids undergo beta oxidation to produce ATP in the mitochondria. Glucose cannot be formed from fatty acids.

Question 30

What do insulin and GH have directly opposing effects on?

Answer 30

• fat catabolism
• glucose utilisation
• fat anabolism
• glycogen production

Question 31

What does GH and insulin do to fat?

Answer 31

Causes fat breakdown

Insulin stimulates fat deposition

Question 32

What do GH and insulin do to glucose utilisation?

Answer 32

GH inhibits glucose utilization

Insulin stimulates glucose absorption

Question 33

How do GH and insulin affect protein synthesis?

Answer 33

They both promote protein anabolism

Question 34

What do insulin and GH do to glycogen?

Answer 34

Insulin stimulates glycogen deposition.

GH encourages glycogenolysis.

Question 35

What happens to glucagon levels in starvation?

Answer 35

They go up as body enters a catabolic phase with increased glycogenolysis

Question 36

What causes ketoacidosis in starvation?

Answer 36

The accumulation of acetyl-CoA

Question 37

What can the majory of amino acids be converted to for ketosis?

Answer 37

After deamination can be converted to acetyl-coA from which acetoacetate can be formed.

Question 38

What does the liver convert fatty acids to in ketosis?

Answer 38

Fatty acid degradation occurs largely in the liver where acetyl-CoA is formed leading to acetoacetate production. This is transported at low levels but with efficient flux to the rest of the body.

Question 39

What is ketosis?

Answer 39

The presence of excessive levels of acetoacetate, beta-hydroxybutyrate or acetone in the blood - due to high fat diet/diabetes/starvation.

Question 40

What limits entry of acetyl-CoA into the citric acid cycle in ketosis?

Answer 40

Oxaloacetate is needed to receive acetyl CoA into the citric acid cycle.

Question 41

How does ketoacidosis cause hyponatraemia?

Answer 41

Ketoacids are easily excreted by the kidney but being strong acids they are excreted combined with Na+ from the extracellular fluid. The resultant hyponatraemia leads to an increased acidosis beyond that occasioned by the direct rise in ketoacid levels.