Regulation of Energy Intake and Body Weight Regulation Flashcards
What part of the brain is intimately involved in both the control of short- and long-term regulation of body weight?
Hypothalamus
The paraventricular nucleus (PVN), ventromedial nucleus (VMN), arcuate nucleus (Arc), and lateral hypothalamus (LH) (Figure 2) regulate food intake and disposition by processing information concerning peripheral energy stores and then stimulating or inhibiting feeding or altering gastric motility and food metabolism/utilization.
What is the “hunger center” involved in short-term regulation of eating?
Lateral Hypothalamus
Stimulation of the lateral hypothalamus (LH) produces voracious eating, even in a food replete animal, and lesions in this region produced aphagia (no eating).
Two peptides have been identified that are expressed in the brain only by neurons in the LH: melanin concentrating hormone (MCH) and orexins (also known as hypocretins).
What peptides are in the lateral hypothalamus and promote hunger?
melanin concentrating hormone and orexines
What is the “satiety center” involved in the short-term regulation of food?
ventromedial nucleus (VMN)
Stimulation of this region results in cessation of eating even in hungry animals. Animals with lesions in this region eat excessively and become obese.
VMN lesions have the effect of “resetting” the regulated weight to a higher level.
Arcuate nucleus
Contains “first order” neurons that promote either food intake or satiety.
Activation of arcuate neurons that produce both neuropeptide Y (NPY) and agouti-related peptide (AgRP) promote feeding while activation of the arcuate neurons that produce both α-melanocyte stimulating hormone (α-MSH) and cocaine and amphetamine-related transcript (CART) promote satiety.
Melanocortin receptors (MCRS)
Activation of MCRs induces satiety.
α-MSH activates MCRs
neuropeptide Y (NPY)
Neuron that stimulates hunger and food intake
increases hunger when injected into the hypothalamus and decreases energy expenditure
Where do long-term signals of weight regulation come from compared to short-term?
Short-Term Signals – meal-related
Long-Term Signals – adiposity-related
What are non-homeostatic mechanisms that affect our energy balance?
Internal inputs: Reward and Motivation Cravings "Thinking about food" Restraint Learned behaviors Attention Cognitive/Executive Decisions
External inputs: Environmental Cues Availability/portions Social Context Time cues
Leptin
‘satiety hormone’ from adipose tissue was identified when the gene that is defective in an obese strain of mice, the ob/ob strain, was cloned
AgRP
Agouti-related peptide
Inhibit the MCRs (inhibiting satiety) so basically increasing hunger
Ghrelin
Secreted from the stomach that induces feeding
Meal-to-meal basis
Gut hormone
“The hunger hormone”
PYY, GLP1
Secreted from distal ileum
Gut hormone
SATIETY signaling meal-to-meal
CCK
Hormone that goes up after a meal
The duodenum signals the presence of nutrients to the brain via the release of cholecystokinin (CCK).
Short-term meal-to-meal signaling
Do overweight or weight-gaining prone individuals have more leptin?
Yes, but still report more hunger
Resistant to leptin?