Regulation of Food Intake Flashcards
Body weight “set point” in rats
- homeostatic regulation of energy intake
- Whether you over or underfeed them, their weight comes back down to or goes back up to regular weight when returned to regular diet
- ?humans
Adaptations to the Environment
Genetics
Increased Energy Expenditure
- Resting energy expenditure
- Thermic effect of food
- Activity (exercise and/or nonexercise)
Reduced Intake/Appetite
- Changes in appetite modulators
- Cognitive and/or behavioral changes
Changes in Substrate Metabolism
-Increased fat oxidation, reduced nutrient assimilation
Physiologic or homeostatic mechanisms of energy balance regulation
short term signals: meal related
long term signals: adiposity related
Non-Homeostatic mech
- reward and motivation
- cognitive/executive decisions
- environmental cues
- social context
hunger center
hypothalamus:
-Lateral Nucleus = “hunger center”
Lesion? aphagia (no eating)
-expresses melanin concentrating hormone (MCH) and orexins. Both induce feeding. Stimulate brainstem motor systems, cranial motor neurosn (trigeminal, facial, hypoglossal)
- Ventromedial nucleus= satiety center
- stimulation? cessation of eating.
- Lesion? eat excessively. (lesion has effect of ‘resetting’ regulated weight to higher level)
- arcuate nucleus:
- Paraventricular nucleus
Leptin
Satiety hormone
Associated with stimulation of catabolic pathways and inhibit anabolic pathways to keep body in balance
-insulin is also considered a marker of adiposity and a homeostatic signal to brain (stop eating)
Leptin: stimulates POMC/CART and inhibits NPY/AgRP (activating satiety circuit and inhibiting feeding circuit)
Neuropeptide Y
stimulates hunger and food intake
MCR
catabolic pathway: reduce intake and increase energy expenditure
NPU stimulates anabolic and inhibits MCR (catabolic pathway)
Ghrelin
from stomach, induces adiposity; stimulates appetite (anabolic pathways)
- receptors in arcuate nucleus (Ghrelin activates NPY and arcuate neurons)
- meal to meal (short term) regulation
PYY, GLP-1
secreted by intestinal tract after meal
- Satiety type hormones (hunger level goes down)
- Stim POMC neurons and catabolic pathways (reduced food intake)
-Meal to meal regulation
Hypothalamus
- direct pathways to reward pathways, limbic systems, cortex (prefrontal, motor, sensory)
- Pathways go in both directions
People who might be prone to gaining weight could be resistant to…
leptin
Obese people do NOT necessarily have MORE…
ghrelin
“problems” with our biologic homeostatic regulation of food intake
Our biologic signals are primarily designed to protect us during times of undernutrition.
Perhaps it’s all about “resistance” to these signals, ie leptin resistance?
Nonhomeostatic regulation of energy intake: internal inputs
Reward Mechanisms Cravings “Thinking” about food Restraint Learned Behaviors Attention
external inputs
Environmental Cues: Sight Smell Taste Availability/Portions Social Context Time cues
When hungry, what is increased (fMRI)? Lean people
Brain areas imp in: attention reward motivation memory
What about in people that are prone to obesity? What is increased (fMRI)?
Obese prone have PERSISTENT: attention reward motivation memory
Arcuate nucleus (hypothalamus)
- contains first order neurons that promote either food intake or satiety.
- Activation of arcuate neurons that produce both neuropeptide Y (NPY) and agouti-related peptide (AgRP) promote FEEDING
- Activation of arcuate neurons that produce both alpha-melanocyte stimulating hormone (alpha-MSH) and cocaine and amphetamine related transcript (CART) promote SATIETY
- alpha-MSH is a product of POMC precursor molecule
arcuate nucleus neurons project to:
PVN: paraventricular nuclei and LH (lateral hypothal)
alpha-MSH activates ___. What blocks effect of alpha MSH at this site?
Site: MCR (Melanocortin receptors)
Blocker? AgRP
Activation of Melanocorti receptors induces saitety
NPY action
- increases hunger
- decreases energy expenditure (inhibits symp n.)
(NPY/AgRP neurons are thought to constitue a feeding system that is opposed by the alpha-MSH/CART satiety system)
Gastric distension
-info carried by vagal afferents to nucleus of tractus solitarius (NTS), relayed to PVN/Arcuate nucleus/LH, amygdala, thalamus. From thal to visceral sensory cortex–> “gastric fullness”
CCK
- duodenum signals brain about presence of nutrients thru release of CCK
- vagal afferents
- area postrema to send info to hypothal
GLP-1
- released when food in ileum (from L cells)
- also on receptors in area postrema via NTS
- signals to reduce food intake
Peptide YY (PYY)
- also from L cells like GLP-1
- anorexic effects by inhibiting hypothalamic NPY/AgRP neurons
Glucose sensitive neurons location
VMN: stimulated by hyperglycemia
LH: inhibited by by glucose
Area of brain involved in drug reward and food reward systems?
Nucleus accumbens and dopamine afferents.
Reciporocal connections between nucleus accumbens and LH
POMC (alpha-MSH/CART) neurons are impacted by what NT?
serotonin
Also evidence that endogenous opioid system plays an important role in regulation of food intake, preference, choice (antagonists suppress intake)
