Food intake and Energy Expenditure

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Lecture 2 & 3: What makes us decrease and increase feeding behavior

Last updated 6:58 PM on 3/24/26
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29 Terms

1
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Homeostasis

Maintains the internal environment within narrow physiological range

Energy intake vs Energy Expenditure is equal

Not as realistic in today’s sedentary society (in the US)

2
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Three components of neuronal response of homeostasis

  • Humoral

  • Visceromotor

  • Somatic

3
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Role of Hypothalamus

  • regulates homeostasis

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Humoral Response

t

5
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Roles of Oxytocin on the boday/brain

  • facilitates bonding

  • reduces anxiety

  • rewards caloric intake

6
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News and Views

study of oxytocin and intake of food in men

context dependent

  • resting state

  • food is chosen

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Glucose

our body’s energy “cash”

  • instant supply of energy needs

  • via food or produced by liver

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Glycogen

our body’s “standby reserve” of energy

  • we break down glycogen when glucose runs low

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Fat

our body’s 3rd reserve of energy and “certificate of deposit”

  • fat forms into triglycerides and energy

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Well-fed state vs Fasting state

  • know briefly, not in detail

<ul><li><p>know briefly, not in detail</p></li></ul><p></p>
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Process of High Blood Sugar to Low

know well

  1. High Blood Sugar

    1. promotes insulin release

<p>know well</p><ol><li><p>High Blood Sugar</p><ol><li><p>promotes insulin release</p></li></ol></li><li><p></p></li></ol><p></p>
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Process of low blood sugar to high

know well

  1. Low blood sugar

    1. promotes glucagon release

  2. Pancreas

  3. Glucagon

    1. simulates glycogen breakdown

    2. Glucose → Liver → Glycogen

  4. Raises blood sugar

<p>know well</p><ol><li><p>Low blood sugar</p><ol><li><p>promotes glucagon release</p></li></ol></li><li><p>Pancreas</p></li><li><p>Glucagon</p><ol><li><p>simulates glycogen breakdown</p></li><li><p>Glucose → Liver → Glycogen</p></li></ol></li><li><p>Raises blood sugar</p></li></ol><p></p>
13
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Type 1 Diabetes

Autoimmune Disease

  • body attacks itself, destroying beta cells as it recognizes it as a foreign body

  • you don’t produce insulin, which is necessary for body to use glucose for energy

  • No glucose regulation

    • issues - brain problems, energy

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Type 2 Diabetes

Insulin Resistance: Tissues cannot respond to insulin

  • Glucose stays in the blood

  • No glucose regulation

    • issues: hard on cells

      • osmotic water loss

      • damage of blood vessels

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Controlling glucose levels

  • diet

  • exercise

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Lipid levels: Adipose Tissue

releases leptin

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Satiety

being satisfied and not having hunger or motivation to seek out food

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Catabolic Factors do what

  • Decrease appetite

  • Decrease food intake

  • Increase metabolism

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Anabolic factors do what

  • Increase appetite

  • Increase food intake

  • Decrease metabolism

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Hunger Homeostatic feedback loops

  • Short-term feeding behavior: Maintenance of blood glucose levels

  • Long-term feeding behavior: Maintenance of fat stores

hunger can also be affected by mood

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Long-term feeding behavior goal

  • Maintain long-term energy stores (fat)

    • fat have 2x energy as glucose, doesn’t require excess water storage like glucose

    • body has set-point for amt of fat

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Role of set-point in the body

rat study: fasting and overfeeding resulted in same weight

reality show: guy went from 444-289lbs back to 450

  • Lipostatic Hypothesis

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Lipostatic Hypothesis

states that the brain monitors fat levels and maintains them at some fixed set-point amount

  • which requires the fat communicates with the brain in some way

a theory suggested a blood-borne hormone played a role

  • Evidence: 1960s study of Parabiosis

    • fused two animals to share the same blood

      • genetically obese mouse and normal mouse

    • 1994: Discovered presence of hormone: Leptin

      • mutation of OB: recessive mutation that causes weight gain

        • reduced and didn’t produce leptin

      • injected obese mice with leptin: restored normal weight

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Leptin

suppresses hunger and feeding, increased energy expenditure, reproductive competence

  • “Starvation signal”

  • lowers amount of food intake

  • lowers amount of body fat

what is leptin deficiency?

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How brain controls/detects leptin levels

  • Leptin theorized that leptin effects hypothalamus

  • Known: leptin activates a-MSH and CART in arcuate nucleus of hypothalamus

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What happens when there’s excess adipose tissue (Humoral, visce., Somatic)

Integrated response

  • Humoral: high secretion of TSH and ACTH, raises metabolic rate of cells in body

  • Visceromotor: higher activity of sympathetic response, raises metabolic rate and body temperature

  • Somatic motor: decrease in feedin behavior

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Where in the brain is leptin binding to coordinate this response that will eventually reduce adipose tissue?

Arcuate Nucleus

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Function of Arcuate Nucleus

  • makes a-MSH and CART

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