1
Q
Foods Effect on Evolution
A
- Food sources were scarce
- Behaviours motivated by obtaining nutrients for survival
- Development of the sense of smell (which plays a part in flavour!)
2
Q
Mechanism Behind Hunger Signals
A
1) Blood Sugar Levels
- Glucose is the preferred source of energy from the brain
- Glucose is stored as glycogen, stored in muscle and liver
- Glucose released by liver to replenish blood glucose levels, regulated by insulin
- Reduced glycogen stores –> hunger
2) NPY (Neuropeptide Y)
- Potent appetite stimulant, neurotransmitter
- High levels lead to activity in hypothalamus
- Increased appetite and food seeking behaviours
3
Q
Blood Sugar Levels in the Body
A
- Pancreas secretes insulin to promote cell uptake of glucose after a meal
- Results in usage and storage of excess glucose as glycogen or adipose
- Decrease in blood sugar
- Liver converts glycogen to glucose
- Increase in blood sugar
- Glycogen in liver depletes
- Hunger!
The liver and pancreas help to buffer extreme swings in B.S levels, and regulate ingestive behaviours.
4
Q
NPY in non human mammals
A
- Effects them in a similar way as humans!
5
Q
Satiation Cues / Meal Cessation
A
Brain receives satiety signals from:
1) Stretch receptors in stomach via vagus nerve (connects gut and brain stem)
- How much is the stomach being stretched? high levels –> decreased NPY activity
- HIGHH levels of ghrelin can inhibit these stretch receptors…
- Could also be in small intestines
2) Cholecystokinin
- Small intestine produces CCK
- Locally slows movement of food from stomach to SI
- Acts on hypothalamus to supress hunger and promote satiety
3) Portal vein circulation
- Portal vein: Vein connecting SI to liver
- Presence of nutrients in portal vein detected by sensitive neurons
- Signals fired to hypothalamus to inhibit NPY
- Glucose in portal vein cuases insulin to rise
6
Q
CCK
+ Rat experiment :(
A
Cholecystokinin
- Hormone secreted by small intestines as food moves through
- Receptors in the brain detect CCK
- Serves as a satiety signal
Rats injected w/ CCK:
- Decreased meal duration
- Increased meal frequency
- Same amount of calories consumed as control (w/o injection)
Therefore, CCK regulates short-term satiety rather than long term consumption.
7
Q
NPY
A
Neuropeptide Y
- Hormone/neurotransmitter
- High levels in the hypothalamus triggers activity that promotes hunger and food seeking behaviour when glycogen reserves deplete
- Related to Reward Driven Feeding
8
Q
Why is Fat the Ideal Form of Long-Term Energy Storage
A
/ Adipose tissue
- Fat has 2x the energy density as glycogen
- 1g fat = 9kcal, compared to 1g carb = 4kcal
- Fat is found in all parts of the body
- Adipose tissue is an endocrine organ
9
Q
Leptin
A
- Hormone secreted by adipose tissue
- Involved in long term energy balance and correlates w/ fat mass
- High leptin levels = interacts w/ receptors on hypothalamus = reduced appetite and food consumption
- Controlled by OB gene
- Leptin indicates low energy stores rather than inhibiting appetite
- Inhibits NPY in hypothalamus
10
Q
Studies of OB Gene in Mice
A
OB Gene Knockout Mouse:
- Leptin production stops
- Appetite increases
- Fat storage increases resulting in obesity
- Reversed w/ leptin injections
Normal Mice Injected w/ Leptin:
- Additional leptin does not result in weight loss
- High enough leptin levels result in leptin resistance (true in humans and animals)
11
Q
Leptin Resistance
A
Beyond certain level, effect of leptin on appetite is reduced
12
Q
Evolutionary Basis of Leptin Function
A
- In history, taking in too many calories was rare
- Hence, leptin adapted to serve as an indicator of low energy stores rather than to reduce food intake
- Decreased leptin = Increased foraging = minimized activity (saves energy)
13
Q
Leptin and NPY interactions
A
NPY is a hunger signal
- NPY increases appetite
- Leptin inhibits NPY, causing it to decrease appetite in energy consumption
Together, leptin and NPY act to regulate weight to optimal levels.
14
Q
Ignoring Hunger: Interactions between NPY, Leptin, and CCK
+ eating eventually :)
A
- Glycogen reserves deplete
- NPY increases, acting as a hunger signal
- Adipose tissue secretes leptin to inhibit hunger, to indicate the need for food is not urgent
Eventually, drive to eat wins.
- As meal is taken, CCK released to prompt short-term satiety
15
Q
Experiments on Mice: NPY & Reward Driven Feeding
A
- NPY injected into brains of satieted rats
- Resulted in…
(1) increase in sucrose consumption
(2) rats work harder for a cue associated w sucrose
(3) increase in saccharin consumption (same taste, less calories)
(4) More carbs, less proteins and fats consumed - Therefore, NPY action promotes unconditional and conditional behaviours leading to increased carbohydrate consumption.
WHY?
- Preexisting preference for carbohydrate amplify NPY-mediated seeking of carbohydrates
- Genetic predisposition towards carbohydrate consumption
16
Q
Endogenous Opioids
A
Naturally occuring chemical substances that have morphine-like analgesic (relieving pain) actions in the body
- Contributes to palatability & reward-driven feeding
- Naloxene reduces intake of saccharine, sucrose, and saline by BLOCKING opioid receptors
17
Q
Naloxene
A
- Drug that blocks opioid receptors
- Reduces intake of saccharin, sucrose, and saline
18
Q
Experiments on Mice: Opioid Receptors
human application
A
Opioid Receptor Knockout Mice:
- Lower preference for saccharine than control mice
Maladaptive reward driven feeding mechanism may contribute to overeating in humans
19
Q
Weight Loss vs Weight Gain
A
- Body guards itself from weight loss more strongly against weight gain
- Evolutionary: Calories and nutrition used to be less certain
- Unintentional maladaptive expression in modern nation (cheap calories and minimal movement)
20
Q
Evolution of Taste
A
Taste is used to assess nutritional quality!
Bitter and sour tastes are associated with poisonous/toxic foods.
- Taste must be acquired for these senses
Sweet, salty, savoury foods are associated with foods that are safe, nutritious, and rich in energy.
- Individuals who could detect these tastes had a survival advantage: access to nutritional foods while avoiding toxic ones
21
Q
Universal Taste Preferences
Why is so?
A
- Universal in babies/infants!
- Certain tastes elicit the same response in all babies
- Healthy infants & unhealthy (brain damage) infants exhibit same response to taste
Experiment:
- Healthy infant elicits acceptance response to sweet & salty foods, rejection response to bitter & sour foods
- Same responses seen in baby w/ hydrocephalus
Hence, taste response is controlled by older and lower regions of the brain.
- Further evidence that taste response is an adaptive mechanism
22
Q
How do Cultural Influences Shape Taste Response?
A
- Highly processed foods are engineered to give you a salty / sweet taste
- Foods we enjoy as adults are learned by experience (as well as individual differences in taste sensitivity…)
23
Q
Differences in Individual Taste Sensitivity
A
- Influenced by number of taste buds on tongue
- Highly sensitive tasters = more taste buds = toxin avoidance and increased nutrition (evolutionary lens)
- Females are more sensitive to sweet and bitter tastes,
- Increasing during first trimester (time period when fetus is most sensitive to toxins)
24
Q
Adaption of Taste Preferences
A
- Adapted for identifying safe, nutritious calorie-rich foods
- Salty, sweet, rich foods give calories which fulfill energy needs
- Taste preferences have yet to adapt to increase in calorie intake in modern society
25
How Are Taste and Smell Unique as Senses?
Able to detect chemical stimuli!
* Depends on receptors interacting w/ small molecules
26
Taste Receptor Cells
* Beginning of taste sensation
* Located on taste buds on tongue, soft palate, and throat (50 - 150 cells per bud)
* Responds to dissolved food molecules
* Action potential fired, **gustatory nerve** sends signals to the medulla
27
Sensory Process of Taste
1. taste buds (w/ taste receptors)
2. Medulla (in brainstem, sent via gustatory nerve)
3. Can either act locally or be sent to thalamus
4.
* Primary: Thalamus --> gustatory cortex (sends info to somatosensory and orbital cortex) (taste and flavour)
* Secondary: Pons --> hypothalamus + amygdala (cessation and feeding)
28
What Tastes Can We Detect?
* Sweet: Energy rich foods
* Salty: Electrolytes
* Bitter, sour: spoiled or harmful
* Umami: Detects glutamate and aspartate
29
Taste Maps are....
**False. **
All areas of the tongue detect all types of taste!
* Each taste bud contains some proportion of all 5 taste receptors
30
Brainstem in Sensory Taste Processing
* Action potential from taste receptor cells sent to brain stem
Taste pathways diverge:
1) --> medulla --> thalamus (relay station) --> somatosensory cortex (texture) OR --> gustatory cortex --> orbital cortex (taste and flavour)
* Then goes to several higher brain regions (gustatory cortex, etc.)
* Processing taste, flavour, texture
2) --> pons --> hypothalamus and amygdala
* Cessation and Feeding
* When to start and stop feeding
* NPY and CCK
31
Hypothalamus & Amygdala in Taste Processing
* Sent from thalamus
* Origin of emotional and hormonal drives behind feeding
* CCK activity and satiety
31
Gustatory Cortex
* Main processing center for taste
* Specific neurons respond to each of the 5 basic tastes
* Connects to somatosensory cortex to connect taste w/ texture
* Connects to orbital cortex to connect waste w/ smell --> flavour!
32
Taste vs. Flavour
* Taste: Senses that the taste buds detect, occurs in the tongue
* Flavour: Combined experience of taste and smell, occurs in the nasopharynx
33
How is Flavour Processed?
* Odourants from meal travel up through back of the throat
* Interacts w/ receptors in nasal cavity that process smell (**retronasal smell**)
34
The Special Case of Spice
* Spice isn't actually a taste...
* Results from **capsaicin**, a chemical that binds to heat/pain receptors in mouth
* Causes receptors to fire action potentials
35
Smell Sensation
The processing of chemical molecules (**odourants**) of stimuli found in the air.
* Smell has a direct link to cortex, not having to go through thalamus
* Evolutionary lens: Smell detected over long distances, aiding in finding food, mates, avoiding predators
36
Smell Sensatory Pathway
Starts with a breath.
1. Odourants enter nasal cavity
2. Dissolves in mucus of nose (allowing for odourants to bind w/ **olfactory cilia/receptors** of the **olfactory bulb**
3. Olfactory receptors fire action potentials / send electrical signals
4. Receptor axons synapse w/ dendrites of **glomeruli**
5. Glomeruli relay signal to higher regions of the brain, where smell contributes to flavour perception (limbic system, olfactory cortex, orbital cortex)
37
Olfactory Cilia
Tiny hair-like structures that cover the receptor surface of the nasal cavity / olfactory epithelium
38
Olfactory Receptor Cells
Detect odor molecules and convert them into nerve signals for the brain.
* Unique smells activate a unique pattern of firing across multiple receptors
* Recieve input from 10 - 20 cilia, responding to a range of stimuli
39
Glomeruli
Receives input from thousands of olfactory receptor cells
* Send action potentials along their axons to higher regions of the brain (limbic system, primary olfactory cortex in temporal lobe, orbital cortex in frontal lobe)
40
What is the primary short-term energy store? long-term?
* Glycogen is the body's preferred short-term energy store
* Fat is a long-term energy store
41
Ghrelin
Hunger/appetite-stimulant hormone
* Produced by cells in the stomach
* Binds directly to neurons in the hunger center of hypothalamus
* Increased ghrelin = increased time after last meal
* Increases dramatically just before a scheduled time for a meal – involved in meal anticipation
* Increases grastic motility to prepare for digestion – source of hunger pangs
* Positive effect on learning as it binds to neurons in hippocampus, helping animals learn which cues in environment are related to food acquisition
* Binds to NPY neurons to make them release more NPY
42
Post-Eating Calm
| /FOOD COMAAAA
* Hypothalamus induces state of calm to focus energy on disgestion following a meal
* Activates nerves to slow heart rate, breathing rate, drowsiness
43
Neuropeptide Y (NPY)
* **Neurotransmitter** (not hormone!) released by neurons in hypothalamus
* Produces sensation of hunger
* NPY neurons binded by ghrelin to make them release more NPY
* Insulin and glycogen inhibit NPY release
44
Why Are Some Foods are Especially Satiating?
* **Liquid calories** are less satiating as it produces less stretching of the stomach and faster digestion of the SI
* Less CCK and stretch-neuron activity
* **High fibre foods** are more satiating as fibre cannot be digested by humans
* Fibre bulks food up w/o the calories
* More firing of stretch-sensitive neurons and CCK
* **Proteins** are more satiating as it bulks up food and sstretches stomach and intestines
* CCK and neurons in portal vein sensitive to amino acids
45
Mint
* Menthol is the chemical that makes mint taste cold
* Binds to receptors in neurons designed to detect cold temperature
* Suvleen believes mint is disgusting
Psych 1XX3
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