Ch. 11 Ingestive Behavior Eating Test 3

Front 1

What are the 2 categories of eating behavior and their purposes?

Back 1

1) Appetitive for behaviors that locate food

2) Consummatory for behaviors that place food in the gut such as biting, chewing, sucking, and swallowing

Front 2

What 3 nutrients are the product of gut digestion?

Back 2

1) Glucose

2) Amino acids

3) Fats

Front 3

What is the storage polymer of the primary source of energy for all tissues. Where is this storage polymer found? What makes this polymer?

Back 3

Glucose can be converted to glycogen in the liver. It is then stored in muscles and the liver.

Front 4

What does adipose tissue store?

Back 4

Glucose and amino acids can be converted to fat and stored in adipose tissue.

Front 5

What is the function of the liver in regards to storage polymers? What storage polymers stay in the liver and which do not? What is the primary nutritional reservoir for the central nervous system?

Back 5

The liver converts glucose to glycogen. It can also convert sugar and amino acids to fat for storage in adipose tissue. The liver does store glycogen but does NOT store fat. The carb polymers of the liver are reserved primarily for the central nervous system

Front 6

What hormone regulates the absorptive of metabolism? Where is this hormone secreted from? Lack of this hormones results in what disease?

Back 6

Insulin which is secreted by islet cells of the pancreas. Lack of insulin is type 1 diabetes mellitus.

Front 7

Insulin permits entry of glucose into all cells except ______. Insulin promotes ____ and _____ of nutrients. Insulin does this by increasing the conversion of ____ to ____ in the liver and muscles and conversion of _____ to fat.

Back 7

Neurons. Utilization and storage. Glucose to glycogen in the liver and muscles and conversion of glucose to fat

Front 8

What molecule facilitates protein synthesis and also fat storage? How does it do this?

Back 8

Insulin facilitates transport of amino acids into cells and transport of fats into adipose tissue

Front 9

What are the 2 factors the stimulate insulin secretion and their mechanisms of action?

Back 9

1) Presence of glucose in the blood stimulates islet cells in the pancreas

2) Activity of parasympathetic axons that innervate the pancreas as a result of reflexes initiated by eating

Front 10

What is the storage polymer of fat? How does the body utilize fat?

Back 10

Triglycerides. The body uses fat by breaking them down by adipose cells. The liver takes up the glycerol and converts it to glucose and the cells can use free fatty acids.

Front 11

What are the 3 sources of glucose for the brain?

Back 11

1) Glycerol converted to glucose in the liver

2) Liver glycogen converted to glucose

3) Muscle protein converted to amino acids which the liver converts to glucose

Front 12

Where and when do ketones originate? What tissues use ketones?

Back 12

Ketones originate from the oxidation of fatty acids during times of fasting for use by all tissues EXCEPT the liver

Front 13

What are the 2 most important factors that delineate the fasting phase of metabolism?

Back 13

We need BOTH

1) Low levels of insulin

2) High levels of glucagon

Front 14

What cells produce both insulin and glucagon?

Back 14

Islet cells of the pancreas

Front 15

When is glucagon secreted? What is the effect of glucagon?

Back 15

When blood-glucose levels fall, glucagon stimulates conversion of glycogen to glucose and promotes breakdown of fats

Front 16

Under what conditions are glucocorticoids released? Where are these secreted from? What do glucocorticoid hormones promote?

Back 16

Glucocorticoids are released during vigorous exercise or stress by the adrenal cortex promoting breakdown and utilization of glycogen

Front 17

In the absence of glucose, the body uses _______ as an energy source

Back 17

fatty acids

Front 18

The factors that initiate a meal are distinct from those that terminate it. What 3 environmental factors can start a meal?

Back 18

1) Habit

2) Conditioned environmental cues

3) Environmental stimuli

Front 19

What environmental stimuli can initiate a meal?

Back 19

1) A clock such as "breakfast time"

2) Sight/smell of food

3) Presence of others

Front 20

What 2 physiological factors start a meal? How are these conditions detected?

Back 20

1) Availability of glucose in the brain as detected by detectors in the medulla

2) Availability of nutrients outside the BBB as monitored by the liver and transmitted via the vagus nerve

Front 21

What is the relationship between meal size and group size?

Back 21

Meal size goes up with group size

Directly proportional

Front 22

How does glucose metabolism differ between the absorptive and fasting phase?

Back 22

Absorptive: Glucose is converted to glycogen. It is used in the brain and as energy for the rest of the body. It is also stored as glycogen and triglycerides.

Fasting: Glucose from glycogen and glycerol and exclusively directed towards the brain

Front 23

What gastrointestinal hormones increases eating. Where else is this produces? How do levels of this peptide hormone differ between fasting and absorptive phases? What evidence do we have that this peptide is also involved in initiation of a meal? What is the other function of this peptide?

Back 23

Ghrelin increases eating and is produced mostly in the stomach and also by neurons in the brain. Peptide levels increase with fasting and are reduced after a meal. Bloodlevels of ghrelin increase shortly before each meal, which suggeststhat this peptide is involved in the initiation of a meal. This peptide is also involved in controlling the release of growth hormone

Front 24

Hypoglycemia can be induced by ___________, leading to hunger. 2-DG induces _____ by competing with glucose for metabolism and transport into the cell. 2-DG also stimulates eating.

Back 24

glucoprivation, glucoprivation,

Front 25

What is lipoprivation? Which compounds can induce lipoprivation? How do they do this?

Back 25

Lipoprivation refers to a lack of fatty acids available to cells. Methyl Palmoxirate (MP) and Mercatoacetate (MA) induce lipoprivation by interfering with the metabolism of fatty acids

Front 26

How does the liver communicate with the brain regarding hunger signals?

Back 26

Liver contains glucoreceptors who's info travel to the nucleus of the solitary tract via the vagus nerve.

Front 27

What about the neural pathways regarding hunger and thirst can allow you to confuse thirst with hunger?

Back 27

The liver transmits hunger signals to the nucleus of the solitary tract just like the baroreceptors do when experiencing hypovolemic thirst. This all converges on the median preoptic nucleus stimulting eating.

Front 28

2-DF stimulates eating. Infusion of this compound into the ____ _____ vein produces immediate eating whereas transection of the _____ nerve prevents the stimulatory effect on eating. Which compound mimics the effects of 2-DG but also increases firing of the pathway that connects the liver to the nucleus of the solitary tract.

Back 28

hepatic portal vein, vagus. 2,5-AM blocks glucose metabolism just like 2-DG AND increases firing rate of the vagus.

Front 29

What is the role of the 4th ventricle in regards to food? What experimental procedure did we use to find this out?

Back 29

Infusion of 5-thioglucose (5-TG) into the 4th ventricle induces eating by blocking glucose metabolism and consequently inducing glucoprivation. Infusion into the 3rd ventricle has no effect when we block the cerebral aqueduct.

Front 30

What is the differential role of the brains ventricles in eating and drinking?

Back 30

The 4th ventricle is involved in eating behaviors whereas the 3rd ventricle is involved in thirst

Front 31

How is ghrelin secretion regulated? How do we know this?

Back 31

Ghrelin secretion is controlled by receptors in the duodenum found in the upper part of the small intestine. We know this because injection of nutrients into the blood does not suppress ghrelin secretion but entry of food into the duodenum does

Front 32

What 3 major factors contribute to feeding termination? What information do these factors rely on?

Back 32

1) Head factors: info from nose, eyes, tongue, throat

2) Gastric factors: Calorie receptors

3) Intestinal factors: Glucose, amino acid, and fatty acid receptors

Front 33

Which of the 3 feeding termination factors contributes the least? How do we know this? How does learning contribute to this mechanism for termination of feeding?

Back 33

Head factors contribute the least as shown by sham-feeding studies. Taste factors allow for learning about the caloric content of different food and can adjust subsequent intakes

Front 34

How did sham-feeding studies contribute to our understanding of the importance of gastric factors in termination of feeding?

Back 34

Sham-studies showed up that the stomach is not requires for feeling of hunger as shown when rats adjusted their meal intake after food removal via a fistula

Front 35

In the stomach, food mixes with _____ and ____ for the digestion of proteins. In the duodenum, food mixes with _____ and _____ enzymes to continue to degradative process.

Back 35

HCl, pepsin, bile, pancreatic enzymes

Front 36

Introduction of food into the duodenum suppresses ghrelin, suppressing hunger, and thus facilitating termination of eating. Food is slowly introduced into the duodenum. The rate of food introduction is controlled by what satiety hormone? What does this hormone do? Where is the site of action for this hormone in the brain?

Back 36

Cholecystokinin = CCK secretion keeps food in the stomach by closing access to the duodenum helping you feel fuller longer. CCK acts on the circumventricular organs

Front 37

Lesioning of what nerve can reduce eating? What is this procedure called? How does this work?

Back 37

Lesioning of the vagus nerve aka vagotomy reduces intake by preventing the inhibitory efferent action of the VMH on CCK secretion, keeping food in the stomach longer.

Front 38

What peptide is secreted directly proportionally to the amount of calories ingested? Where are the cells that express this peptide?

Back 38

Peptide YY = PYY is expressed by cells in the intestine

Front 39

Injection of glucose into the _____ cavity reduced eating in hungry animals while similar IV injections did not. Injection of glucose into the ____ ____ vein produced long-term satiety in hungry animals. This vein is a direct route the the ______ which has glucoreceptors and plays an important role in starting and stopping meals

Back 39

peritoneal, hepatic portal, liver

Front 40

What hexose can can suppress eating upon infusion into the hepatic portal vein but cannot cross the BBB?

Back 40

Fructose

Front 41

What have force feeding studies taught us about the relationship between food intake and body weight?

Back 41

Food intake falls as body weight increases

Front 42

What have starvation studies taught us about the relationship between gastric satiety factors and body weight?

Back 42

gastricsatiety factors are less effective when body weight has been reducedbelow normal levels

Front 43

The fat cells of the body secrete ____ protein to suppress food intake and stimulate metabolism. The genetically obese ob mouse lacks the gene that produces the aforementioned protein, but daily administration of _____ protein normalized weight.

Back 43

leptin

Front 44

The more and larger the fat cells, the more ____ is released. This then reaches receptors in the LH, arcuate, supraoptic, and paraventricular nuclei which suppresses production and release of ______. The _____ normally triggers hunger. Activation of the initial receptor also increases levels of _________-_______ hormone and _______ which suppresses hunger.

Back 44

leptin, NPY (Neuropeptide Y), neuropeptide Y, corticotropin-releasing, melanocortin

Front 45

What part of the brain is essential for controlling feeding? What experimental procedure elucidated this? What about this brain region allows for feeding?

Back 45

Only the brain stem is essential as shown by decerebration which involves transection between the diencephalon and midbrain. The brain stem has the motor neurons needed for eating, hunger detection, and satiety signals

Front 46

Lesions of the __/___ abolish both glucoprivic and lipoprivic eating. This area receives information from where?

Back 46

AP/NST (Area Postrema and the Nucleus of the Solitary Tract) receives taste info from the tongue and hunger signals from the liver

Front 47

What are the 2 hypothalamic regions are involved in feeding? Lesions to these centers produces what respectively?

Back 47

Lateral hypothalamus lesions produce under eating since it's the "feeding center"

Ventromedial hypothalamus lesions produce overeating since it's the "satiety center"

Front 48

Excitation of _____ _____ cells in the brain by glutamate stimulates eating. These cells contain 2 peptide neurotransmitters. What are these called? Infusion of these neurotransmitters induces _____. These neurons project to brain areas that modulate ______. What happens if we stimulate neurons?

Back 48

Lateral hypothalamus

Melanin-concentrating hormone and Orexin

Eating

Metabolism

Stimulation of neurons

Front 49

What nucleus houses neurons that secrete the peptide that stimulates ravenous eating and increases energy conservation aka reducing metabolism? What is the name of the peptides released by this neuron? What factors modulate secretion of this neuron?

Back 49

The arcuate nucleus has neuropeptide Y secretory neurons. They also secrete AGRP.

NPY and AGRP levels increase with hunger and decrease with satiety

Front 50

What are the 2 ultimate effects of stimulation of the arcuate nucleus?

Back 50

1) Conservation of energy via decreased insulin secretion, decreased fatty acid breakdown, and decreased body temp

2) Promotion of eating/reduction of metabolic rate

Front 51

What pathway do the projections of the arcuate nucleus take in order to conserve energy?

Back 51

Arcuate nucleus --> Paraventricular nucleus --> Brain stem nuclei that control ANS

Front 52

What pathway do the projections of the arcuate nucleus take in order to promote feeding?

Back 52

Arcuate nucleus --> Lateral hypothalamus

Front 53

What region of the hypothalamus modulates metabolism?

Back 53

Paraventricular hypothalamus

Front 54

What are orexigens? What are the 4 orexigens of relevance? Where are these orexigens found? What about the connectivity of orexigenic regions allows for it's ability to modulate metaboism?

Back 54

Orexigens are appetite-inducing chemicals.

1) Melanin-concentrating hormone (MCH)

2) Orexin

3) Neuropeptide Y = NPY

4) Agouti-related peptide = AGRP

Found in the hypothalamus. These axons project to neurons in the spinal cord that control the autonomic nervous system

Front 55

Where is the site of action for leptin? How does it effect these neurons?

Back 55

Receptors on neurons that release NPY and AGRP in the arcuate nucleus. It is inhibitory

Front 56

What is the site of action for NPY and AGRP?

Back 56

NPY and AGRP secreting neurons project to the lateral hypothalamus to stimulate MCH and Orexin

Front 57

Why does weed make you hungry in terms of it's effect on hypothalamic feeding regions?

Back 57

THC mimics endocannabinoids which facilitate release of MCH and Orexin

Front 58

Where are the anorexigenic peptide secreting neurons found? What are these compounds called? Where is their site of action? What are their respective functions?

Back 58

The arcuate nucleus contains CART (Cocaine and amphetamine-regulated transcript) neurons which secrete CART and a-MSH (alpha melanocyte-stimulating hormone). They both bind to the MC4-R (melanocortin-4 receptor) where they both inhibit feeding.

Front 59

Where does AGRP bind? What else binds here? What are their respective effects?

Back 59

a-MSH (anorexigenic) and AGRP (orexigenic) both bind to MC4-R where they exert opposite effects

Front 60

What BMI is considered obese and what is considered overweight?

Back 60

Obesity = BMI>30

Overweight = BMI>25

Front 61

Metabolic efficiency is reflected in differences in what 2 factors?

Back 61

1) Non-exercise activity thermogenesis (NEAT)

2) Genetic background

Front 62

What obesity surgery can result in bacterial overgrowth and vitamin deficiencies? How does this procedure result in weight loss?

Back 62

Intestinal bypass which reduces food absorption

Front 63

What serotonin agonist can be used to suppress appetite? What are the associated health problems with use of this drug?

Back 63

Fenfluramine can lead to cardiac problems

Front 64

What herbal preparation can reduce appetite?

Back 64

Ephedrine

Front 65

How can we prevent fat absorption pharmacologically?

Back 65

Xenical