Biochemistry- Why eat

Question 1

Why do we feel hunger? Give physiological and psychological reasons

Answer 1

Physiological reasons:
o Metabolic fuels
o Amino acids (protein turnover)
o Vitamins and minerals (replace losses)

 Psychological reasons
o Social aspects of food and meals
o Hedonistic value
o Psychological value

Question 2

What are the main hormones and signals involved in hunger

Answer 2

Ghrelin (a peptide) is the only known circulating orexigenic (appetite stimulant) hormone. This surges before every meal
(with and without feeding schedules) and injections stimulate hunger and feeding.

 Production of ghrelin by the stomach decreases in response to nutrients in digestion (especially carbohydrates and protein).
 Ghrelin stimulates processes in anticipation of digestion (e.g. gastric acid secretion).
 Orexigenic signals cause you to eat more.
 Anorexigenic signals cause you to eat less.

Question 3

What are the satiety signals

Answer 3

Satiety signals include a large number of peptides that are released in response to meals,
as well as gastric distension:

 These peptides are produced during meals by the gastro-intestinal tract and related
organs. They interact with receptors on nerves that innervate the GI tract, especially the
vagus nerve.
 Different satiety signals are released for different macronutrients.
 Some satiety signals affecting digestion (e.g. inhibit gastric emptying).
 Satiety signals interact synergistically to give a feeling of fullness, at high levels nausea.

Cholecystokinin causes
animals to finish meals
more quickly
 Bombesin
 Amylin
 Glucagon
 Glucagon-like peptide 1

Question 4

What are adiposity signals

Answer 4

Leptin and insulin are responsible for long term regulation:
o Leptin is primarily secreted by white adipose tissue with levels reflecting subcutaneous body fat.
o Insulin is secreted in response to carbohydrate intake, but the amount secreted also corresponds to visceral body
fat (fat surrounding organs).
o Leptin and insulin can both enter the brain and stimulate receptors on nerve endings in the hypothalamus.
o Leptin and insulin increase the brain’s sensitivity to satiety signals.
 Obesity is associated with both insulin and leptin resistance, possible as a result of this, the overall system defends against
weight loss more strongly than weight gain.

Question 5

Describe how these signals can integrate at the NTS

Answer 5

In the brain, leptin and insulin receptors are at a high density in the hypothalamic arcuate nuclei (ARC). The ARC contains
neurons that produce neuropeptide Y (NPY) (makes people feel more hungry) and pro-opiomelanocortin (POMC) (makes
people feel less hungry), these neurons innervate the paraventricular nucleus (PVN) and the lateral hypothalamic area
(LHA).
 The PVN and LHA in turn secrete neuropeptides that alter the sensitivity of the nucleus of the solitary tract to
gastrointestinal satiety signals from the vagus nerve.
 High levels of insulin and leptin, cause the secretion of POMC, stimulating the PVN, and increase the sensitivity of the NTS to
satiety signals, resulting in smaller meals.

Question 6

How do we have food preferences?

Answer 6

Taste is said to be a major determinant in food choices, although others will apply.
 Some preferences are innate, but likes and dislikes can be learnt.
 Preferences are influenced by taste, smell, texture, visual appeal, post-ingestive signals and environmental cues.
 Preferences can also be influenced by pairing liked and unliked flavours.
 Taste can be affected by internal factors, such as sodium deficiency.
 Food preferences can/may be a predictor of future obesity.

Question 7

Describe different tastes and the molecular affinity towards each of them

Answer 7

1. Sweet
    Detection of carbohydrate
    Salivary amylase breaks down starch to release sugars.
   There is an innate preference for sweetness.
    Detection involves G-protein coupled receptors on taste
   receptor cells.
2. Salt
    Sodium is a physiological requirements.
    Sensitivity to and preference for salt has been shown to
   fluctuate according to the body’s needs.
    Detection involves various ion channels, some sensitivity
   to sodium in particular.
    Anions modulate saltiness sensation.
3. Sour
    There is an innate aversion to sourness, part of the body’s
   mechanism to regulate body pH.
    An indicator of food ripeness.
    Detection involves an intracellular decrease in pH.
4. Bitter
    Detection of a wide range of potentially toxic compounds.
    Heritable variations
    Some association with obesity in non-tasters of a
   particular bitter compound.
    Detected by G-protein coupled receptors.

4.1. Genetic variation in bitter perception
 The largest family of taste receptors (TAS2R) encodes the
bitter taste receptors, and shows greater variation than
other families.
 Taste blindness has been observed for PROP (6-npropylthiouracil). The common versions of this allele lead
to a recessive (non-taster)/dominant (taster) inheritance
pattern.
 PTC is similar to the glucosinolates in cruciferous
vegetables.
 Non-tasters prefer sweet, high-fat foods, and have a
higher risk of alcoholism.
 PROP-tasters have a lower preference for citrus fruit and
cruciferous vegetables.

5. Umami (savoury)
    Detection of amino acids/small peptides.
    Synergistically enhanced by 5’ ribonucleotides.
    Enhances palatability of food in general.
    Detected by G-protein coupled receptors.
6. Fat
    Contributes to perception of fat soluble flavour
   molecules, also contributes to perception of texture (e.g.
   creamy).
    Heightens pleasurable sensation of sweetness.
    Preference of high-fat foods is associated with obesity.
    PUFA (polyunsaturated fatty acid) (released by lingual
   lipase) may also interact with ion channels, enhancing the
   tastes sensed.

Question 8

Name and describe 4 processes driven by hydrolysis of ATP (producing energy)

Answer 8

. Endothermic reactions
 Enzymes can couple endothermic reactions to the breakdown of ATP, altering the equilibrium of both reactants in favour of
the products.
 Enzymes can also degrade the pyrophosphate product of a reaction, rendering the original reaction irreversible.

2. Metabolic trapping
    Glucose is able to leave or enter the cell via transporters that cannot bind glucose-6-P.
    A large proportion of resting metabolic rate is simply for maintaining gradients across the cell membrane.
    By phosphorylating intermediate products of the glycolytic pathway, they cannot bind to GLUT transporters and so are
   trapped within the membrane.
    Glucose is converted into glucose-6-phosphate by hexokinase which requires ATP. G-6-P cannot leave the cell.
3. Muscle contraction
    The movement of the thick filaments relative to the thin filaments gives rise to the contraction or shortening of the muscle
   fibre. The binding and hydrolysis of ATP are responsible for this motion.
    The action potential that stimulates muscular contraction depolarises the cell.
    ATP is needed to re-establish normal concentration gradients, and maintain them between contractions.
4. Signal transduction
    Covalent modification of proteins is a very common mechanism for altering the function of enzymes.
    Phosphorylation is by far the most common covalent modification of proteins.
    The negative charge on the phosphate can have a large effect on the 3D conformation of the protein.
    The phosphorylated amino acid can also act as a binding site for other proteins.
    Some signal transduction pathways are amplified using phosphorylation cascades. When the receptor binds to a hormone,
   it results in the activation of a kinase that phosphorylates and activates another kinase and so on.
    ATP is used in the formation of cAMP which activates protein kinase A.

Question 9

What are the different types of amino acids and why do we need protein?

Answer 9

Protein is required in the diet for maintenance, growth and during injury/disease.
 Amino acids are grouped as:
o Essential: cannot be synthesised de novo by the organism.
o Conditionally essential: synthesis is limited (or can’t make enough) under special pathophysiological conditions.
o Dispensable: can be synthesised by the organism.

 The main use of amino acids is for:
o Protein synthesis, synthesis of other nitrogenous compounds
o Constitute a fuel
o Maintenance: replace lost protein by oxidation, lost epithelial cells, modified proteins/amino acids.
o Growth: protein deposition in growth, pregnancy and lactation.
o Injury/disease: certain disease states (burns, infection and cachexia) are associated with a loss of protein
(oxidisation/gluconeogenesis).

Question 10

Why do we need micronutrients

Answer 10

There are a large variety of nutrients that are needed in relatively small amounts, but are essential for optimal health:
o Vitamins (e.g. vitamin A).
o Minerals (e.g. iron).
o Fatty acids (e.g. omega-3 series of fatty acids).
 These micronutrients serve a wide variety of purposes: structural roles, coenzymes, components of signalling pathways.
 Absence from the diet results in malnutrition diseases.
 In addition, there exist other components of food that although they not technically nutrients, are believed to have health
benefits (e.g. fibre, lycopene (in tomatoes) and plant sterols (vegetable oils)).