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2X Study > 4 - Systems to Cells > Flashcards

4 - Systems to Cells Flashcards

1
Q

Give an overview of glucoses role in metabolism.

A
  • It is a good fuel for complete oxidation and is involved in biosynthetic reactions.
  • Stored as starch, glycogen etc.
  • Required for normal function of the brain and nerves.
  • In excess: glycogen within muscle and liver or triglycerides in adipose tissue.
  • Low levels: storage molecules broken and become exporters of fatty acids and glucose.
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2
Q

What is the role of insulin?

A
  • Stimulated by intake of glucose (increase in levels)
  • Released by pancreatic B-cells
  • Tissues take up sugar for oxidative phosphorylation, and muscles and liver cells store as glycogen.
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3
Q

What do glucagon and insulin have in common (3)?

A
  • released from pancreas
  • polypeptide hormones
  • bind to specific receptors
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4
Q

What is the role of glucagon?

A
  • Stimulated when blood sugars are low
  • Released from pancreatic a-cells
  • Stimulates glycogen and lipid breakdown (gluconeogenesis (glucose production from amino acids or lactate).
  • Increases cAMP levels which activates protein kinase A for phosphorylation.
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5
Q

What is the difference in glucose use in low and high levels of exercise?

A

Low - use of free fatty acids and blood glucose.
High - use of glycogen, muscle degeneration (stores) etc.

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6
Q

How can an enzymes activity be regulated?

A

Via reversible covalent modification.
The phosphorylation- addition of P (-2) transferred from ATP by kinases.
The removal of the phosphate is catalysed by phosphatases.
It may turn the enzyme on/off.
It alters the 3D conformation due to high charge density - often make salt bridges with arginine or lysine residues.
It is reversed by kinase/phosphatase system.

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7
Q

What are the three methods of enzyme regulation?

A
  1. Changing rate of biosynthesis/degradation levels
  2. Changing activity
  3. Changing location
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8
Q

How is the direction and speed of metabolic pathways controlled?

A

By enzymes as both pathways favourable - steps are irreversible.
> If we want to reverse a step we usually require a different enzyme.
RDS - rate determining step.

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9
Q

Give two examples of rate determining steps in the glycolytic (glycolysis) pathway.

A

1 - phosphorylation of glucose by hexokinase or glucokinase
2 - phosphorylation of fructose-6-phosphate.

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10
Q

What is diabetes and its two types?

A

Diabetes is the dysregulation of glucose homeostasis.
T1D - b-cell destruction and autoimmune (no insulin).
T2D - b-cell dysfunction and insulin resistance. This could be due to prolonged high blood sugar (constant need for b-cells causes dysfunction).

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11
Q

What is leptin?

A

Single mutation which helps the study of diabetes - causes a lack of hunger in an organism so they keep eating.

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12
Q

Give an example of altered carbohydrate metabolism.

A

Bears - during hibernation they store masses of food with altered metabolism - can turn on/off insulin resistance to maintain blood sugar.

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13
Q

What form of insulin is biologically active and why?

A

Only the mature form is biologically active to ensure there is no accidental release.
It would be disastrous if even a small amount of insulin is released during low blood sugar.

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14
Q

Why is the accurate control of GLUT2 important and how is this done?

A

It is a highly accurate and controlled process which must be directly proportional. It creates a linear relationship as to ensure not too much (hyperglycaemia) or too little insulin is released in proportion to the blood sugar levels. A key facet of this is the low affinity of GLUT2.

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15
Q

How do we achieve diffusion of glucose through the plasma membrane and why would it be difficult without?

A

> Glucose is polar and therefore interacts with water well.
The plasma membrane is made of hydrophilic heads and hydrophobic lipid tails.
When we try push a hydrophilic molecule through this it would be very energy intensive.
The use of a transporter (GLUT2) means little energy is required - facilitative diffusion transporters.

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16
Q

Why is compartmentalisation important?

A

Different compartments mediate different functions to correctly process insulin - e.g. if preproinsulin was released it would cause no harm.
It leads to specialisation and hence greater efficiency.
The ability to package insulin into secretory vesicles at high concentrations is key - creates highly efficient systems and allows for ease of regulation.

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17
Q

What is the inverse relationship between affinity and Km?

A

Km is 1/2 vmax (enzyme working at half max velocity).
The higher the Km, the lower the enzyme affinity - if we have a low Km, this means low substrate concentrations are making our enzyme work quickly. The Km is an important measure of the affinity of an enzyme or transporter for its substrate.

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18
Q

Give an example of affinity and Km relationship.

A

GLUT2 has a high km, meaning it has a lower efficiency, but it means it does not plateau in key blood sugar levels due to it not having reached its max activity, and so it is able to accurately sense changes in blood sugar so can proportionally convert insulin release - linear trend.

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19
Q

How do beta-cells respond to changes in extracellular glucose concentrations?

A

They rapidly change ATP/ADP ratio - high ATP levels. Glucose phosphorylation in b-cells uses low affinity enzyme glucokinase (hexokinase alternate) as it is not as saturated so phosphorylation rate is directly proportional to intracellular glucose.
Glucose transporter and glucokinase are less efficient but have made a glucose sensor.

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20
Q

What causes the insulin cascade?

A

A single molecule of insulin activates a kinase that can phosphorylate many target molecules - amplification - causing this cascade.

21
Q

Describe SH2 domains.

A
  • Recruited by insulin receptors
  • Bind phosphotyrosine
  • Pocket for P-Tyr residue to fit
  • Second binding pocket is hydrophobic and so binds to isoleucine - confers specificity - residue side chain.
22
Q

What is GLUT4 vital for and where is it stored/expressed?

A

Specialised form of glucose transporter expressed in fat and muscle - goes to cell surface in response to insulin binding - triggered by Akt.
Stored in specialised secretory vesicles in absence of insulin.

23
Q

How can glucose uptake be stopped or slowed?

A

Inhibiting Akt or knocking down genes for Akt - causes GLUT4 not to dock and fuse with membrane.

24
Q

What effects does insulin have (3)?

A
  1. Inhibits lipolysis
  2. Increases glucose transport
  3. Glycogen synthesis and cell-specific effects like lipid droplet formation in fat cells to others.
25
Q

Describe STRs and how we can use them for phenotype-gene association.

A

Short tandem repeats - we all have the same sequences but differ in the number of repeats. We inherit STRs and different STRs can be mapped to different positions on the X-chromosome.
The strategy is to look for STRs co-inherited with phenotype - nearest will be 100% inherited with phenotype, and this lessens the further the STRs are.

26
Q

How would we find an associated gene to a particular phenotype?

A

Say it was X-linked, we could map the genes in the chromosomal region.

27
Q

What are candidate genes?

A

A gene when a mutant might cause the mutant phenotype we observe, within our identified chromosomal region.

28
Q

What gene was identified for the inappropriate aggression phenotype?

A

Monoamine oxidase genes - MOXA and MOXB. They function to metabolise excess neurotransmitters which calm fight or flight - mutant genes will have a longer cooldown period.

29
Q

How can mouse models be used for gene-phenotype studies, using an example.

A

Used due to similar genes. They generated a transgenic MOXA (correlated with MOXA deficiency) mouse mutant via gene deletion to abolish MOXA activity. Control mice vs mutants showed increased restlessness, attacking and escape/biting etc.

30
Q

What is Nail Patella Syndrome?

A

Autosomal condition which is co-inherited with ABO blood group gene (on same chromosome).

31
Q

What is gene mapping?

A

Process by which a particular phenotype is assigned to a particular gene.

32
Q

What are single gene conditions, giving three examples.

A
  • Mostly not inherited as they normally involve multiple genes and traits.
  • Tay-Sachs, sickle-cell and CF.
33
Q

How much DNA do different twins share?

A

Twin studies: monozygotic identical twins share 100% DNA, dizygotic non-identical twins are similar to those of siblings (50% DNA).

34
Q

How do we quantify heritability, using an example.

A

It is a measure of how well differences in genes account for differences in traits.
MS - partially due to inheritance, more prevalent in those further from equator (lack vitamin D).
If one twin has MS - 20% likely in identical, 5% in non-identical.
Heritability = (20-5)*2 = 30%

35
Q

What is a linkage analysis?

A

We look at a trait which commonly affects families. We find a pre-disposing allele from an affected ancestor, but after generations the area around this mutation will shrink due to recombination with other chromosomes - founder mutation.

36
Q

Describe complex phenotypes and their association with genome wide association studies.

A
  • SNPs - main source of variation
  • GWAS - DNA sequences provided from a variety of individuals and we want to find a pattern.
  • Selectively choose population - pick those with desired alleles and control for characteristics.
  • Manhattan plot - higher up, more frequently inherited.
37
Q

What are the current recommendations for exercise (3)?

A
  • Some PA is better than none
  • 150-300 of moderate, 75-150 of intense (a week)
  • Muscle-strengthening 2x a week
38
Q

What two events will diabetics experience due to low exercise?

A

Enter a hyperglycaemic state meaning:
1 - Glucose toxicity (decrease in insulin secretion and increase in resistance)
2 - Endothelial dysfunction (impacts tissues and increases risks)

39
Q

What are the effects of enhanced PKC and oxidative stress?

A

These impact our vascular function. The PKC pathway is activated by an increase in diacylglycerol - mediated by cellular signals which increase pro-inflammatory cytokine production, causing kidney and nerve damage. Oxidative stress leads to increase in ROS production, causing endothelial dysfunction.

40
Q

How does exercise help manage T1D and T2D?

A

Exercise increases glucose utilisation, leading to euglycemia (normal). It manages blood sugar levels independently of insulin via increasing ATP consumption and promoting carb use. This reduces levels and provides a route to euglycemia, giving long-term control. It also benefits insulin sensitivity and GLUT4 activity.

41
Q

Why is aerobic and resistance training important?

A
  • Improves insulin sensitivity
  • Metabolic impact of ~72hrs
  • Promotes oxidation of fatty acids (anti-inflammatory)
  • Improves lipids, bp, other metabolic parameters
  • Does not require weight loss to work
  • Lower risk of adverse health outcomes with better grip strength
  • Muscle contraction > increased GLUT4 transporter movements
  • Long-term enhances insulin independence
  • Combined yields best effects
42
Q

What can chronic training cause?

A

Negative impact - temporary post-exercise hyperglycaemia > gluconeogenesis.
The body does not know the length of exercise, so there is an upregulation of glucose, which increases blood sugar levels.

43
Q

What is the impact of carbohydrates?

A

High carb content foods increase blood glucose so should be avoided - the amount of carbohydrates is the primary determinant. There are simple and complex carbs.

44
Q

What is GI and give high/low examples.

A

GI is the glycaemia index which is a measure of how quickly food elevates your blood glucose after eating.
High - white bread, white rice.
Low - lentils, broccoli, spinach, nuts.

45
Q

What is the Mediterranean diet?

A
  • Blue zone
  • Macronutrients
  • Healthy fats, veg, whole grains
  • Limited red meat and processed foods
  • Reduces inflammation and oxidative stress
46
Q

What is the ketogenic diet?

A
  • Low in carbs and high in fat
  • Risks include change in dominant substrate (ketogenesis)
  • Ketoacidosis, keto flu and nutrient deficiencies
47
Q

Why is BBQ a risk for glucose levels?

A

Uses high GI foods, overeating, and cooking meat at high temps can produce advanced glycation end products which increase oxidative stress and inflammation.

48
Q

Give four foods which are beneficial to our metabolism.

A
  • Green tea (anti-oxidant)
  • Coffee (stimulates CNS, increasing metabolism)
  • Red wine/cocoa - risks recommending these
49
Q

What is gluconeogenesis?

A

Gluconeogenesis is a process that transforms non-carbohydrate substrates (such as lactate, amino acids, and glycerol) into glucose. Therefore, Insulin inhibits gluconeogenesis while glucagon stimulates it.

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