Regulation of Energy Intake and Body Weight Regulation Flashcards

1
Q

What part of the brain is intimately involved in both the control of short- and long-term regulation of body weight?

A

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.

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2
Q

What is the “hunger center” involved in short-term regulation of eating?

A

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).

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3
Q

What peptides are in the lateral hypothalamus and promote hunger?

A

melanin concentrating hormone and orexines

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4
Q

What is the “satiety center” involved in the short-term regulation of food?

A

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.

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5
Q

Arcuate nucleus

A

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.

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6
Q

Melanocortin receptors (MCRS)

A

Activation of MCRs induces satiety.

α-MSH activates MCRs

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7
Q

neuropeptide Y (NPY)

A

Neuron that stimulates hunger and food intake

increases hunger when injected into the hypothalamus and decreases energy expenditure

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8
Q

Where do long-term signals of weight regulation come from compared to short-term?

A

Short-Term Signals – meal-related

Long-Term Signals – adiposity-related

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9
Q

What are non-homeostatic mechanisms that affect our energy balance?

A
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
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10
Q

Leptin

A

‘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

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11
Q

AgRP

A

Agouti-related peptide

Inhibit the MCRs (inhibiting satiety) so basically increasing hunger

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12
Q

Ghrelin

A

Secreted from the stomach that induces feeding
Meal-to-meal basis
Gut hormone
“The hunger hormone”

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13
Q

PYY, GLP1

A

Secreted from distal ileum
Gut hormone
SATIETY signaling meal-to-meal

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14
Q

CCK

A

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

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15
Q

Do overweight or weight-gaining prone individuals have more leptin?

A

Yes, but still report more hunger

Resistant to leptin?

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16
Q

Do signals not work properly in overweight people? What are the theories behind this?

A

Very possible

Our biologic signals are primarily designed to protect us during times of undernutrition.
Perhaps it’s all about “resistance” to these signals, ie leptin resistance?
Perhaps it’s just much more complicated

17
Q

MRI scan studies when show lean and overweight people picture of food

A

When lean people are hungry, increased brain activity when you look at pictures of food in brian regions that are important for: Attention, Reward, Motivation, Memory. When fed, that activity decreases.

When obese people: are fasted, they have less activity than lean people, but when they’re fed their activity goes up.

Activity of lean people and overweight people on MRI studies are opposite.

18
Q

Glucose and hunger-signaling

A

Hypoglycemia stimulates eating and hyperglycemia inhibits eating.

19
Q

Insulin and weight balance

A

Functions as a long-term regulator of food intake, energy balance, and adiposity in a similar manner as leptin.

Circulates at levels that parallel body fat mass, and both fasting and meal- or glucose-stimulated insulin concentrations are well correlated with body fat content.

Insulin receptors are located in the glucose sensitive regions of the hypothalamus and brainstem, and it is transported into the brain by specific transporters.

20
Q

What part of the brain is likely involved in the food-reward pathway?

A

Nucleus accumbens

Like opioid and drug reward