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26 Cards in this Set
- Front
- Back
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Why types of medications affect feeding behavior?
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Neuroleptics
Anti-convulsants Chemotx SSRI's Drugs of Abuse |
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What is cachexia?
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Loss of body mass that cannot be reversed nutritionally: even if the affected patient eats more calories, lean body mass will be lost, indicating there is a fundamental pathology in place.
Cachexia is seen in patients with cancer, AIDS |
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What is the relationship between body weight and feeding behavior?
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Over the long haul, body weight controls feeding and not vice-versa.
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Role of lateral hypothalamus? Result of lesion?
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Lat Hthal: Feeding center
If lzn, animal ceases to eat (Lateral Hypothalamic Syndrome) |
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Role of ventromedial hypothalamus? Result of lesion?
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VM Hthal: Satiety center
Lesion leads to hyperphagia; never satisfied |
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Where is leptin produced?
Relation to body fat mass? Effect of injections on obese mice lacking Ob gene? Location of leptin receptors? |
Leptin produced by adipocytes
Blood levels of leptin proportional to body fat mass Injection of leptin into CSF of mice lacking Ob gene (can't produce leptin) caused long-term decline in feeding Leptin receptors in arcuate nucleus of hthal |
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What does the lipostatic hypothesis state?
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Leptin secretion provides negative feedback to the brain to keep fat levels constant (modulates FEEDING behavior)
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Where is the arcuate nucleus located?
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Ventromedial Hypothalamus
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Anorectic vs Orexigenic Circuit in response to Leptin
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Orexigenic:
Leptin INHIBITS NPY/AgRP neurons of arcuate nuc, which normally stimulate Lat Hthal (promote feeding) Thus inhibiting feeding bhrv Anroectic Circuit: Leptin excites alphaMSH/CART neurons of arcuate nucleus, which then inhibit lateral Hthal, thus inhibiting feeding behavior *Leptin has a dual mechanism* |
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What influence's the arcuate nucleus's sensitivity to leptin?
What does this help achieve? |
Genes, hormones, NT's
Helps achieve a "Set Point"--ponderostat |
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Why doesn't leptin administarion work for every obese patient?
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Defective or missing leptin receptors in arcuate nucleus
Defects in arcuate nucleus don't allow activation of alpha-MSH/CART or inhibition of NPY/AgRP neurons |
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What is ghrelin?
Where is it produced? When? Where are its receptors? Effect on feeding behaviors? |
Ghrelin is a peptide that is highly concentrated in the stomach
Released when stomach is empty Receptors in Hthal and ant pituitary Effect: hyperphagia and obesity |
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Effect of gastric bypass surgery on ghrelin levels?
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Flattens normal oscillation of ghrelin levels in gastric bypass pts
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Anorectic Circuit vs Orexigenic Circuit: Ghrelin
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Anorectic:
Ghrelin inhibits alpha-MSH/CART neurons which normally inhibit feeding bhvr Orexigenic: Ghreline excites NPY/AgRP neurons which then stimulate lateral hthal to stimulate feeding Net Effect: Stimulate feeding |
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Ghrelin levels in patients with Prader-Willi?
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Prader-Willi pts have elevated fasting levels of ghrelin; pts never feel full, always hungry
PW is the most common genetic cause of obesity! |
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Compare ghrelin plasma levels for:
Obese caucasian vs Lean caucasian Pima indians |
Obese caucasians have lower ghrelin levels (paradoxical)
Pima indiands have lower ghrelin levels (paradoxical)--population has large rate of obesity |
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Describe 4 mechanisms of satiety.
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1) Gastric/gut distention, vagal activation
2) Release of CCK, vagal activation 3) Rise in plasma insulin 4) Rise in plasma glucose |
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Anorectic or Oxigenic:
CCK |
Anorectic (inhibit feeding)
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Anorectic or Oxigenic:
Insulin |
Anorectic (inhibit feeding)
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Anorectic or Oxigenic:
Peptide YY |
Anorectic (inhibit feeding); from bowel
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Anorectic or Oxigenic:
Neuropeptide Y |
Orexigenic (stimulate feeding)
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Anorectic or Oxigenic:
Hypocretin |
Hypocretin = Orexin
Orexigenic (stimulate feeding) |
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Anorectic or Oxigenic:
Ghrelin |
Orexigenic (stimulate feeding); stimulates GH secretion
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Effect of seeing food on 5-HT levels? Eating food?
Effect of 5-HT levels on feeding? Role of SSRI's? |
See food, eat food-->increased 5-HT levels
SSRI's like Prozac have some success on tx of eating disorders But high levels of 5-HT inhibit feeding/appetite Role is unclear |
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What are examples of short-term appetite control signals?
Long-term? |
Short-term controls:
Glucose Ghrelin Insulin Vagus Smell Bowel distention CCK Taste Long Term: Leptin |
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Why is it that hedonic factors begin as positive reinforcers of feeding and then become negative reinforcers? The stimulus is unchanged.
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Hedonic factors = taste/smell (don't change)
But gastric distention, CCK, acute blood changes, etc. somehow cause psychological change so you stop eating (Frito cycle). Side note: DA plays a role in feeding (reward pw's) |
