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PSYC270 > Feeding Behavior > Flashcards

Feeding Behavior Flashcards

1
Q

What is the difference between enzymes in the saliva, stomach, and intestines?

A

Saliva: break down carbs
Stomach: break down proteins
Intestines: break down carbs + proteins + fat

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2
Q

What is tryptophan and its effects?

A

Helps melatonin production, aiding sleepiness
Increased by eating high carb diet

Enters brain by active transport protein that it shares with phenylalanine
When eating carbs there is an increase in insulin secretion, moving sugars and phenylalanine to storage which decreases competition making it easier for tryptophan to reach the brain

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3
Q

Describe sham-feeding

A
  • Everything swallowed leaks out of a tube connected to the esophagus/stomach
  • Individuals eat and swallow without becoming satiated
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4
Q

What is the role of the duodenum in feeding?

A
  • Absorbs nutrients
  • Nerves from duodenum inform about distension, type and amount of food
  • Distension releases cholecystokinin (CCK) hormone
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5
Q

What is the role of CCK?

A
  • Constricts sphincter between stomach and duodenum causing stomach to hold contents and fill quickly, hastening stomach distension
  • Limits current meal size
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6
Q

Hormones secreted by pancreas

A

Insulin: secreted by beta cells
Glucagon: secreted by alpha cells

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7
Q

What are the differences between insulin and glucagon?

A

Insulin:

- Decreases blood glucose levels
- Promotes glycogen synthesis in liver
- Inhibits fat mobilization and promotes fat storage

Glucagon:
- Increases BG levels, acting in opposition to insulin

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8
Q

What is the mechanism to which glucose is stored after a meal?

A
  1. Pancreas increases the release of insulin before (sight and smell), during, and after a meal
  2. Insulin enables glucose to enter cells (can enter brain cells without insulin)
  3. Excess glucose goes to either:
    • Liver cells where it is transformed to glycogen for storage
    • Fat cells where it is turned into fat for storage
  4. After a meal, blood glucose (BG) decreases, insulin decreases, and glucose enters cells more slowly and hunger increases
  5. Pancreas increases glucagon release which stimulates the liver to convert stored glycogen to glucose
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9
Q

What happens if insulin levels constantly remain high?

A

BG goes into cells (liver + fat) long after a meal

- BG decreases because glucose is leaving the blood without any new entering, increasing hunger

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10
Q

Compare Type I and Type II Diabetes

A

Type I:

  • Autoimmune system destroys beta cells in pancreas causing a loss of insulin, glucose cannot be used
    • Present in children and has heritability
    • Glucose is 3x more than normal, but little enters the cell due to decreased insulin levels
    • Individuals eat more than normal but excrete most glucose and lose weight

Type II:

- Not taking up glucose because of a lack of insulin receptors
- BG remains too high
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11
Q

What is the role of leptin?

A

Only found in vertebrates, produced by fat cells (the more fat cells, the more leptin) for long term feeding behavior regulation

Signals brain about fat reserves:

- Low levels of leptin signalling increases hunger and decrease activity 
- High levels of leptin signalling decreases hunger and increase activity
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12
Q

Compare time restricted feeding and intermittent fasting

A

Time restricted feeding:
- Restrict amount of time not eating and eating every day

Intermittent fasting:
- Not chronic calorie restriction

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13
Q

Compare the standard macronutrient breakdown and a low carb diet

A

Standard breakdown: 50% carbs, 30% fats, 20% protein

Low carb: <20% carbs

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14
Q

How is BMI calculated and what are the categories?

A

BMI = m/h^2

<18.5 kg/h^2: underweight
18.5-25: normal
25-30: overweight
>30: obese

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15
Q

What are the types of obesity heritability?

A
  1. Syndromal obesity: gene causes a medical problem that includes obesity
  2. Monogenetic obesity: 1 gene leads to obesity without other physical or mental abnormalities
    • Ex. mutation of melanocortin receptor gene
  3. Polygenetic/common obesity: many genes that each slightly increase the probability of obesity
    • Ex. variant of FTO gene increase the probability by 2/3
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16
Q

How does fructose effect satiety?

A

Little effect on leptin and insulin, so you do not feel satiated and store most of its calories as fat

17
Q

What is bulimia nervosa?

A
  • Alternate between binges of overeating and strict dieting, some induce themselves to vomiting
  • 1.5% women, 0.5% men
  • Have increases in ghrelin productions
18
Q

What is anorexia nervosa?

A
  • Refusal to eat enough to maintain healthy weight
  • 1% women, 0.33% men
  • Extensive physical activity
  • Abnormalities in dopamine release
19
Q

What is the role of the arcuate nucleus?

A

Contains leptin receptors
Input comes from hormones and cells in amygdala, BFb, thalamus
1. Neurons sensitive to hunger signals stimulated by ghrelin (inhibits PVN)
2. Neurons sensitive to satiety signals stimulated by:
- glucose satiety cells and prompts pancreas to release insulin
- Leptin released by body fat
- Nicotine
=> sends excitatory signal to PVN by releasing melanocortins and glutamate

20
Q

What is the role of ghrelin?

A

Neurotransmitter that binds to the same receptors as GHRH
Released by the stomach in food deprivations, triggers stomach contractions
Acts on arcuate nucleus to increase appetite

21
Q

What is the role of the PVN?

A

Receives excitatory and inhibitory input from arcuate nucleus
Important for satiety, inhibits LH by releasing orexin
Electrical/excitotoxic lesions causes overeating
- Disinhibition of LH
- Eat larger meals but not more frequently

22
Q

What do the hunger neurons in the arcuate nucelus release?

A

GABA + neuropeptide Y (NPY) + agouti-related peptide (AgRP)

23
Q

What is the role of melanocortins?

A

Receptors in PVN limit food intake

- Damage leads to overeating

24
Q

What is the role of orexin?

A

Increases persistence in seeking food, activity and general motivation

25
Q

What is the role of the amygdala?

A

Output to lateral hypothalamus:

  1. Inhibits eating during illness and mediates aversion to foods previously associated with illness
  2. Stimulates eating in response to tasty foods
26
Q

What is the role of the lateral hypothalamus?

A

Input form PVN, stimulation causes increased eating
Controls insulin secretion and alters tastes responsiveness
Contains orexin receptors
Lesions causes aphagia and adipsia

27
Q

Where does LH project to?

A
  1. Nucleus of the tracts solitarius (NTS) — part of taste pathway
    • Alters taste sensation and salivation response
    • Makes food taste better when hungry
  2. Cortex
    • Facilitates ingestion and swallowing
    • Causes cortical cells to increase response to taste, smell, sight of food
  3. Pituitary gland
    • Increases secretion of hormones that increase insulin secretion
  4. Spinal cord
    • Controls autonomic responses (ex. digestive secretion)
    • Damaged lateral hypothalamus has trouble digesting foods
28
Q

Damage to LH in rats

A

Damage leads to food and water refusal
- Kills neurons in lateral hypothalamus and interrupts axons containing dopamine passing through

Recovery after damage:
  1. Aphagia and adipsia: rat refuses food and drink; force fed to stay alive
  2. Anorexia: eats a small amount of palatable food and sweetened water
    - Does not eat enough to stay alive
  3. Adipsia: eats enough to stay alive but at a lower than normal weight
    - Refuses plain water
  4. Near-recovery: eats enough to stay alive but at a lower than normal weight
    - Drinks plain water at meal times to wash down food
    - During stressful conditions, refuses food and water
29
Q

What is the role of the ventral medial hypothalamus?

A

Output inhibits feeding (promotes satiety)

30
Q

Damage to the VMH

A

Normal sized meals but eats more frequently
- Large effect must have a lesion extending out of VMH and invading nearby axons
Stomach empties faster than normal
Increases insulin production and much of meal is stored as fat
- Gain weight even if they do not overeat
- Moves BG into storage even when BG is low
- Cells starve resulting in increased hunger

31
Q

Eating Restriction and AD transgenic mouse study

A

3 groups for transgenic mice:
- 3xTgAD, AL, 3xTgAD, CR, 3xTgAD, IF
Body weight measured week
- Effects of CR but not IF
At 17 months:
- Cr + IF + NonTg, AL had better performance than 3xTgAL, AL in water maze

32
Q

Findings of eating restriction and AD mouse study

A

Hippocampus A-beta levels in transgenic mice:

- Lower in CR than AD
- No difference between IF and AD

Tau levels in hippocampus:

- No difference in total amount of tau
- Phosphotau was lower in CR than AD

PSYC270 (6 decks)

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