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FoM - normal function > carbohydrates > Flashcards

carbohydrates Flashcards

1
Q

what are the main carbohydrates in our diet?

A

Monosaccharides
- Glucose & Fructose (fruit, honey)

Disaccharides
- Lactose & Maltose & Sucrose (milk, table sugar, beer)

Oligosaccharides
- Peas, beans, lentils - not digested but lack of them in diet leads to poor health (gut cancer)

Polysaccharides
- Glycogen (meat)
- Starch (cereal, potato, rice)
- Cellulose & Hemicellulose - indigestable but they increase faecal bulk and decrease transit time

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2
Q

what are the functions of carbohydrates?

A

Highly oxidizable
- Sugar and starch molecules have “high energy” H atom-associated electrons
(major energy source)
- Carbohydrate catabolism is the major metabolic process for most organisms

store potential energy
- Starch in plants
- Glycogen in animals

they have structural and protective functions
- in plant cell walls
- extracellular matrixes of animal cells

Contribute to cell-cell communication
- ABO blood groups & Immune marking

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2
Q

what are 3 monosaccharides?

A

Glucose

Galactose

Fructose

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2
Q

what are disaccharides? give 3 examples:

A

they are sugars formed from two monomers/monosaccharides that are linked together by glycosidic bonds.

  1. Maltose
  2. Lactose
  3. Sucrose
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3
Q

what are glycosidic bonds?

A

they are covalent bonds that form when a hydroxyl group of one monosaccharide reacts with an anomeric carbon of another monosaccharide.

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4
Q

what is an anomeric carbon?

A

it is the carbon on a sugar that has four different groups around it, which allows two different left and right handed mirror images of each other (enantiomers).

It is usually the carbon-1 or the alpha carbon.

It stabilises the structure of glucose.

It is the only residue that can be oxidised.

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5
Q

what is maltose?

A

it’s a disaccharide sugar that is a product of the break-down of starch.

It contains an anomeric C-1 which is available for oxidation, so it is termed a reducing-sugar.

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6
Q

whst is lactose?

A

Lactose is a disaccharide sugar mainly found in milk, it is formed from a glycosidic bond between galactose and glucose.

It has an anomeric C-1 on the glucose which is available for oxidation, so it is a reducing-sugar.

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7
Q

what is sucrose?

A

it’s a common disaccharide sugar made only by plants, it consists of approx 25% of dietary carbohydrates.

It does not have a free anomeric C-1 so it is not available for oxidation, hence it is a non-reducing sugar.

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8
Q

what are polysaccharides? give two examples:

A

Polysaccharides are sugars that contain more than ten monosaccharide units, they have long chains, which might be made up of the same or differing monomer species.

e.g. Starch & Glycogen

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9
Q

what are homo/heteropolysaccharides?

A
  1. Homopolysaccharides}- Single monomeric species
  2. Heteropolysaccharides - Two or more monomeric species
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10
Q

what is starch?

A

is a polysaccharide sugar that is made up of two types of glucose polymer:

amylose and amylopectin

These glucose polymers together form alpha helices

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11
Q

what are amylose and amylopectin?

A

Amylose (20-25% of starch)

  • Linear polysaccharide, D-glucose residues in
    (α1→4) glycosidic bond.

Amylopectin (75-80% of starch)

  • Branched polysaccharide, (α1→4) glycosidic bonds
  • (α1→6) glycosidic bonds cause branches and they occur every 24-30 residue
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12
Q

what is glycogen?

A

it’s a polysaccharide sugar used in animal cells to store glucose.

  • It is a polymer of glucose (α1→4) glycosidic bond linked sub-units with (α1→6) glycosidic bond causing branches every 8-12 residues.
  • It is more extensively branched than Starch
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13
Q

where is 90% of glycogen found in our body?

A

Liver (replenish blood glucose)

Skeletal Muscle (catabolism produces ATP for contraction)

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14
Q

how and when are (α1→4) glycosidic bonds formed?

A

(α1→4) glycosidic bonds is formed between the carbon-1 of one monosaccharide and carbon-4 of the other monosaccharide through a hydroxyl group

(α1→4) glycosidic bonds are formed when the OH on the carbon-1 is below the glucose ring

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14
Q

what is an (α1→6) glycosidic bond? when is it formed?

A

it’s a covalent bond formed between the -OH group on carbon 1 of one sugar and the -OH group on carbon 6 of another sugar, which causes branching.

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15
Q

why do some carbohydrates attach to proteins?

A

it might:

↑ Protein’s solubility and stability

  • Influence protein folding and conformation
  • Protection from degradation
  • Communication between cells
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16
Q

what are glycoproteins?

A

they are proteins that have carbohydrates covalently attached to them.

located in outer plasma membrane and extracellular matrix, in the blood.

Within cells in the secretory system
(Golgi Apparatus, Secretory Granules)

they have a low carbohydrate content compared to protein

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17
Q

what are glycosaminoglycans? give an example:

A

they are un-branched polymers, known as mucopolysaccharides, made from repeating units of hexuronic acid and an amino-sugar, which alternates through the chains.

Function - Mucus & Synovial fluid around joints.

e.g. Hyaluronic acid that makes up the ground substance, giving it a gel-like form.

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18
Q

what are proteoglycans?

A

they are proteins that have a high content of carbohydrates, which are formed from Glycosaminoglycans covalently bonded to proteins.

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19
Q

where are proteoglycans located? what is their function?

A

Location: The surface of cells or between cells in the extracellular matrix.

Role: involved in the Formation of connective tissue

20
Q

what are mucopolysaccharidoses?

A

they are a group of genetic disorders caused by the absence or malfunction of the enzymes that are required for the breakdown of glycosaminoglycans (GAGs).

21
Q

what does build up of GAGs in connective tissue lead to?

A
  • Damage in cellular architecture and function
  • Severe dementia, heart problems, endothelial structure problems.
  • Stunted bones, inflammed & damaged joints.

e.g. Hurler, Scheie, Hunter, Sanfilippo syndromes

22
Q

what does hurler syndrome lead to?

A

Severe developmental defects
* Stop developing at 4 yrs → death at around 10 yrs

  • Clouding and degradation of the cornea
  • Arterial wall thickening
  • Dementia caused by
    (build-up of cerebrospinal fluid (CSF) & enlarged ventricular spaces)
23
Q

how is glucose absorbed in the intestines?

A

Inside the the lumen of the intestines there is a high [Na+] and [Glucose] after eating.

Glucose is absorbed through an indirect ATP-powered process:

Sodium-Glucose symporters on the Apical surface are used to diffuse Na+ and Glucose together into the epithelial cell with the concentration gradient (Low cellular Na+) caused by the ATP-Driven Sodium/Potassium Pump.

Na+ is removed from the cell through the Sodium/Potassium Pump.

Glucose is transported into the blood through a Glucose uniporter (GLUT2).

This system works even if glucose goes against its concentration gradient.
(i.e. when blood glucose is high)

23
Q

how do we digest carbohydrates? starting from the mouth to jejunum:

A

Mouth → Salivary amylase hydrolyses (α1→4) glycosidic bonds of starch

Stomach→ No carbohydrate digestion

Duodenum → Pancreatic amylase hydrolyses (α1→4) glycosidic bonds of starch

Jejunum → Final digestion by mucosal cell-surface enzymes:

  • Isomaltase - hydrolyses (α1→6) glycosidic bonds
  • Glucomylase - Removes glucose from non-reducing ends
  • Sucrase - hydrolyses sucrose
  • Lactase - hydrolyses lactose

Final products are monosaccharides → Glucose, Galactose, Fructose

24
Q

what does galactose and fructose do?

A

Galactose has a similar mode of absorption as glucose, utilising gradients to facilitate its transport.

Fructose binds to channel protein (GLUT5) and simply moves down its concentration gradient
(high in gut lumen, low in blood)

25
Q

what happens after absorption of glucose through the intestinal epithelium cells?

A

Glucose diffuses → hepatic portal vein → liver

Glucose is phosporylated into Glucose 6-phosphate by hepatocytes.

It is trapped in the liver cells because GLUT transporters can’t recognise it anymore.

26
Q

what ae the causes of disaccharide deficiencies?

A

non-genetic results from:

  • Intestinal infection
  • Inflammation of gut lining
  • Drugs injuring the gut wall
  • Surgical removal of the intestine

Characterised by abdominal distension and cramps

Diagnosis → intestinal enzyme secretion test (Lactase, Sucrase, Maltase)

26
Q

what is lactose intolerance?

A

Lactose intolerance is the most common disaccharidase deficiency because most human populations lose lactase activity after weaning.

If lactase is lacking, then ingestion of milk doesn’t work→ disaccharidase deficiency symptoms

These symptoms are caused by:

  • Undigested lactose break down causes gas and irritant acid build up
  • Lactose is osmotically active, so water is drawn from gut into lumen → diarrhoea

Avoiding symptoms by:

  • no milk products / lactase supplements / treated milk products
27
Q

what is glucokinase

A

Glucokinase is an enzyme that facilitates phosphorylation of glucose to glucose-6-phosphate, it is mainly found in the liver.

Glucokinase has a high Km (low affinity - takes more substrate) and a high Vmax for glucose

but doesn’t grab much glucose at low concentrations

High Vmax means it can phosphorylate glucose quickly, thus most absorbed glucose is trapped in the liver when glucose is high after eating a meal

Glucokinase is not easily satisfied → High Vmax

28
Q

what is hexokinase?

A

Hexokinase is an enzyme that facilitates phosphorylation of glucose to glucose-6-phosphate, it is found in tissues other than the liver.

Hexokinase has a low Km (high affinity - takes less substrate) and a low Vmax for glucose.

but can grab glucose even at low concentrations

Hexokinase is easily satisfied → Low Vmax

29
Q

what is the fate of glucose-6-phosphate (G6P)

A

Pentose phosphate pathway → pentoses (5-C)

Glycolysis

(Substrate-level phosphorylation)
G-6-P → 2 Pyruvate and forms 2 ATP

(Oxidative phosphorylation)
uses oxygen - combustion!

2 Pyruvate goes through Citric Acid Cycle → CO2 + H2O + Lots of ATP

Storage of G-6-P as Glycogen (to be used later)

30
Q

what happens to glycogen if blood glucose is low in liver?

A

Glycogen → G-1-P → G-6-P → Glucose

Glucose 6-phosphatase (G6Pase) is an enzyme, found in liver, that hydrolyses G-6-P resulting in a free phosphate group and free glucose, to allow it to diffuse through the cells.

31
Q

what happens to glycogen if blood glucose is low in skeletal muscle?

A

Glycogen → G-1-P → G-6-P → Lactate

This is done through glycolysis

32
Q

describe the synthesis of glycogen (glycogenesis):

A
  1. Glycogenin begins the process by covalently binding Glucose monomers together from Uracil-Diphosphate (UDP)-Glucose, making chains of 8 Glucose residues.

UDP-Glucose → UDP + Glucose

Then the glucose are bound together to form a (α1→4) linear chain.

  1. Glycogen synthase extends the Glucose chain by adding glucose monomers to the non-reducing end.
  2. The chains formed by Glycogen synthase are broken by Glycogen-branching enzyme and reattached via (α1→6) glycosidic bonds to give branching points.
33
Q

describe the degradation of glycogen (glycogenolysis):

A
  1. Glucose monomers are removed one at a time from the non-reducing ends as Glucose-1-phosphate (G-1-P) using glycogen phosphorylase.
  2. Glucose near the branch is removed in a 2-step process by de-branching enzyme:

a) Transferase activity of de-branching enzyme removes a set of 3 glucose residues and attaches them to the nearest non-reducing end via a (α1→4) bond.

b) Glucosidase activity of debranching enzyme then removes the final glucose by breaking the branching (α1→6) bond to release free glucose.

  1. This leaves an unbranched, linear chain for degrading or building.
34
Q

what happesn to the degraded glycogen?

A

in muscle → Glycolysis (substrate level phosphorylation) → ATP for muscle contraction

In liver → G6-Pase converts G-6-P to glucose which moves to blood.

35
Q

what is von gierke’s disease?

A

it’s characterized by G6-Pase deficiency in liver, kidney, and intestine, so you can’t breakdown glycogen to glucose.

Symptoms:-

High [Liver glycogen]: normal structure but lots of it

Low [Blood glucose]: fasting hypoglycaemia
- glycogen can’t be used as an energy source, all glucose must come from diet.

High [Blood lactate]: lacticacidaemia
- lactate (made by skeletal muscle) can’t be reconverted to glucose in the liver

Treatment:- regular carbohydrate feeding

36
Q

what is mcardle’s disease?

A

it’s characterized by skeletal muscle glycogen phosphorylase deficiency.

Symptoms:-

  • High [muscle glycogen] – normal structure but lots of it
  • Weakness and cramps after exercise
  • No increase in [blood glucose] after exercise

Treatment:-
* Avoid strenuous activity
* “second wind”
- Exercise briefly (anaerobically), wait for the pain to subside, continue to exercise (aerobically using oxidative phosphorylation of fatty acids)

36
Q

why are most symptoms not apparent in resting state?

A

as muscles use glucose/fatty acids from blood.

37
Q

Describe the overall free energy of Glycolysis:

A

glycolysis has a high -ΔG so it is an exergonic, energy-giving process.

38
Q

under anaerobic conditions why must NAD+ be regenerated?

A

to maintain NADH/NAD+ redox balance

It is replenished by:
2 Pyruvate + 2 NADH→ 2 Lactate + 2 NAD+

Pyruvate is reduced to Lactate, while NADH is oxidized to NAD+

39
Q

Why must NAD+ be replenished after being converted to NADH in Glycolysis?

A

Because without NAD+ the full process of Glycolysis cannot be achieved.

NAD+ is limited in the cell (it comes from the vitamin - niacin)

All the fates that pyruvate is subjected to will produce NAD+ to replenish it, as it is required for the reduction of various intermediate metabolites.

40
Q

What happens to pyruvate after Glycolysis?

A
  1. Pyruvate → Acetaldehyde → Ethanol
  • Process done by Yeast and other microorganisms.
  • Oxidation of NADH drives the reduction of Acetaldehyde to Ethanol, this NAD+ then goes on to be recycled in glycolysis again (redox balance) under anaerobic conditions
  1. Pyruvate → Lactate (Under anaerobic conditions)
  • Pyruvate is reduced to lactate via fermentation
  • Oxidation of NADH drives the reduction of Pyruvate to Lactate, which in turn replenishes stores of NAD+ for further glycolysis
  1. Pyruvate → acetyl CoA (under aerobic conditions)
  • Occurs within the mitochondria.
  • NADH formed in this reaction will later give up it’s hydride ion (:H-) to the respiratory chain.
41
Q

Why can’t gluconeogenesis be an exact reverse of glycolysis?

A

because 3 out of the 10 glycolysis reactions have a large -ΔG which makes them irreversible.

Instead the cell bypasses those 3 reactions with enzymes that catalyse a separate set of irreversible reactions.

41
Q

describe the fate of blood lactate

A

When muscles don’t receive enough O2 to make ATP via Oxidative Phosphorylation

ATP is made via Substrate-level Phosphorylation producing Lactic Acid (Anaerobic glycolysis)

Lactate is converted to Glucose in the liver by a process called Gluconeogenesis

The liver repays the oxygen debt run up by the muscles.

This is called (Cori Cycle) = the process of anaerobic glycolysis then lactate conversion to pyruvate and then gluconeogenesis to produce glucose

42
Q

what are the 4 reactions that sidestep the 3 irreversible reactions of glycolysis to form glucose (gluconeogenesis)

To allow for independent control of the glycolysis and gluconeogenesis pathways
and prevent them cancelling each other out.

A

In the mitochondria and cytosol
——————————————

Reaction-A:

Pyruvate → Oxaloacetate (OAA)
Catalyst - pyruvate carboxylase (adds carbon)

Intermediate Reaction:

OAA → Malate (crosses mitochondrial membrane) → OAA (in cytosol)
Catalyst - (M) malate dehydrogenase Catalyst - (C) malate dehydrogenase

Reaction-B:

OAA → Phosphoenolpyruvate (PEP)
Catalyst - PEP carboxykinase (PEPCK) (removes carbon and adds phosphate)

In the cytosol (cytoplasm)
———————————–

PEP goes through Intermediate Reversible Reactions:

         PEP →→→ F-1,6-bisP

Reaction-C:

F-1,6-bisP → F-6-P
Catalyst - fructose-1,6-bisphosphatase (hydrolysis - only cleavage of phosphate)

Reaction-D:

G-6-P → Glucose
Catalyst - glucose 6-phosphatase (hydrolysis - only cleavage of phosphate)

No phosphoryl group transfer to ADP because that would be energetically unfavourable

43
Q

what is fructose and galactose similar to glucose?

A

they are two monosaccharides do not have specific pathways like Glycolysis of glucose, but they can jump into glycolysis at various points.

Fructose in adipose tissue → F-6-P

fructose in liver → DHAP / GA3-P

Galactose → G-6-P

44
Q

Explain the role of PEP carboxykinase (PEPCK) in PEPCKmus mice.

A

Overexpression of PEPCK gives a lot of Phosphoenolpyruvate (PEP) in muscle from lactate after exercising, therefore gluconeogenesis is highly active in these animals.

Lactate → Pyruvate → PEP

Lactate in their muscles ends up in the citric acid cycle, providing ATP for muscle function.

44
Q

how does drinking affect gluconeogenesis (formation of glucose)? and what homeostatic malfunctions could it lead to?

A

Gluconeogenesis requires NAD+ to function well.

When drinking:

These processes require NAD+ which reduces and inhibits gluconeogenesis

Because gluconeogenesis from the Lactate Pathway requires NAD+ to begin:

Homeostatic malfunctions:

  • ↑ [Blood Lactate] - Lacticacidaemia
  • ↓ [Blood Glucose] - Hypoglycaemia
45
Q

Substrate-level phosphorylation vs Oxidative/Respiration-linked phosphorylation.

What’s the difference?

A

“substrate-level” requires soluble enzymes and chemical intermediates, when a phosphate group is transferred
from a pathway intermediate to ADP, making ATP

“oxidative” or “respiration-linked” involves membrane bound enzymes and gradients of protons, mainly talking about the electron transport chain.

FoM - normal function (20 decks)

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