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YR2SEM1 > Food2150 Set 3 > Flashcards

Food2150 Set 3 Flashcards

1
Q

How is taste stimulated?

A

when chemical compounds activate specialized receptor cells in the oral cavity

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2
Q

How was taste buds thought to work and how they actually work?

A
  • all in different areas of the tongue
  • pretty even all-around tongue
  • triggered by contact taste bud cells (TBCs) of tongue
  • primarily reside in circumvallate, foliate, and fungiform papillae
  • taste buds are low down: everything you taste has to be somewhat soluble to access them
  • each taste bud has 50-100 TBCs
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2
Q

What is taste used to do?

A
  • used to identify nutritious food items
  • Making poor food selections when foraging entails wasted energy from eating foods of low nutrient and energy content, but also the harmful and potentially lethal ingestion of toxins
  • drives a primal sense of ‘acceptable” or unacceptable for what is sampled
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3
Q

What are type 1 cells: what taste are they responsible for and how do they communicate?

A
  • salty
  • maintain supporting structure (base) of buds
  • unsure how they communicate
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3
Q

What are the 5 tastes?

A
  • bitter, sour, sweet, salty, umami
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4
Q

What are type 2 cells: what taste are they responsible for and how do they communicate?

A
  • sweet, umami, bitter
    -rely on hormones synthesized by TBCs and their cognate receptors
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4
Q

What are chemosensory organs?

A
  • taste cells that each make a different flavour and communication
  • individually, are not unique to the tongue; found in nearly every organ
  • all 4 together only found on tongue
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5
Q

How does the gut work as a chemosensory organ?

A
  • largest hormone-producing organ in body
  • gastrointestinal epithelial cells function as molecular sensors involved in multiple processes related to food intake and digestion
  • many identified in the gut also expressed in TBCs
  • satiety hormones
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5
Q

What are type 3 cells: what taste are they responsible for and how do they communicate?

A
  • sour
  • form conventional neuronal synapses with sensory afferent intragemmal nerve (neural pathwork)
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5
Q

What are type 4 cells?

A
  • small heterogeneous group of cells located toward the base of the taste bud
    structure
  • can differentiate into any of the 3 cells
  • quiescent precursor cells and immature taste cells
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6
Q

How does overeating work with taste?

A
  • humans may want to eat even when full
  • we see apple pie: even though we are stuffed from thanksgiving we want to eat it because it tastes good
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6
Q

What are the different families for the taste receptors? (What are the G protein-coupled receptors (GPCRs)?

A

type 1 family (T1Rs: sweet and umami)
type 2 family (T2Rs: bitter)
type 3 family (+TIR2s: sweet, +T1R1: umami)

epithelial sodium ion channel (ENaC): salty
acid-sensing ion channels (ASICs): sour

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7
Q
A
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7
Q

How does flavor sensing in utero work?

A

cry-face: kale-exposed (bitterness)
laughter: carrot-exposed (sweeter)

we, from birth, do not like bitter flavours

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8
Q

How does genetic variation affect our taste?

A
  • ability to taste bitter thiourea compounds may have important implications as a marker for dietary patterns and chronic health in children
  • some children sensitive to bitter may require strategies to consume them
  • children insensitive to it may have greater intakes of high-fat foods and excess body weight (affected by other factors as well)
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9
Q

What does the PROP phenotype?

A
  • bitterness
  • associated to food acceptance, dietary intake, obesity risk in children
  • affects chronic health conditions, food/beverage preferences, chemosensory perception
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10
Q

What is the AH-B theory for sweetness?

A
  • An electronegative atom (B) must be 3
    angstroms from a H-bonding proton (HA)
  • It is attracted by the lipophillic (gamma)
  • Typically CH3 or phenyl
  • based on glucose (sweet- sugar)
  • know triangle !
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11
Q

What are taste receptors?

A
  • an electronegative atom (B) must be 3A from a H-bonding proton (HA) and attracted by the lipophillic (gamma) groups
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12
Q

What taste receptors does bitter require?

A
  • May use the same receptor as sweet receptors
  • Bitter molecules have a polar group and a hydrophobic group
  • One polar group interact differently than two polar groups
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13
Q

What taste receptors does sour require?

A
  • AH/B theory is used for sour (AH or B receptor binds with H3O+)
  • Sour compounds are acids (carboxylic acids) -COOH
  • Suggest the AH or B receptor interacts with H3O+
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14
Q

What taste receptors does salty require?

A
  • Complex flavour sensation
  • Described as a combination of sweet, bitter
    and sour
  • It is believed that cations cause salty and
    anions modify the salty taste
  • Not much is known about salty perception
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15
Q

What taste receptors does umami require?

A
  • Often amino acids
  • Defined as savoury and delicious
    sensation
  • MSG, GMP, IMP
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16
Q

What is the Scoville scale?

A
  • measures the amount of capsaicin
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17
Q

What is pungency?

A
  • oral sensation
  • Spicy
  • Capsaicinoids
  • Very hydrophobic compounds
  • scoville scale!
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18
Q

What is astringency?

A
  • oral sensation
  • Perceived as a dry feeling in the mouth
  • Tannins in Red Wine
  • Often confused with bitterness
  • Compounds complex with protein in saliva and they form
    precipitates on the tongue
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19
Q

What is menthol-cooling?

A

World’s most sold flavor- menthol
* Menthol solutions below oral temperature fell cooler than water of the same temperature (cold enhancement)
* L-menthol cools more effectively than d-menthol, but d-menthol attenuated warmth at least as much as l-menthol
* toothpaste, chewing gum or candies
* menthol binds to a cold receptor, increasing intracellular calcium
causing the same nerve stimulus as contact with cold water

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20
Q

What are the 7 sensations of smell?

A

Desirable:
- camphor
- floral
- mint
- ether
Non desirable:
- acrid
- putrid
- musk
* be able to differentiate enantiomers

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21
Q

How do we smell (aroma)?

A
  • Nose lined with mucous membranes with receptors connected to the olfactory nerve
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22
Q

Describe camphor scent

A
  • smells like menthol
  • used in asian sweets
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23
Q

Describe floral scent

A
  • Sage, orange, rosemary, cinnamon
  • Important for the food industry
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24
Q

Describe mint scent

A
  • Mint leaves
  • Spearmint, mint, peppermint
  • Extensively used in foods
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25
Q

Describe ether scent

A
  • good scent
  • Most smells associated with fruits
  • Grapes, wintergreen, apples
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26
Q

Describe acrid scent

A
  • bad scent
  • Smells like burning / smoke
  • Smoked and cured meat smell
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27
Q

Describe putrid scent

A
  • bad scent
  • Rotten foods
  • Short chain aldehydes and ketones
  • Breakdown of protein & lipids
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27
Q

Describe musk scent

A
  • bad scent
  • Old spice
  • Not used in the food industry
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28
Q

What is specific of odour?

A
  • different mirrors cause different scents (enantiomers)
  • left-handed and right-handed
  • (L: spearmint, R: caraway)
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29
Q

What is the science of conditioned reflexes?

A
  • Pavlov to rejected Sechenov’s ‘psychic’ salivary
    secretion hypothesis and proposed instead it
    was of a reflex nature was involved
  • not permanent but
    temporary or a conditioned one
  • discovered that reflex mechanisms were not of
    psychic activity but instead experimentally proven
    theory of conditioned reflexes
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30
Q

Describe long term eating

A

APPETITE
- psychological drive to eat
- might not be hungry, still going to have a piece of chocolate
- Influences (Social, biological and psychological)

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31
Q

Describe short term eating

A

HUNGER
- Our biological drive to eat (starts food-seeking behaviour)
- Low glucose in the brain – Neuropeptide Y released
- Eat (glucose returns)- Alpha-melanotropin

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31
Q

Describe NPY

A
  • NPY is a potent orexigenic peptide: Increases
    motivation to eat and delays satiety by augmenting
    meal size
  • produced in hypothalamus
  • increases food intake
  • first trigger that makes you start to seek food
  • secretes before you start to eat
  • preps digestion system to receive food
  • from swallowing to gastric contractions, pushes food out of stomach into duodenum
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32
Q

Describe the nervous system

A
  • Connected network of cells, tissues, and organs (autonomic nervous system; fight or flight)
  • Parasympathetic Nervous System (not active thought; feed and breed, rest and digest; digestive system)
  • Increases blood flow to intestine during digestion,
    peristalsis
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32
Q

How do we get our biological drive to eat?

A
  • gut–brain axis involves neural, immune and endocrine signalling pathways
  • nervous, immune, endocrine
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33
Q

Describe long term stoping

A

SATIETY
- Perception of fullness after meal
- Once stomach empties
- Ghrelin is released starting the cycle over again: stomach returns to initial state

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33
Q

Describe short term stoping

A

SATIATION (first stop; when it extends a certain point; full)
- how long until hunger returns: satiety
- Perception of fullness
- Psychological (amount consumed)
- Mechanical (distension & ileal break)
- Hormonal (CCK & PYY)

34
Q

Describe the endocrine system

A
  • uses hormones
  • Collection of physically
    disconnected organs that that
    communicate through hormones
  • Hormones are moved through
    the circulatory system.
  • Digestion, sensory perception of
    fullness
34
Q

What are the NPY family of biologically active peptides?

A
  • control our drive to eat
  • NPY
  • peptide YY (PYY)
  • pancreatic polypeptide (PP)
34
Q

Describe PYY

A
  • reduces food intake
  • reduces contractions
  • produced in large intestine, goes to vagus nerve
34
Q

Describe the immune system

A
  • Cytokines small protein fragments (peptides) mediate homeostasis & immune control as part of the innate immune system
  • lots of biologically petide in foods we eat, and our body NPY, PP, PYY
  • through an intricate interplay with mutually dependent positive and negative feedback mechanisms
35
Q

Describe PP

A
  • that PP is absent in obese children with Prader-
    Willi syndrome by increasing food seeking behavior
  • following a meal it secretes
  • present in overweight children
36
Q

How does fiber, fat, carbs, and protein satiate

A

Satiation, Satiety
FIBER: +++, +
FAT: +, +++
CARBS: ++, +
PROTEIN: +++, +++

37
Q

What are the 6 key stages to oral processing solid food?

A
  1. first bite
  2. comminution
  3. granulation
  4. bolus formation and processing
  5. swallow
  6. residue
    1,2 are mechanics
    3 is tribology
    4-6 is rheology and tribology
    crispy, crunchy, rough, sticky, smooth (takes less time left-right to process)
    - dry food needs more mastification as you need it to be more moist
    - 1st bite needs most force
37
Q

What is the mouth process model?

A
  • Before a food may be swallowed, its ‘degree of
    structure’ must have been reduced below the level of plane ABCD, and its ‘degree of lubrication’ must have crossed plane EFGH
  • ex: dry cracker breaks down structure fast, but hard to eat if mouth dry
37
Q

What is the Cephalic phase?

A
  • Gastric secretions begin before consuming food
  • Importance of thought, sight, smell, and taste of food in the cephalic phase
  • Talking about food for 30 min (without sight, smell, or taste) increased acid secretion & increased serum gastrin (hormone that stimulates acid production)
  • cultural and individual specific; universal
  • lost: if you cook something constantly
  • visual and sensory: increases
38
Q

What are glycemic carbs to monosaccharides?

A

polysaccharides-dextrins-maltose
(salivary amylase breaks up the two transitions)

38
Q

Describe lingual lipase and its contents and hydrolyzation

A
  • Secretion in oral cavity
  • Acidic lipases
  • Do not require bile salts or co-lipases (are not secreted until the intestine)
  • Medium-chain triglycerides were hydrolyzed at rates 5-8-fold higher than long-chain triglycerides
38
Q

Describe Asp, His, Ser in lingual lipase

A

ser: strong nucleophile
asn: electronegative withdrawing
- does not need to be located near each other in protein, or in same place
- attacks covalent bonds: 2 fatty acids from lipas (triglyceride)

38
Q

Describe the process of amylose to maltose

A
  • digest very efficiently
  • straight
  • A-1,4 bound glucose molecules
  • smallest section amylase can break it down (disaccharides +)
38
Q

Describe lingual lipase

A
  • best at cleaving sm1 and sm3 (our digestive system does not cleave position 2 (so 1 or 3) (very ineffective)
  • takes off 1 of fatty acids
  • lipase has small or no effect
  • important for pre-term infants: they do not have built digestion system
  • function enzyme arises from how protein folds
39
Q

What is maternal lipase?

A
  • Found in breastmilk
  • Stable to pH 3.5, resists degradation in the stomach
  • Requires bile acids so it does not become active until reaching the duodenum
  • Enough breast milk lipase is present in a feeding to hydrolyze all the breast milk triglycerides ingested within half an hour
  • Studies demonstrate improved efficiency absorption for the premature
    infant when fed non-pasteurized human breast milk
  • does most of digestion for baby
  • important for infant nutrition
  • breaks down fat
  • baby is born: pH of baby’s child is not nearly as high as adult
  • formula feeding: poo is more liquidy/messy, they are not eating fat
39
Q

What is the distal stomach?

A

antrum and the pylorus

39
Q

Describe the process of amylopectin to maltose

A
  • branched
  • A-1,4 and some 1,6 (we cannot break down 1,6)
  • less complete digestion
39
Q

What is the fundus?

A
  • proximal stomach
  • Comprised of the cardia, fundus, and body
39
Q

What do the 2-3L of gastric fluids a day include?

A

mucus, acid intrinsic factor, & enzymes

39
Q

What is zymogen?

A
  • an inactive precursor of an enzyme
  • requires a biochemical change (such as a hydrolysis reaction revealing the active site) for it to become an active enzyme
  • parietal cells make HCl, chief cells and HCl create pepsinogen
  • pepsin and pepsinogen in cycle
39
Q

What are some features of the stomach

A
  • Pyloric sphincter: Junction between the stomach and the small intestine
  • Fundus, Antrum, Cardia: secrete mucin
  • Thick folds, known as rugae, parietal cells secrete HCl (pH 1-2)
  • chief cells secrete pepsinogen & gastric lipase
  • pepsinogen: active precursor converts
    to proteolytic pepsin contact with acid
  • grind food particles until they pass through the
    pyloric sphincter
  • Food reservoir, where ingested food will remain until it moves to the distal end
39
Q

What is the mucous layer of stomach secretions?

A
  • protects the inner cells and musculature of the stomach
  • Foveolar cells produce mucus & bicarbonate (HCO3−) ions
  • important for protecting the gastric epithelium from its own acid secretions.
  • makes sure you cannot self-digest stomach
  • parietal cells
  • intrinsic factor: Glycoprotein binds to vitamin B12
    allowing for absorption at the terminal ileum
39
Q

What is the vagovagal reflex?

A
  1. food causes distension
  2. Release of acetylcholine, Causes relaxation
  3. leads to parietal cells
  4. creates pepsinogen and HCl
  5. full
    - controls contraction of the gastrointestinal muscle layers in response to distension by food
39
Q

Describe antral contraction waves

A
  • Elastic capacity to maintain more constant flow of
    digesta (chyme) to small intestine
  • 3-5 contractions going at the same time
  • continues into food emptied of stomach
  • once it enters into duodenum
  • food getting pushed to pyloric sphincter, food that can’t gets through gets moved against wall again
39
Q

How do enzymes and mucus work in stomach secretions?

A
  • parietal cells make HCl
  • chief cells make pepsinogen
  • pepsinogen in constant circle with pepsin
  • gastric pits
  • zymogens released into oral captivity
39
Q

Describe zymogens

A
  • an inactive precursor of an enzyme. It requires a biochemical change (such as a hydrolysis reaction revealing the active site) for it to become an active enzyme
  • because organs made from proteins
40
Q

Describe pepsin

A

active enzyme: cleaves proteins, pH drops and denatures proteins (they unfold; increased SA; enzyme has more space to act

40
Q

What are the digestive products of a triglyceride?
*EXAM Q

A
  • 2 fatty acids
  • 1 SN2 monoglyceride
40
Q

What does nucleophilic attack on a triglyceride?

A

SN1 and SN3 do not cleave off at same time

40
Q

What is the protein (catalytic functional) triad?

A
  • does the nucleophilic attack
  • Asp, His, Ser
  • acts on SN1 and SN3
40
Q

How does gastric emptying and satiety refer to solid and liquids?

A
  • takes longer for gastric emptying for solids than liquids
40
Q

What does ghrelin influence?

A
  • food preference
  • mood
  • stimulates appetite (hypothalamus)
  • growth hormones (pituitary)
  • inhibits insulin
  • increases cardiac output: nutrients ready to be absorbed, gives larger reservoir of blood to intestine for nutrients being digested
40
Q

Compare leptin and ghrelin

A

Leptin:
- suppresses appetite
- long-term regulation of energy
- from adipose tissue
Ghrelin:
- stomach emptying
- stimulates hunger
- fast-acting regulation of energy

40
Q

What can happen if you take ozempic without diabetes?

A
  • weight loss: acts on GLP-1
  • can paralyze gastric system (can’t eat solid foods: peristalsis)
40
Q

What are the steps of satiety?

A
  1. psychological
  2. vasovagal reflex
  3. nutrient sensing
  4. gut microbiome (we don’t think of its effects much, but has big effect)
41
Q

What happens if we impair villi?

A
  • due to food-borne infection
  • we see osmotic gradient occur; water diarrhea
  • if they rupture; blood diaarhea
42
Q

What is the physiology of small intestine?

A
  • cross-section of small intestine
  • villi
  • epithelia cell with microvilli
43
Q

What does salivary amylase act on?

A
  • acts between polysaccharides and dextrins
  • acts between dextrins and maltose
  • from mouth; carb digestion
44
Q

What does pancreatic amylase act on?

A
  • acts between polysaccharides and dextrins
  • acts between dextrins and maltose
  • from pancreas; carb digestion
45
Q

How do glucose, fructose, and galactose get transported?

A
  • glucose and galactose: rely on transporters to move them across epithelium
  • fructose has to be converted into glucose to transport the brush border
  • lactose physically anchored on epithelial lining (site of absorption)
46
Q

How does lipid digestion work?

A
  • cholesterol produces bile acid
  • bile is conjugated (taurine; amino sulfonic acid)
  • CCK causes gallbladder contraction, secretes all bile and digestive enzymes you need
  • intestine connected to gallbladder
47
Q

What can humans digest?

A
  • no beta configurations
  • only alpha 1,4
48
Q

What is emulsifier?

A
  • Allows for the mixing of the aqueous and oil phases into small droplets
  • Increasing the interface for the lipase-catalyzed reaction
  • when you eat fat: you never really eat straight fat/oil surfactants to mix them are bad for you, but create long shelf life
  • bile has to displace surface that is not fat
  • bile req. to make surface to hydrolyze
  • small molecule with a lot of hydroxyl group, can sit at surface of droplet, with lipase it can access oil in droplet
49
Q

How does pancreatic lipase work?

A

salivary lipase -> gastric lipase -> pancreatic lipase-> ASP,HIS,SER acts on triglyceride to make 2 monoglycerides
- Part of SCFA does not reach plasma, it is
metabolized in the cell lining of the
gastrointestinal wall

50
Q

What is Co-lipase?

A

prevent inhibitory effect of bile salts on lipase catalyzed duodenal hydrolysis of long-chain triglycerides

51
Q

Describe assimilation (absorption)

A

The lymphatic system takes fat soluble compounds from the GI tract through the thoracic duct to the bloodstream
- fat component determines if a drug must be taken with or without food (fat soluble, do not have to with water soluble)
* not controlled
* fats do not go through the liver
* most drugs are fat soluble, since they do not go through the liver, they get into our body more rapidly

52
Q

What is the end of the small intestine and large intestine?

A
  • glucagon-like peptide 1 acts on:
  • brain (appetite suppresion)
  • stomach (slows gastric emptying, decreases HCl secretion)
  • gallbladder (secretes insulin, decreases glucagon)
  • gall bladder acts on insulin
  • insulin acts on decreasing glucose production and glucose uptake, and brain
53
Q

What is the ileal break?

A
  • Entry of nutrients into the duodenum and jejunum activates the duodenal and jejunal “brakes”
  • Negative feedback mechanisms that influence the function of the proximal gastrointestinal tract
53
Q

How does intestinal protein digestion work?

A
  • dependent on where it can cut protein up
  • shorter proteins (peptides); do not form structures like beta-sheets
53
Q

How are microbial effects beneficial in the large intestine?

A
  • Further breakdown of undigestables
  • By-products can also be absorbed
  • E. coli produces certain B vitamins
  • Lactic acid bacteria produce healthful nutraceutical compounds
  • microorganisms can digest organisms you cannot
54
Q

What do trypsin and chymotrypsin act on?

A

trypsin: K, R
chymotrypsin: W, Y, F

55
Q

What are some active and inactive enzymes (zymogens) of intestinal protein digestion?

A

inactive: chymotrypsinogen, trypsinogen
active: chymotrypsin, trypsin

55
Q

How does protein absorption work?

A

food protein gets chewed, through stomach (pepsin) at very acidic pH, than through long intestine at slightly acidic pH, to the brush border

55
Q

What is the colon responsible for in the large intestine?

A
  • Water reabsorption & feces formation: diarrhea can lead to dehydration
  • Mineral reabsorption: diarrhea can lead to mineral depletion
  • Microbial fermentation
  • Breakdown of complex carbohydrates,
  • Absorption of volatile fatty acids
  • Detoxification and protection
  • to increase bile, increase fiber intake
56
Q

How does the gut microbiota change between infants?

A
  • mode of delivery
  • type of infant feeding
  • gestational age
  • hospitalization and antibiotic use
56
Q

How are microbial effects undesirable in the large intestine?

A
  • growing microbes may produce toxic sulphur compounds, carcinogens, gases causing flatulence, bloating
  • metabolites enter circulation and have neurological effects
57
Q

What are the three dominate phyla in the colon?

A
  • bacteroidetes, firmicutes, actinobacteria
  • Complex environment populations influence each other
  • Populations evolve with age (Firmicutes/Bacteroidetes ratio
    especially)
58
Q

What do Bacteroides mainly produce vs Firmicutes?

A

B: acetate and propionate
F: butyrate

59
Q

Why may microbial effects be undesirable?

A

may produce:
- toxic sulphur compounds
- carcinogens
- gases (flatulence)

60
Q

Why may microbial effects be beneficial?

A
  • Further breakdown of indigestible
  • By-products can also be absorbed
  • E. coli produces certain B vitamins
  • Lactic acid bacteria produce healthful nutraceutical compound
61
Q

What is symbiosis?

A
  • A microbial positive adaptation on or inside the body
62
Q

What is dysbiosis?

A

microbial imbalance or maladaption

63
Q

Where do SCFAs produce and what is butyrate?

A

microbial fermentation
- an essential energy substrate for cellular metabolism in the colonic epithelium

64
Q

What does dysbiosis manifest as?

A
  • inflammatory bowel disease & IBS
  • obesity & MetS
  • asthma & hypertension
    (D) mood & behavior hormone signaling

YR2SEM1 (10 decks)

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