Hormone responses to signals of hunger and satiety

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Biology

34 Terms

1

Are cases of obesity increasing globally?

Yes

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2

What are some of the negative results of obesity?

  • Type 2 diabetes

  • Heart disease

  • Stroke

  • Some types of cancer

  • Sleep apnea

  • Hypercholesterolemia

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3

What happens in the body during a well-fed state versus a fasting state?

  • Well-fed:

    • Brain: Food → glucose, free fatty acids, amino acids. Glucose powers the brain and muscles

    • Liver: Glucose → glycogen. Stored in liver and muscles

    • Pancreas: Insulin facilitates glucose transportation

  • Fasting state:

    • Brain: Free glucose and ketone bodies power the brain

    • Liver: Glycogenesis breaks down stored glycogen. Lipolysis releases free fatty acids and glycerol.

    • Pancreas: Glucagon is released

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4

What signaling molecules are involved in the regulation of energy balance?

  • Orexigenic signaling molecules- increase appetite

  • Anorexigenic signaling molecules- decrease appetite

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5

What are the internal signals that influence feeding behavior?

Available energy: glucose, fatty acids, ketone bodies

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6

How does the body use glucose?

  • Glucose can be oxidized into energy: glucose + oxygen = CO2 + H2O + ATP

  • All body cells can use glucose for fuel (glycogenesis= Breaking down glycogen)

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7

How does the body use fatty acids?

  • All cells in the body can use fatty acids (via lipolysis)

  • Mostly the heart uses fatty acids

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8

What is the role of insulin in the body?

Insulin brings glucose into cells (except in the brain)

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9

What happens with the absence of insulin?

  • Hyperglycemia- high blood sugar

  • Diabetes mellitus

    • Type 1- Can’t make insulin

    • Type 2- Body becomes insensitive to insulin

  • Diabetes insipidus- Problems with ADH

    • Results in the inability to keep water in, and frequent urination

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10

How does the body store fuel?

  • Glycogen- Glucose → glycogen, and stored in the liver and muscle (insulin needed for storage)

  • Fatty acids- Food → fatty acids (fuel)

  • Triglycerides- Fatty acids + glycerol = triglycerides (don’t need insulin for storage)

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11

How does insulin influence hunger?

  • Insulin is secreted before you eat (controlled by internal clock + cephalic cues [food smell]), and increases hunger

  • Insulin promotes glucose storage + prevents triglyceride breakdown

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12

What are glycogen and triglycerides used for?

They are broken down into glucose and fatty acids

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13

What area of the body needs a constant source of glucose?

The brain

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14

How do we get energy out of (break down) the storage?

  • Epinephrine- Released from the adrenal medulla. Breaks down glycogen and triglycerides.

  • Glucagon- Released from pancreatic alpha cells. Breaks down glycogen

  • Glucocorticoids- (corticosterone/cortisol) released from the adrenal cortex. Leads to breakdown of glycogen

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15

What is the glucostatic hypothesis? What is the main problem with it?

  • Brain monitors glucose levels.

  • When glucose levels fall below a critical level, we get hungry

  • Eating restores glucose levels and hunger

  • Problem: People with diabetes have high levels of glucose, but are often hungry

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16

What is the Lipostatic hypothesis? What is the main problem with it?

  • Brain monitors fat stores

  • When fat stores fall below a critical level, we get hungry

  • Eating restores body fat and hunger

  • Problem: Humans get hungry after just 4 hours, but don’t lose weight

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17

What was the experiment to test glucose vs fatty acids?

  • Energy availability is limited from either glucose or fatty acids

  • 2-Deoxy-D-glucose (2DG)- Inhibits glycolysis (turning glucose into energy)

    • Blocks glucose- increases food intake + hyperglycemia

  • Methyl palmoxirate- Inhibits lipolysis (breaks down triglyceride into glycerol and fatty acids)

    • Blocks fatty acid metabolism- Increases food intake

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18

Which is a stronger signal to eat food, glucose or fatty acids?

Both are strong signals

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19

What area of the body can strongly detect energy levels?

The liver- Nutrients infused through a vein (hepatic portal vein) in the liver decreases food intake. 2DG applied here increases food intake.

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20

What does a large dose of insulin do?

Reduces blood glucose levels, makes animals hungry

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21

What do ketone bodies do in the brain?

Makes the brain “fed”, does not inhibit insulin-induced food intake

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22

What does fructose do in the brain?

Makes the liver “fed”, inhibits insulin-induced food intake

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23

What happens if there is a “fed” liver and a “starved” brain?

  • Blocks insulin-induced feeding

  • Due to the vagus nerve (where the liver monitors glucose levels to the CNS)

  • Cutting the vagus nerve blocks the effects of fructose in the liver

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24

What are two rodent models for genetic obesity?

  • Obese (ob/ob) mouse

  • Zucker rat

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25

What does leptin do to ob/ob mice? Why?

  • Makes them thin

  • ob/ob mice lack the leptin gene

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26

What are zucker rats?

  • Rats that have a mutation of the leptin receptor

  • Gene therapy to replace the missing receptor reverses the effects

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27

What is ghrelin?

  • A gut peptide made by stomach cells.

  • It rises before meals and falls after

  • Ghrelin injections increase hunger

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28

Why is it unlikely that ghrelin directly affects hunger signaling?

There are many other peptides that can decrease food intake

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29

What is the dual center theory? Is it correct?

  • The lateral hypothalamus is the hunger center, the ventromedial hypothalamus is the satiety center

  • This theory is wrong

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30

Why is the dual center hypothesis incorrect?

  • Lesions of lateral hypothalamus results in sick mice (due to cutting dopamine off)

  • Lesions of the ventromedial hypothalamus results in obese mice (due to increased fat stores, and insulin disruption)

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31

What are the most popular amine and peptide neurotransmitters?

  • Neuropeptide Y- increases food intake, has its own receptors, made by arcuate neuron

  • AGRP- increases food intake, binds to another receptor (melanocortin), made by arcuate neuron

  • POMC (α-MSH)- inhibits food intake, binds to melanocortin receptors, a melanocortin, made by arcuate neuron

  • CART

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32

What do GI hormones do?

Serve as satiety signals that converge on the dorsal hindbrain

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33

What are the two main areas of the neural circuit involved with food intake?

  • Paraventricular nuclei of hypothalamus (PVH)

    • Arcuate neurons project here

  • Arcuate nuclei of hypothalamus (Arc)

    • Ghrelin, leptin, and insulin act here

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34

What are incretins?

  • A group of metabolic peptide hormones that lower blood glucose

  • Glucagon-like-peptide 1 (GLP-1) and Gastric inhibitory protein (GIP)

  • Stimulate insulin release, inhibit glucagon release (ultimately lowering blood glucose)

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