Carbohydrates Flashcards

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1
Q

Carbohydrate

A

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.

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2
Q

Monosaccharide`

A

Most basic fundamental sugar like glucose, galactose and fructose.

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3
Q

Disaccharides

A

Compound of two monosaccharides in dehydration synthesis like sucrose and lactose

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4
Q

Polysaccharides

A

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

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5
Q

Oligosaccharides

A

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

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6
Q

Simple Carbohydrate

A

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

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7
Q

Complex Carbohydrates

A

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

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8
Q

What by and where is fructose absorbed?

A

GLUT5 in the intestinal lumen on enterocytes.

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9
Q

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

A

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

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10
Q

What does increased fructose consumption lead to?

A

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

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11
Q

TXNIP

A

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

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12
Q

How does fructose affect lipid metabolism and contribute to steatosis?

A

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.

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13
Q

De Novo Lipogenesis

A

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

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14
Q

Acetyl-Coa

A

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

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15
Q

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

A

Acetyl-COA are what fatty acids are synthesised from

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16
Q

Where is de novo lipogenesis contained and why?

A

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.

17
Q

What is the metabolic pathway of fructose in hepatocytes?

A

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.

18
Q

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

A

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

19
Q

How does chronic fructose consumption affect DNL regulaton?

A

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

20
Q

SREPB1c

A

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

21
Q

Why is the sweetness of fructose bad?

A

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.

22
Q

What is the mechanism fructolysis in relation to glucose metabolism?

A

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.

23
Q

What is the movement pathway for fructose upon consumption?

A

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.

24
Q

How is fructose metabolised in adipose tissue/muscle

A

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

25
Q

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

A

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

26
Q

Explain the basics of enzyme kinetics.

A

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.

27
Q

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

A

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.

28
Q

Why does fructose metabolism occur faster than glucose?

A

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.

29
Q

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

A

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

30
Q

Allosteric Modulation

A

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

31
Q

Lipogenic Program

A

A process where fatty acids and glycerol convert into fats.

32
Q

CPT1A enzyme

A

Enzymes essential in translocation of fatty acids into the mitochondria

33
Q

What is an alternative pathway for fructose in the Liver?

A

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

34
Q

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

A

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.

35
Q

How does F1P effect glucokinase KM?

A

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

36
Q

What are all possible pathways for fructose in the liver?

A

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