Regulation of Feeding

Question 1

What does the regulation of body weight require?

Answer 1

A balance between food intake and energy expenditure

Question 2

Which is stronger? Mechanisms that induce feeding or mechanisms that reduce feeding?

Answer 2

Mechanisms that induce feeding as a result of evolutionary pressures to seek and store food

Question 3

Which mechanisms control feeding?

Answer 3

Homeostatic and non-homeostatic. The two systems overlap and communicate in different capacities

Question 4

What is the Prandial State?

Answer 4

The period prior to and during meal consumption (anabolic metabolism)

Question 5

What is the Post-absorptive State?

Answer 5

The period between meals (catabolic metabolism)

Question 6

How is glucose used as a primary energy source?

Answer 6

Glucose is converted to adenosine triphosphate (ATP) which is the primary energy source in the cell

Question 7

How does the body regulate energy homeostasis?

Answer 7

Through distal and proximal cues. Feeding usually ceases before proximal cues peak, indicating that animals use the distal and intermediate cues to estimate food consumption

Question 8

What are distal cues?

Answer 8

External cues such as grocery store logos or food items

Question 9

What are proximal cues?

Answer 9

Internal cues such as blood glucose and nutrient levels. They provide the body with feedback about its metabolic and nutritional state

Question 10

What neural systems or structures are involved in homeostatic mechanisms?

Answer 10

Hypothalamus, Nucleus of the solitary tract (NTS), Adiposity signals (proximal cue, long-term, such as leptin, insulin, etc), Satiation signals (proximal cue, short-term, such as CCK, etc)

Question 11

What neural systems or structures are involved in non-homeostatic mechanisms?

Answer 11

Amygdala, Accumbens, Paraventricular nucleus of the thalamus (PVT), Ventral tegmental area (VTA), Hedonic stress (distal cue)

Question 12

How does the brain receive signals about the current energy state of the body?

Answer 12

Through short-term signals (signals rising and falling around meals) such as ghrelin, insulin, PYY, CCK, mechanosensory receptors in the digestive tract; and long-term signals (signals regarding energy stores) such as leptin

Question 13

What factors affect the short-term regulation of food intake?

Answer 13

Orexigenic factors (appetite stimulant) and anorexigenic factors (appetite suppressant). Blood glucose levels must be well-regulated across the prandial and postabsorptive states (therefore cues must anticipate blood glucose levels)

Question 14

What are examples of orexigenic factors?

Answer 14

Grehlin, NPY (Neuropeptide Y), AgRP (Agouti-related peptide). Ghrelin stimulates the release of NPY and AgRP which stimulates feeding

Question 15

What are examples of Anorexigenic factors?

Answer 15

CCK (cholecystokinin), PYY (peptide tyrosine-tyrosine), CART (cocaine and amphetamine-related transcripts), aMSH (alpha melanocyte stimulating hormone), Insulin, Glucagon

Question 16

How is ghrelin related to the short-term regulation of feeding?

Answer 16

Ghrelin increases with fasting and decreases after a meal. It increases before a meal suggesting a role in initiating eating. Ghrelin antagonists inhibit feeding. Ghrelin injections increase eating and can cause weight gain over time (cause subjects to have increased feelings of hunger). Ghrelin is produced in the stomach

Question 17

How is CCK related to the short-term regulation of feeding?

Answer 17

CCK is present in cells lining the duodenum. CCK can act as a satiety signal (injections suppress feeding). It acts as both a neuropeptide and a peptide hormone

Question 18

What is the duodenum?

Answer 18

Beginning of the small intestine, controls bile secretion, monitors presence of fats, releases CCK

Question 19

How is PYY related to the short-term regulation of feeding?

Answer 19

PYY decreases feeding. It is a hormone released by the gut proportional to the number of calories ingested. Injections can cause subjects to feel less hungry (correlates with levels of satiety)

Question 20

What is the glucostatic theory?

Answer 20

The hypothesis that low glucose levels trigger eating. However, there is not strong evidence to support it (injections do not have a huge effect on food consumption)

Question 21

What is hypoglycemia?

Answer 21

When the level of glucose in the blood drops below what is healthy

Question 22

How is insulin related to the short-term regulation of feeding?

Answer 22

Large injections of insulin cause hypoglycemia and glucoprivation (stimulates eating). Insulin converts and stores glucose and allows non-neural cells to use it (without insulin only brain cells can use glucose).

Question 23

Is body weight regulated over the long term or short term?

Answer 23

Long-term (bodies will adapt to diets over the long term to stay within a certain weight range)

Question 24

How is leptin related to the long-term regulation of feeding?

Answer 24

Leptin is secreted by well-nourished fat cells (more fat in fat cells means more leptin signal). Injections of leptin can reduce obesity (however there has been limited impact in treating obesity). High levels of leptin desensitize the brain to hunger signals. Low levels provide a stronger hunger signal. Leptin levels help the body regulate weight.

Question 25

What signals inhibit feeding neurons?

Answer 25

PYY, Leptin, Insulin, CCK

Question 26

What inhibits AgRP?

Answer 26

Insulin and PYY

Question 27

What stimulates the release of aMSH?

Answer 27

Insulin and leptin

Question 28

What hypothalamic regions are implicated in feeding?

Answer 28

Lateral Hypothalamus (LH) stimulation produces eating and drinking (lesions lead to adipsia and aphagia), Ventromedial Hypothalamus (VMH) stimulation suppresses eating (lesions lead to obesity)

Question 29

What are examples of appetitive mechanisms?

Answer 29

External such as appearance, smell, and taste; and internal such as time or size of last meal

Question 30

Are we regulated more by nutritional needs or appetitive mechanisms?

Answer 30

Appetitive mechanisms (Most of our feeding has to do with circadian rhythms, conditioned habits, and the perceived value of the food item)

Question 31

What do different regions in the Lateral Hypothalamus accomplish?

Answer 31

Some promote eating, some promote food ‘liking’, some suppress ‘liking’

Question 32

What happens when the insula cortex is inactivated?

Answer 32

Cue-guided behavior is disrupted (but not feeding behavior)

Question 33

How is the insular cortex related to the regulation of feeding?

Answer 33

The insular cortex is related to the processing of taste, changes in food preferences, and the control of food intake. The insular cortex responds to taste-predictive cues

Question 34

What are DREADDs?

Answer 34

Designer Receptors Exclusively Activated by Designer Drugs. hM3Dq is the primary excitatory DREADD used

Question 35

How do hunger signals modulate insular cortex activity?

Answer 35

Activation of AgRP neurons in the arcuate nucleus of the hypothalamus restores cue-related activity in the insula (because the activation of AgRP neurons induces a hunger-like state)

Question 36

How are the AgRP neurons and the insula connected?

Answer 36

Activation of AgRP neurons leads to excitation of Periventricular nucleus of the thalamus (PVT) neurons which project to the BLA (which then go to the Insula)

Question 37

How are PVT neurons related to the regulation of feeding?

Answer 37

Involved in feeding behaviour and addiction. Inhibition of neurons leads to increases in food intake. Excitation of neurons disrupts cue-guided behaviour

Question 38

How is the BLA related to the regulation of feeding?

Answer 38

BLA seems to be providing information to insula about the current value of the food. Inactivation of BLA neurons projecting to the insula disrupts activity in insula neurons