Regulation of Feeding Flashcards
What does the regulation of body weight require?
A balance between food intake and energy expenditure
Which is stronger? Mechanisms that induce feeding or mechanisms that reduce feeding?
Mechanisms that induce feeding as a result of evolutionary pressures to seek and store food
Which mechanisms control feeding?
Homeostatic and non-homeostatic. The two systems overlap and communicate in different capacities
What is the Prandial State?
The period prior to and during meal consumption (anabolic metabolism)
What is the Post-absorptive State?
The period between meals (catabolic metabolism)
How is glucose used as a primary energy source?
Glucose is converted to adenosine triphosphate (ATP) which is the primary energy source in the cell
How does the body regulate energy homeostasis?
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
What are distal cues?
External cues such as grocery store logos or food items
What are proximal cues?
Internal cues such as blood glucose and nutrient levels. They provide the body with feedback about its metabolic and nutritional state
What neural systems or structures are involved in homeostatic mechanisms?
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)
What neural systems or structures are involved in non-homeostatic mechanisms?
Amygdala, Accumbens, Paraventricular nucleus of the thalamus (PVT), Ventral tegmental area (VTA), Hedonic stress (distal cue)
How does the brain receive signals about the current energy state of the body?
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
What factors affect the short-term regulation of food intake?
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)
What are examples of orexigenic factors?
Grehlin, NPY (Neuropeptide Y), AgRP (Agouti-related peptide). Ghrelin stimulates the release of NPY and AgRP which stimulates feeding
What are examples of Anorexigenic factors?
CCK (cholecystokinin), PYY (peptide tyrosine-tyrosine), CART (cocaine and amphetamine-related transcripts), aMSH (alpha melanocyte stimulating hormone), Insulin, Glucagon
How is ghrelin related to the short-term regulation of feeding?
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
How is CCK related to the short-term regulation of feeding?
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
What is the duodenum?
Beginning of the small intestine, controls bile secretion, monitors presence of fats, releases CCK
How is PYY related to the short-term regulation of feeding?
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)
What is the glucostatic theory?
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)
What is hypoglycemia?
When the level of glucose in the blood drops below what is healthy
How is insulin related to the short-term regulation of feeding?
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).
Is body weight regulated over the long term or short term?
Long-term (bodies will adapt to diets over the long term to stay within a certain weight range)
How is leptin related to the long-term regulation of feeding?
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.
What signals inhibit feeding neurons?
PYY, Leptin, Insulin, CCK
What inhibits AgRP?
Insulin and PYY
What stimulates the release of aMSH?
Insulin and leptin
What hypothalamic regions are implicated in feeding?
Lateral Hypothalamus (LH) stimulation produces eating and drinking (lesions lead to adipsia and aphagia), Ventromedial Hypothalamus (VMH) stimulation suppresses eating (lesions lead to obesity)
What are examples of appetitive mechanisms?
External such as appearance, smell, and taste; and internal such as time or size of last meal
Are we regulated more by nutritional needs or appetitive mechanisms?
Appetitive mechanisms (Most of our feeding has to do with circadian rhythms, conditioned habits, and the perceived value of the food item)
What do different regions in the Lateral Hypothalamus accomplish?
Some promote eating, some promote food ‘liking’, some suppress ‘liking’
What happens when the insula cortex is inactivated?
Cue-guided behavior is disrupted (but not feeding behavior)
How is the insular cortex related to the regulation of feeding?
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
What are DREADDs?
Designer Receptors Exclusively Activated by Designer Drugs. hM3Dq is the primary excitatory DREADD used
How do hunger signals modulate insular cortex activity?
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)
How are the AgRP neurons and the insula connected?
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)
How are PVT neurons related to the regulation of feeding?
Involved in feeding behaviour and addiction. Inhibition of neurons leads to increases in food intake. Excitation of neurons disrupts cue-guided behaviour
How is the BLA related to the regulation of feeding?
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
