Food2150 Set 3 Flashcards
1
Q
How is taste stimulated?
A
when chemical compounds activate specialized receptor cells in the oral cavity
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
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
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
3
Q
What are the 5 tastes?
A
- bitter, sour, sweet, salty, umami
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
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
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
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)
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
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
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
7
Q
A
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
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)
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
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 !
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
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
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+
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
15
Q
What taste receptors does umami require?
A
- Often amino acids
- Defined as savoury and delicious
sensation - MSG, GMP, IMP
16
Q
What is the Scoville scale?
A
- measures the amount of capsaicin
17
Q
What is pungency?
A
- oral sensation
- Spicy
- Capsaicinoids
- Very hydrophobic compounds
- scoville scale!
18
What is astringency?
- 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
19
What is menthol-cooling?
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
20
What are the 7 sensations of smell?
Desirable:
- camphor
- floral
- mint
- ether
Non desirable:
- acrid
- putrid
- musk
* be able to differentiate enantiomers
21
How do we smell (aroma)?
* Nose lined with mucous membranes with receptors connected to the olfactory nerve
22
Describe camphor scent
- smells like menthol
- used in asian sweets
23
Describe floral scent
* Sage, orange, rosemary, cinnamon
* Important for the food industry
24
Describe mint scent
* Mint leaves
* Spearmint, mint, peppermint
* Extensively used in foods
25
Describe ether scent
* good scent
* Most smells associated with fruits
* Grapes, wintergreen, apples
26
Describe acrid scent
* bad scent
* Smells like burning / smoke
* Smoked and cured meat smell
27
Describe putrid scent
* bad scent
* Rotten foods
* Short chain aldehydes and ketones
* Breakdown of protein & lipids
27
Describe musk scent
* bad scent
* Old spice
* Not used in the food industry
28
What is specific of odour?
- different mirrors cause different scents (enantiomers)
- left-handed and right-handed
- (L: spearmint, R: caraway)
29
What is the science of conditioned reflexes?
- 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
30
Describe long term eating
APPETITE
- psychological drive to eat
- might not be hungry, still going to have a piece of chocolate
- Influences (Social, biological and psychological)
31
Describe short term eating
HUNGER
- Our biological drive to eat (starts food-seeking behaviour)
- Low glucose in the brain – Neuropeptide Y released
- Eat (glucose returns)- Alpha-melanotropin
31
Describe NPY
- 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
32
Describe the nervous system
- 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
32
How do we get our biological drive to eat?
- gut–brain axis involves neural, immune and endocrine signalling pathways
- nervous, immune, endocrine
33
Describe long term stoping
SATIETY
- Perception of fullness after meal
- Once stomach empties
- Ghrelin is released starting the cycle over again: stomach returns to initial state
33
Describe short term stoping
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
Describe the endocrine system
- 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
What are the NPY family of biologically active peptides?
- control our drive to eat
- NPY
- peptide YY (PYY)
- pancreatic polypeptide (PP)
34
Describe PYY
- reduces food intake
- reduces contractions
- produced in large intestine, goes to vagus nerve
34
Describe the immune system
- 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
Describe PP
- 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
How does fiber, fat, carbs, and protein satiate
Satiation, Satiety
FIBER: +++, +
FAT: +, +++
CARBS: ++, +
PROTEIN: +++, +++
37
What are the 6 key stages to oral processing solid food?
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
What is the mouth process model?
- 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
What is the Cephalic phase?
- 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
What are glycemic carbs to monosaccharides?
polysaccharides-dextrins-maltose
(salivary amylase breaks up the two transitions)
38
Describe lingual lipase and its contents and hydrolyzation
- 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
Describe Asp, His, Ser in lingual lipase
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
Describe the process of amylose to maltose
- digest very efficiently
- straight
- A-1,4 bound glucose molecules
- smallest section amylase can break it down (disaccharides +)
38
Describe lingual lipase
- 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
What is maternal lipase?
* 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
What is the distal stomach?
antrum and the pylorus
39
Describe the process of amylopectin to maltose
- branched
- A-1,4 and some 1,6 (we cannot break down 1,6)
- less complete digestion
39
What is the fundus?
- proximal stomach
- Comprised of the cardia, fundus, and body
39
What do the 2-3L of gastric fluids a day include?
mucus, acid intrinsic factor, & enzymes
39
What is zymogen?
- 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
What are some features of the stomach
- 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
What is the mucous layer of stomach secretions?
- 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
What is the vagovagal reflex?
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
Describe antral contraction waves
- 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
How do enzymes and mucus work in stomach secretions?
- parietal cells make HCl
- chief cells make pepsinogen
- pepsinogen in constant circle with pepsin
- gastric pits
- zymogens released into oral captivity
39
Describe zymogens
- 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
Describe pepsin
active enzyme: cleaves proteins, pH drops and denatures proteins (they unfold; increased SA; enzyme has more space to act
40
What are the digestive products of a triglyceride?
*EXAM Q
- 2 fatty acids
- 1 SN2 monoglyceride
40
What does nucleophilic attack on a triglyceride?
SN1 and SN3 do not cleave off at same time
40
What is the protein (catalytic functional) triad?
- does the nucleophilic attack
- Asp, His, Ser
- acts on SN1 and SN3
40
How does gastric emptying and satiety refer to solid and liquids?
- takes longer for gastric emptying for solids than liquids
40
What does ghrelin influence?
- 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
Compare leptin and ghrelin
Leptin:
- suppresses appetite
- long-term regulation of energy
- from adipose tissue
Ghrelin:
- stomach emptying
- stimulates hunger
- fast-acting regulation of energy
40
What can happen if you take ozempic without diabetes?
- weight loss: acts on GLP-1
- can paralyze gastric system (can't eat solid foods: peristalsis)
40
What are the steps of satiety?
1. psychological
2. vasovagal reflex
3. nutrient sensing
4. gut microbiome (we don't think of its effects much, but has big effect)
41
What happens if we impair villi?
- due to food-borne infection
- we see osmotic gradient occur; water diarrhea
- if they rupture; blood diaarhea
42
What is the physiology of small intestine?
- cross-section of small intestine
- villi
- epithelia cell with microvilli
43
What does salivary amylase act on?
- acts between polysaccharides and dextrins
- acts between dextrins and maltose
- from mouth; carb digestion
44
What does pancreatic amylase act on?
- acts between polysaccharides and dextrins
- acts between dextrins and maltose
- from pancreas; carb digestion
45
How do glucose, fructose, and galactose get transported?
- 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
How does lipid digestion work?
- 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
What can humans digest?
- no beta configurations
- only alpha 1,4
48
What is emulsifier?
- 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
How does pancreatic lipase work?
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
What is Co-lipase?
prevent inhibitory effect of bile salts on lipase catalyzed duodenal hydrolysis of long-chain triglycerides
51
Describe assimilation (absorption)
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
What is the end of the small intestine and large intestine?
- 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
What is the ileal break?
* 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
How does intestinal protein digestion work?
- dependent on where it can cut protein up
- shorter proteins (peptides); do not form structures like beta-sheets
53
How are microbial effects beneficial in the large intestine?
* 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
What do trypsin and chymotrypsin act on?
trypsin: K, R
chymotrypsin: W, Y, F
55
What are some active and inactive enzymes (zymogens) of intestinal protein digestion?
inactive: chymotrypsinogen, trypsinogen
active: chymotrypsin, trypsin
55
How does protein absorption work?
food protein gets chewed, through stomach (pepsin) at very acidic pH, than through long intestine at slightly acidic pH, to the brush border
55
What is the colon responsible for in the large intestine?
- 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
How does the gut microbiota change between infants?
- mode of delivery
- type of infant feeding
- gestational age
- hospitalization and antibiotic use
56
How are microbial effects undesirable in the large intestine?
* growing microbes may produce toxic sulphur compounds, carcinogens, gases causing flatulence, bloating
- metabolites enter circulation and have neurological effects
57
What are the three dominate phyla in the colon?
* bacteroidetes, firmicutes, actinobacteria
* Complex environment populations influence each other
* Populations evolve with age (Firmicutes/Bacteroidetes ratio
especially)
58
What do Bacteroides mainly produce vs Firmicutes?
B: acetate and propionate
F: butyrate
59
Why may microbial effects be undesirable?
may produce:
- toxic sulphur compounds
- carcinogens
- gases (flatulence)
60
Why may microbial effects be beneficial?
* Further breakdown of indigestible
* By-products can also be absorbed
* E. coli produces certain B vitamins
* Lactic acid bacteria produce healthful nutraceutical compound
61
What is symbiosis?
- A microbial positive adaptation on or inside the body
62
What is dysbiosis?
microbial imbalance or maladaption
63
Where do SCFAs produce and what is butyrate?
microbial fermentation
- an essential energy substrate for cellular metabolism in the colonic epithelium
64
What does dysbiosis manifest as?
- inflammatory bowel disease & IBS
- obesity & MetS
- asthma & hypertension
(D) mood & behavior hormone signaling
