What are examples for positive and negative food signals?
positive:
Ghrelin
negative:
Leptin (signals brain that fat cell is full)
Insulin GLP1
What are some influecing factors in food intake?
Hedonic control of eating (pleasure related aspect)
Eating disorders (conditions disurpting normal patterns)
Microbiome
Name key entities involved in regulating and modulating food intake.
How and why is energy stored in the body?
—> to buffer constant energy demand
long term: triglycerides
short term: glucogen (glucose)
Which states can the body be in?
prandial state (after eating)
nutrients abundant in blood stream
—> storage molecules are synthesized (anabolic phase)
postabsobative state (fasting phase, between meals)
storage molecules are broken down (catabolized)
—> provide body with continous supply of fuel for cells
What energy balance do you have if you are either obese or starvation?
obese
intake and storage of energy consistently exceeds energy usage of body
—> storage fat increases
—> body becomes obese
starvation
not enough energy is taken up to meet the needs
—> body goes in starvation
Where is the Hypothalamus located and what are functions?
underneath the thalamus, connected to pituitary (central hormone release)
Homeostasis includes:
regulation of body temperature
composition of blood fluids
blood pressure
control of feeding
What are the three functional zones of the hypothalamus?
periventricular —> receives input from other zones
medial —> secretes hormones into blood stream
lateral —> secretes hormones into blood stream (includes pituitary)
What are the main differences between the symphathetic and parasympathetic nervous system?
Symphathetic
—> prepares body for activity
four f’s (fight, flight, fright, sex)
final transmitter: Noradrenaline (norepinephrine)
Parasympathetic
—> prepares for digestion, regeneration, growth, …
final transmitter: acetylcholine
What is the enteric nervous system?
in inner walls of esophagus, stomach, gut, pancreas and gall bladder
major nerve sets: Plexus myentericus and Plexus submucosus
has more or less autonomous functions —> ‘little brain’
sensory functions (stretch, tension, chemoreception)
motor functions (control gut movements, production of enzymes, …)
—> integration with CNS via sympathetic and parasympathetic fibers
What is the parabiosis experiment?
Hypothesis: signal from fat cells to brain defect
mice with ob-/ob- mutation were abnormally fat
—> shared blood circulation
—> ob mice became thinner
signale molecule: Leptin
Leptin is an important signal molecule in the control of energy storage. Describe its function, where and how it works.
produced in fat cells when these are sufficiently filled with lipids
Receptors in the arcuate nucleus (hypothalamus)
High level of Leptin: Activates Paraventricular nucleus, inhibits lateral hypothalamic area —> inhibit feeding behavior
Low level of Leptin: Inhibits Paraventricular nucleus, activates lateral hypothalamic area —> stimulate feeding behavior
What effects do lesions in ventromedial hypothalamic and lateral hypothalamic areas in mice have?
ventromedial hypothalamic lesions —> overeating and accumulation of fat
lateral hypothalamic lesions —> disruption of food intake —> anorexia
What is the Nucleus arcuatus?
‘brain sensor’ that responds to varying levels of leptin in blood stream
Why is the simple assumption: lateral hypothalamus = hunger center and medial hypothalamus = feeding center, not appropriate (esp. in humans)?
In humans, more areas are involved:
nucleus arcuatus
nucleus paraventricularis
hypothalamica lateralis.
What happens with a high level of leptin? And what are the specific transmitters?
nucleus acruatus neurons —> a-MSH/ CART transmitters
activate nucleus paraventricularis —> releases anabolic hormones (ACTH, TSH)
inhibits lateral hypothalamic area —> inhibits feeding behavior
transmitter: a-MSH, CART
What happens with a low level of leptin? And what are the specific transmitter?
nucleus arcuatus neurons —> release AgRP, NPY transmitters
inhibit paraventricular nucleus
activate lateral hypothalamic —> stimulates feeding
transmitter: AgRP, NPY
Name important signals involved in the short-term regulation of food intake.
Hunger signals (orexigenic):
Ghrelin: in stomach wall, released in blood when stomach empty —> stimulates appetite by activation of NPY and AgRP neurons
Satiety signals:
Insulin: released by the pancreas as a reaction to glucose in the blood
Cholecystokinin: released by the intestine wall, mostly after fatty foods (similar to GLP1, NPYY)
Gastric distension: stretching of stomach walls —> vagus nerve to brain
Are Ghrelin levels low or high during fasting?
high
What are signals of long-term energy storage?
Leptin and Insulin
What are the different phases of Insulin level?
substrate phase —> glucose appears in blood
cephalic phase —> presentation of food
gastric phase —> start of eating
What are the three brain areas that control ingestive behavior?
Hindbrain: meal size control
Hypothalamus: drive to eat
Cortico-limbic-system: provides cognitive, executive, and emotional support for ingestive behavior
What is the hedonic evaluation of food?
determines expected amount of pleasure obtained by a certain type of food
Name the four brain areas that regulate the hedonic evaluation of food and what they process/evaluate.
Orbitofrontal cortex and amygdala: reward value of food
Insula: taste of food
Nucleus accumbens and dorsal striatum: receive dopaminergic input and regulate the motivational properties of food (what would I do in order to get it)
Lateral hypothalamus: food-seeking behaviors
Describe the self-stimulation experiment(s) performed on mice and their outcomes.
Experiment:
rat with an electrode in the lateral hypothalamus where stimulation is rewarding
animal can stimulate itself by pressing a lever
stimulation strength is adjusted to threshold (so that animal maintains self-stimulation)
Observation:
repeated self-stimulation and stopped eating
Dopamine: shown to be associated with wanting food but has no connection to enjoying
Conclusion:
dissociation between wanting food and liking food
When rats have access to “yummy” food drugs, the reward thresholds go up (stimulus from self-stimulation needs to be higher).
What are the effects of human weight gain on the brain?
decreased availability of dopamine receptors (D2R)
aim of D2R loss: subjects would not continue to search for food
but: if food is constantly available → continue eating
What is the connection between food, mood, and serotonin?
serotonin levels rise in anticipation of food and spike during a meal (esp. with carbohydrates —> derived from tryptophan)
serotonin is a critical neurotransmitter for mood control
drugs that elevate serotonin levels are also strong appetite suppressants
What is the involvement of the amygdala in food intake? Also, mention the role of PKC-delta cells and Htr2a-cells.
Amygdala: responds to harmful stimuli —> leads to thread avoidance
PKC-delta cells (in the central nucleus): signal bad food —> terminate food intake
Htr2a-cells:
involved in appetite behavior
activation of these cells: make a particular food item more rewarding —> higher intake
inactivation of these cells: inhibits consumption
What is the involvement of the Cerebellum in food intake?
decreases hedonic value of food
might act as a brake on neural networks that promote food intake
What are the two contrasting perspectives regarding whether the metabolic drive or the hedonic drive holds predominant control over food intake?
Bottom-up: Metabolic signals modulate processing of cognitive and reward functions
Top-down: Cognitive and emotional brain circuits may override homeostatic regulation (dieting, hunger, strike)
Homeostatic mechanisms in the body-brain communication keep body weight around a set point.
What are factors that play role in Eating disorders?
-Biological Factors,
What are the differences between the three main eating disorders?
Anorexia nervosa:
low weight, food restrictions, fear of gaining weight, strong desire to be thin
increased 5-HT (Serotonin) and decreased DA (Dopamine)
Binge eating:
binge eating episodes, negative psychological and social problems (mild version of Bulimia)
impulsive/ compulsive disorder, with little impulse control in decision-making (medial PFC)
Bulimia nervosa:
binge eating with subsequent purging (e.g. vomiting)
Why look at the microbiome when studying feeding behavior?
microbiota gets altered through diet (western diet —> dysbiosis)
dysbiotic microbiota may alter communication between the gut and brain, contributing to mood alterations, social behavioral alterations, and cognitive alterations
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