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Diet in Health and Disease > Pshysiological Control of Appetite > Flashcards

Pshysiological Control of Appetite Flashcards

1
Q

Define Appetite

A

The integrated response to the sight, smell, thought or taste of food that initiates or delays eating

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2
Q

Define Hunger

A

A painful sensation caused by a lack of food, this initiates food-seeking behaviour

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3
Q

Define Hypothalamus

A

Brain centre that controls activities such as maintenance of water balance, regulation of body temperature, and control of appetite

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4
Q

Define Endocrine System

A

It is a collection of glands that secrete hormones directly into the circulatory system to affect a distant target organ

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5
Q

Define Neurotransmitters

A

Are endogenous chemicals that transmit signals across a synapse from one neuron to another ‘target’ neuron

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6
Q

Define Hormones

A

Any member of a class of signalling molecules produced by glands in multicellular organisms that are transported by the circulatory system to target distant organs to regulate physiology and behaviour

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7
Q

Short-term regulation of body weight is governed by the following:

A

Hunger (postabsorptive), appetite and satiety (postprandial)
The physical trigger for hunger > satiety.

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8
Q

Long-term regulation of body weight is governed by the following:

A

Feedback mechanism - adipocytokines (signalling protein is released from the adipose mass when normal body composition is disturbed).
This mechanism plays a greater role in younger persons than older adults.

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9
Q

Define Satiation

A

Prompts the termination of eating.
Controls energy intake in one sitting.

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10
Q

Define Satiety

A

Fullness that persists after eating. Controls length of time until next meal/snack.

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11
Q

Facts about Macronutrients and Fat Storage

A
  • The body prefers to use CHO as an energy source
  • Only excess intake of CHO and Protein will be turned into fat
  • Fat will remain as fat for storage
  • Physical activity encourages the burning of dietary fat (Beta-oxidation)
  • A high CHO diet decreases Beta-oxidation
  • Most endurance athletes burn fatty acids for energy
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12
Q

Fat and Fat Storage

A

Most fat is stored directly in adipose tissue.
The body has the ability to store fat as triglycerides.

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13
Q

CHO and Fat Storage

A

Limited CHO can be stored as glycogen. 2/3 of glycogen is stored in the muscles, and the rest is stored in the liver.
Most CHO is used as an energy source.
Excessive CHO will be synthesized into fat (for storage).

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14
Q

Protein and Fat Storage

A

Protein is primarily used for tissue synthesis.
Adults generally consume more protein than needed for tissue synthesis.
Excess protein is used as an energy source.
Some protein will be synthesized into fat (for storage).

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15
Q

How do fat cells form and expand?

A

The cells can expand to store more fat (hypertrophy). Once filled to capacity, stimulate the production of more fat cells.
Weight loss leads to the shrinking of the adipocyte size but no change in the number of cells.
Enzymes control the size of the fat cells.
Lipoprotein lipase (LPL) increases lipogenesis.
Hormone-sensitive lipase (HSL) stimulates lipolysis.
Heavier people have increased activity of LPL.

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16
Q

How many adipocytes does an adult hold?

A

30-50 billion, which holds between 0.4-0.5 micrograms of fat each
Adipocytes of obese individuals contain 0.6-12 micrograms of fat per cell.

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17
Q

Explain the Healthy Eating Cycle

A

Hunger - Anticipation - Eat - Pleasure - Fullness - Satisfaction

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18
Q

What is Hedonistic Regulation?

A

Reward input

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19
Q

What are Endorphins?

A

Neurotransmitters produced by the pituitary gland and the hypothalamus - the brain’s pleasure chemicals.
They enhance the desire for food by the smell, sight, or taste of foods.

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20
Q

Examples of Endorphins

A

Dopamine
Serotonin

21
Q

What are the satiety regulators?

A

The hypothalamus.- When feeding cells are stimulated, they signal us to eat. When satiety cells are stimulated, they signal us to stop eating.
The sympathetic nervous system.- When activity increases, it signals us to stop eating. When activity decreases, it signals us to eat.

22
Q

Which centres of neural control does the hypothalamus contain?

A

Temperature
Hunger
Appetite
Thirst

23
Q

What is Leptin?

A

A peptide released by adipose cells that circulates at levels related to fat reserves.
It serves as an indicator of the body’s total energy stores and provides a mechanism for controlling hunger.
In obesity, it loses function to control hunger.

24
Q

Explain cholecystokinin (CCK)

A

Gut hormones at the brain level inhibit food intake. Stimulate pancreatic enzymes.

25
Q

Explain glucagon-like-peptide-1 (GLP-1)

A

A gut hormone released in the presence of glucose-rich food: delays gastric emptying time and promotes satiety.

26
Q

Explain Ghrelin

A

The hunger hormone, is a peptide hormone secreted by the gastric mucosa on an empty stomach during fasting. This hormone decreases rapidly after a meal.

27
Q

Explain Peptide YY-3-36 (PYY-3-36)

A

It is secreted in the small bowel in response to foods. In obesity, it loses the ability to inhibit energy intake.
Peptide YY is a short (26 aa’s) peptide released from cells in the ileum and colon in response to feeding.
In the blood, gut, and other periphery elements, PYY reduces appetite; similarly, when injected directly into the CNS, PYY is also anorexigenic, i.e., it reduces appetite.

28
Q

Explain Thyroid hormones

A

Modulates the tissue responsiveness to the catecholamines secreted by SNS.
A reduction in thyroid hormone:
- reduces the SNS activity
- decreases adaptive thermogenesis

29
Q

What are the environmental factors that influence satiety?

A

Temperature, humidity and availability.

30
Q

What are the emotional factors that influence satiety?

A

Stress and mood.

31
Q

What are the CNS factors that influence satiety?

A

Hypothalamus and vagus nerve

32
Q

What are the metabolic influences on satiety?

A

Energy requirements, neurotransmitter levels, insulin, and various hormones.

33
Q

What is the Kwashiorkor disease?

A

It is an acute form of childhood protein energy malnutrition.
Characterised by inadequate protein intake, but with reasonable calorie intake.
Represents a maladaptive response to starvation.

34
Q

What are the symptoms of Kwashiorkor disease?

A

Mild anaemia, apathetic, thin upper arm, usually underweight, finger leaves a hole (skin), flaking paint rash, large liver.

35
Q

What are the energy-depleted end products?

A

CO2
H2O
NH3

36
Q

What are the precursor molecules of Anabolism?

A

Amino acids, sugars, fatty acids and nitrogenous bases.

37
Q

Explain the insulin and glucagon feedback loops

A
  • Low blood sugar promotes glucagon release (pancreas).
    Glucagon stimulates the breakdown of glycogen (liver)
    Raises blood sugar.
  • High blood sugar promotes insulin realise (pancreas).
    Insulin stimulates glucose uptake from the blood. Stimulates the formation of glycogen. Lowers blood sugar.
38
Q

Explain the Well-feed state

A
  • Protein hydrolysed to amino acids in the intestine and absorbed and passed into the hepatic portal vein.
  • Most amino acids pass through the liver and are not catabolised in the liver unless concentrations are very high.
  • Amino acids are used by the liver and the other organs for protein synthesis.
    Excess amino acids are catabolised by the liver to yield urea. Carbon elements are used mainly for fatty acid synthesis.
    Dietary fatty acids are delivered to adipose tissue in chylomicrons; lipase releases fatty acids that are taken up and stored as triglycerides.
    High insulin promotes the synthesis of glycogen and adipose tissue.
39
Q

What is starvation?

A

It is defined as the post-absorptive period: all food has been digested, and no glucose is coming in from the gut.
It is an adaptive hypo-metabolic state.
Eventually, the body converts fatty acids to ketone bodies, which can be used by the brain as an energy source.
Muscle mass can, therefore, be spared in favour of using fat/triglycerides as an energy source.
Physiological processes are designed to protect lean tissue as much as possible and preserve glucose for brain metabolism.

40
Q

How much glucose does the brain need a day?

A

120g

41
Q

Explain starvation response 1st stage

A
  • insulin + glucagon
    + gluconeogenesis - glycogenolysis
    Glycogen is broken down to glucose
    Lipogenesis is reduced
    Fats are split into glycerol and fatty acids
    Fatty acids are used as a source of energy by skeletal muscles
    Glycerol can be used to make a small amount of glucose
    Most of the circulating glucose comes from the deamination of amino acids
42
Q

Explain 2nd stage of starvation

A

This can last for several weeks
Fats are the main energy source (from adipose tissue).
The liver metabolises fatty acids into ketone bodies.
After 3 days to a week of fasting, the brain begins to use ketone bodies and glucose as a source of energy.
Non-essential proteins are used, and de-amination is first.
Protein sparing is key.

43
Q

Explain ketogenesis

A

Acetyl CoA is broken down into ketone bodies

44
Q

Explain 3rd stage of starvation

A

Survival can depend on the amount of fat stored.
Protein reserves are depleted once the fat stores are depleted.
Switch to proteins as the major energy source.
Muscles are rapidly depleted including heart muscle.
Cell function degenerates.

45
Q

Explain the 3 phases of starvation

A

Post-absorptive
Gluconeogenic
Protein Conservation

46
Q

Statements about leptin

A

It is produced by the adipose tissue.
It signals the amount of fat stores.

47
Q

Statements about Ghrelin

A

It is produced when the stomach and small intestine are empty of food, particularly proteins and fats.
Resistance to grhelin lead to excessive hunger and obesity.

48
Q

Explain Wegovy/semaglutide drug for the treatment of obesity

A

Semaglutide is a glucagon-like peptide-1 analogue and it acts to enhace the production of insulin and increase the sensation of fullness and so reduce appetite.

Diet in Health and Disease (16 decks)

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