Carbohydrates

Question 1

Carbohydrate

Answer 1

Oxygen, carbon and hydrogen macromolecules being an important energy source, regulator of blood glucose and insulin metabolism, cholesterol and triglyceride metabolism and assist in fermentation.

Question 2

Monosaccharide`

Answer 2

Most basic fundamental sugar like glucose, galactose and fructose.

Question 3

Disaccharides

Answer 3

Compound of two monosaccharides in dehydration synthesis like sucrose and lactose

Question 4

Polysaccharides

Answer 4

Long chain polymers of polysaccharides connected by glycosidic bonds like amylose and cellulose.

Question 5

Oligosaccharides

Answer 5

A polymer of about 3-10 monosaccharides connected by glycosidic bonds, like amylose.

Question 6

Simple Carbohydrate

Answer 6

Mono/Disaccharides easily utilised for energy where consumption results in rapid rise in blood sugar and insulin secretion.

Question 7

Complex Carbohydrates

Answer 7

Oligo/Polysaccharides forming more complex chemical structures with longer digestion rates and more gradual effects on blood sugar increase.

Question 8

What by and where is fructose absorbed?

Answer 8

GLUT5 in the intestinal lumen on enterocytes.

Question 9

What is the function of Fructose as a substrate for bacterial fermentation?

Answer 9

It leads to gas and bacterial metabolite formation, affecting intestinal motility causing abdominal pain and bloating.

Question 10

What does increased fructose consumption lead to?

Answer 10

Increased adaptability to it, inducing TXNIP which binds/regulates GLUT5-mediated intestinal fructose transport.

Question 11

TXNIP

Answer 11

Intestinal thioredoxin-interacting protein is a powerful inhibitor of tumour growth and angiogenesis

Question 12

How does fructose affect lipid metabolism and contribute to steatosis?

Answer 12

Activation of the lipogenic program, increasing VLDL triglyceride secretion and additionally supresses hepatic fatty acid oxidation, a process responsible for adipocyte lipolysis, where fats are hydrolysed.

Question 13

De Novo Lipogenesis

Answer 13

A process converting excess carbohydrates into fatty acids which are esterfied to storage triacylglycerols that can provide energy for beta oxidation.

Question 14

Acetyl-Coa

Answer 14

A protein begingin the final common pathway of the three major myocardium substrates; free fatty acids, glucose and lactate.

Question 15

What does Acettyl-COA do in hepatic de novo lipogenesis?

Answer 15

Acetyl-COA are what fatty acids are synthesised from

Question 16

Where is de novo lipogenesis contained and why?

Answer 16

Contained in the liver, where due to difference in fructose/glucose metabolism, has a higher fraction of diet-derived fructose available for conversion to fat via DNL.

Question 17

What is the metabolic pathway of fructose in hepatocytes?

Answer 17

Fructose is phosphorylated into F1P, then cleaved into dihydroxyacetone phosphate and glyceraldehyde, where GAH is phosphorylated by triose-kinase to form G3P, both fructose-derivatives entering glycolytic and gluconeogenic pathways.

Question 18

Why is DNL’s generation of malonyl-CoA important?

Answer 18

Malonyl-CoA is a metabolite limiting FA oxidation through inhibition of CPT1A enzymes, this inhibition increasing fatty acid availability for production.

Question 19

How does chronic fructose consumption affect DNL regulaton?

Answer 19

It increases trans-reg of DNL by activation of TF’s promoting lip-syn.

Question 20

SREPB1c

Answer 20

A gene required for glucose metabolism and fatty acid/lipid production

Question 21

Why is the sweetness of fructose bad?

Answer 21

It increases food palatability, worsening food behaviour and overconsumption, which additional addiction inducing behaviours like dependance and binding by stimulation of dopaminergic pathways, and leading to leptin resistance, an appeptie supressor.

Question 22

What is the mechanism fructolysis in relation to glucose metabolism?

Answer 22

It has most the same enzymes and metabolic intermediates, differing in that fructose predominantly synthesises in the liver for liver replenishment of glycogen/triglyceride synthesis.

Question 23

What is the movement pathway for fructose upon consumption?

Answer 23

It absorbs passively via GLUT5 in the small intestine with high binding affinity for fructose, where entry into the bloodstream is done so by GLUT2.

Question 24

How is fructose metabolised in adipose tissue/muscle

Answer 24

Hexokinase forms fructose-6-phosphate, of which enters glycolysis

Question 25

What are the enzymatic kinetics for hexokinase in relation to fructose metabolism in adipose-tissue/muscle?

Answer 25

Hexokinase has higher Km for fructose than glucose, thus glucose is a more favourable substrate, competitively inhibiting fructose phosphorylation.

Question 26

Explain the basics of enzyme kinetics.

Answer 26

Km refers to concentration of substrate permitting enzyme to achieve half Vmax(reaction rate when enzyme is fully saturated by substrate), so enzymes with high Km have low affinity for its substrate, requiring greater concentration.

Question 27

How is fructose metabolised in the liver/kidney and intestine?

Answer 27

Fructokinase degrades F1P into DHAP and GAH by aldolase/aldolase B, DHAP incorporates into glycolysis via triosephosphate isomerase whilst GAH phosphorylated by triose kinase into GAH3P, which can degrade by glycoylsis or serve as a gluconeogenesis substrate.

Question 28

Why does fructose metabolism occur faster than glucose?

Answer 28

It has ability to bypass rate limiting step of glycoslysis catalysed by phosphofructokinase 1, resulting in unimpeded conversion of excess fructose into cholesterol/triglycerides which increase body fat and raise lipid levels.

Question 29

Why does glucokinase have high Km and allosteric activity and why is this important?

Answer 29

Due to inhibitory glucokinase-regulatory proteins which decrease glucokinase affinity for fructose.

Question 30

Allosteric Modulation

Answer 30

Binding of substance to receptor, altering conformation of other site of a receptor, increasing/decreasing receptor affinity of other molecules.

Question 31

Lipogenic Program

Answer 31

A process where fatty acids and glycerol convert into fats.

Question 32

CPT1A enzyme

Answer 32

Enzymes essential in translocation of fatty acids into the mitochondria

Question 33

What is an alternative pathway for fructose in the Liver?

Answer 33

Conversion in the triose-phosphate pool which holds equilibrium with glycerol 3-phosphate, used to synthesise the glycerol backbone.

Question 34

How does SREBP1c relate to chronic fructose consumptions affects on DNL?

Answer 34

SPREBP1c is regulated by nutrients and hormones, mainly insulin, thus in chronic fructose consumption which can lead to hyperinsulinemia, increases SREBP1c expression, increasing lipid synthesis.

Question 35

How does F1P effect glucokinase KM?

Answer 35

Relieveing inhibitory glucokinase regulatory proteinsby fructose-1 phosphate, a positive allosteric modulator of glucokinase by binding/stablising the regulatory proteins.

Question 36

What are all possible pathways for fructose in the liver?

Answer 36

DNL, Lipogenic Program, Fatty acid Oxidation, tries 3 phosphate pool, GIP regulation and glycolysis.