Neurobiology of Feeding Behaviour Flashcards

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1
Q

Lactase

A

-Is an intestinal enzyme that is necessary for metabolizing lactose, the sugar in milk

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2
Q

Sham-feeding

A

-A procedure in which everything that an animal swallows leaks out a tube connected to the esophagus or stomach

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3
Q

What is the main signal to end a meal?

A
  • Distension in the stomach (ie. an enlargement or ballooning effect)
  • Later research found that meals end after distension of either the stomach OR the duodenum
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4
Q

What part of the body conveys information to the brain about the stretching of the stomach walls?

A

-The vagus nerve

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5
Q

Duodenum

A
  • The part of the small intestine adjoining that stomach
  • Is a major site for absorbing nutrients
  • Nerves from the duodenum inform the brain not only about distension, but also about the type and amount of nutrition
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6
Q

How do your intestines know what you ate?

A
  • You have taste receptors in your digestive tract, similar to the ones on your tongue
  • They do not provide you with a conscious experience, but they do alter brain activity to influence your sense of satiety
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7
Q

What does distension of the duodenum release?

A

-Releases the hormone cholecystokinin (CCK)

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8
Q

Cholecystokinin (CCK)

A
  • Is released by distension of the duodenum
  • Limits meal size in two ways:
    1. First, CCK constricts the sphincter muscle between the stomach and the duodenum, causing the stomach to hold its contents and fill more quickly than usual
    2. Second, CCK stimulates the vagus nerve to send signals to the hypothalamus, causing cells there to release a neaurotransmitter that is a shorter version of the CCK molecule itself

-CCK produces short-term effects only, therefore, it can’t really be manipulated to help people lose weight. It limits the size of the meal, but an animal that has eaten a smaller than usual meal compensates by overeating at the next meal

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9
Q

What are 2 ways that CCK increases satiety?

A
  1. When the duodenum is distended, it releases CCK, which closes the sphincter muscle between the stomach and the duodenum. CCK therefore increases the rate at which the stomach distends
  2. Also, neural signals from the intestines cause certain cells in the hypothalamus to release CCK as a neurotransmitter, and at its receptors, it triggers decreased feeding
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10
Q

What two pancreatic hormones regulate the flow of glucose into cells?

A

-Insulin and Glucagon

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11
Q

What is the process going on before, during, and even after meals? (in relation to insulin and glucose)

A

-Immediately before a meal, as well as during and after a meal, the pancreas increases release of insulin, which enables glucose to enter the cells

  • Some of the excess glucose produced by a meal enters the liver, which converts it to glycogen and stores it
  • Some also enters fat cells, which convert it to fat and store it
  • The net effect prevents blood glucose levels from rising too sharply
  • As time passes after a meal, the blood glucose level falls, insulin levels drop, glucose enters the cells more slowly, and hunger increases
  • The pancreas increases release of GLUCAGON, stimulating the liver to convert some of its stored glycogen back to glucose
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12
Q

Simple process of hunger and insulin levels?

A
  • Hunger
  • ->Eating
  • ->Blood glucose increase, insulin release decreases
  • ->Insulin helps glucose enter cells for use or storage, hunger decreases
  • ->Blood glucose levels decline, insulin level decrease
  • ->Feel hungry and cycle repeats
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13
Q

Leptin

A
  • Tells your body you’re FULL!! (ie. it decreases your appetite)
  • Is limited to vertebrates
  • The body’s fat cells produce leptin: The more fat cells, the more leptin
  • Leptin signals your brain about your fat reserves
  • When your fat reserves decrease, leptin levels decline, and you react by eating more and becoming less active, to save energy
  • When leptin levels return to normal, you eat less and become more active
  • A mutation in the leptin gene does not make leptin, and therefore your brain reacts as if its body has no fat stores and must be starving
  • Mice with this mutation will eat as much as possible, conserve their energy by not moving much, and fail to enter puberty
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14
Q

What area of the brain is considered the master area for controlling appetite?

A

-The arcuate nucleus of the hypothalamus

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15
Q

Arcuate nucleus

A

-The arcuate nucleus has one set of neurons sensitive to hunger signals and a second set sensitive to satiety (full) signals

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16
Q

Ghrelin

A
  • Part of the input to the hunger-sensitive cells comes from axons releasing the neurotransmitter ghrelin
  • The stomach releases ghrelin during a period of food deprivation, where it triggers stomach contractions
  • Ghrelin also acts on the hypothalamus to increase appetite
17
Q

What are the several types of input that the satiety-cells of the arcuate nucleus receive?

A
  • Distension of the intestines triggers neurons to relase the neurotransmitter CCK, a short-term signal
  • Blood glucose (short-term signal) directly stimulates satiety cells in the arcuate nucleus and prompts the pancreas to release insulin, which also stimulates the satiety cells
  • Body fat releases leptin, a long-term satiety signal
  • Nicotine also stimulates the satiety neurons, therefore smoking decreases appetite
18
Q

Where does much of the output of the arcuate nucleus go?

A
  • To the paraventricular nucleus (PVN) of the hypothalamus

- Certain types of cells in the paraventricular nucleus inhibit the lateral hypothalamus, an area important for eating

19
Q

Melanocortins

A
  • Melanocortin receptors in the paraventricular nucleus are important for limiting food intake, and anything that damages these receptors leads to overeating
  • Axons from the satiety-sensitive cells of the arcuate nucleus deliver an excitatory message to the paraventricular nucleus, releasing melanocortins
20
Q

What is orexin’s two roles in feeding?

A
  1. First, it increases animals’ persistence in seeking food

2. Second, orexin increases activity and motivation in general

21
Q

Name three HORMONES that increase satiety and one that increases hunger

A

Increase satiety:

  • Leptin
  • Insulin
  • CCK

Increase hunger:
-Ghrelin

22
Q

Which neuropeptide from the arcuate nucleus to the paraventricular nucleus is most important for satiety?

A

-Melanocortins

23
Q

What are the inhibitory transmitters at play when the paraventricular nucleus limits the lateral hypothalamus?

A
  • This inhibitory transmitters here are a combination of:
  • GABA
  • neuropeptide Y (NPY)
  • agouti-related peptide (AgRP)
24
Q

Lateral Hypothalamus

A
  • Controls insulin secretion, alters taste responsiveness, and facilitates feeding in other ways
  • Output from the paraventricular nucleus acts on the lateral hypothalamus, which includes so many neuron clusters and passing axons that it has been compared to a crowded train station
  • An animal with damage in this area refuses food and water, reverting its head as if the food were distasteful
  • In contrast, stimulation to the lateral hypothalamus increases the drive to eat
25
Q

What are the ways that the lateral hypothalamus promotes eating?

A
  • Axons from the lateral hypothalamus to the NTS (nucleus of the tractus solitarius), part of the TASTE pathway, alter the taste sensation and the salivation response to the tastes. When the lateral hypothalamus detects hunger, it sends messages that make the food taste better
  • Axons from the lateral hypothalamus extend into several parts of the CEREBRAL CORTEX, facilitating ingestion and swallowing and causing cortical cells to increase their response to the taste, smell, or sight of food
  • The lateral hypothalamus increases the pituitary gland’s secretion of hormones that increase insulin secretion
  • The lateral hypothalamus sends axons to the SPINAL CORD, controlling autonomic responses such as DIGESTIVE SECRETIONS. An animal with damage to the LH has trouble digesting foods

In simple form: Activity of the lateral hypothalamus improves taste, enhances cortical responses to food, and increases secretion of insulin and digestive juices

26
Q

Ventromedial hypothalamus (VMH)

A
  • Output from the ventromedial hypothalamus inhibits feeding, and therefore damage to this nucleus leads to overeating and weight gain
  • Rats with damage to the VMH eat normal-sized meals, but they eat more frequently. One reason for this being that they have increased stomach motility and secretions, and their stomach empties faster than normal. Another reason is that the damage increases insulin production, and therefore much of each meal is stored as fat
27
Q

Damage to the paraventricular nucleus vs damage to the ventromedial area?

A
  • Rats with damage to the paraventricular nucleus eat larger than average meals
  • In contrast, rats with damage to the VMH eat normal sized meals, but they eat more frequently
28
Q

Bulimia nervosa

A
  • Is a condition in which people alternate between binges of overeating and periods of strict dieting
  • Many, but not all, induce themselves to vomit
  • On average, people with bulimia show a variety of biochemical abnormalities, including increased production of ghrelin, a hormone associated with increased appetite. The biochemistry however is probably a result of the binges and purges, rather than a cause
29
Q

Anorexia nervosa

A
  • Anorexia nervosa is characterized by a refusal to eat enough to maintain a healthy body weight
  • People with anorexia do not regard food as tasting bad, rather they express an exaggerated fear of growing fat
  • Those with anorexia also engage in extensive physical activity which may be motivated by temperature regulation (ie. cold environment causes people to exercise more to gain heat, but this causes them to lose more weight when they are already eating so little)
30
Q

What are the 3 ways that obesity is partly under genetic control?

A
  1. Syndromal obesity occurs if a gene leads to both obesity and other medical problems
  2. Monogenic obesity results from a single gene that does not impair other body functions
  3. Common obesity is influenced by many genes, as well as environmental factors
31
Q

What is the effect of a hypothalamic lesion in these areas?

  • Lateral hypothalamus
  • Ventromedial hypothalamus
  • Paraventricular nucleus
A

Lateral hypothalamus:
-Lesion causes undereating, weight loss, and low insulin levels (because of damage to cell bodies); underarousal, underresponsiveness (because of damage to passing axons)

Ventromedial hypothalamus:
-Lesion causes increased meal FREQUENCY, weight gain, and high insulin levels

Paraventricular nucleus:
-Lesion causes increased meal SIZE, especially increased carbohydrate intake during the first meal of the active period of the day