Intake

Question 1

What is the main goal of regulating feed intake?

Answer 1

To balance fat levels to meet needs and energy balance

Question 2

What is the difference between adipose cells, adipose tissue, and adiposity?

Answer 2

Adipose cells are fat cells
Adipose tissue is fat tissue
Adiposity is the amount of fat tissue

Question 3

What are “easy keepers?”

Answer 3

Animals that store extra fat

Question 4

Why might anorexia occur in an animal?

Answer 4

Sickness or abuse; the animal is using their fat reserves

Question 5

Why is a health weight or energy balance different for different animals?

Answer 5

Genetic differences

Question 6

What is the number one companion animal health issue?

Answer 6

obesity

Question 7

What does it mean when we say intake is a “redundant” regulation system?

Answer 7

Intake has many signals that contribute to it or affect it

Question 8

What are the major principles of intake?

Answer 8

1. Animals eat to meet their energy requirement. They do not eat to get essential nutrients, but to meet energy requirements.
2. The goal to meet demand and maintain a certain fatness “set-point” (i.e. energy maintenance requirements)
3. Daily intake is a matter of the number of size of meals
4. Many sensors to monitor nutrient status in short and long term status that are combined in the brain

Question 9

What is an important predictor of intake when it comes to diet?

Answer 9

The energy density of the diet

Question 10

What do we expect to happen to intake as diet energy density changes?

Answer 10

For feeds lower in energy density, we expect the animal to have to eat more of it to reach their energy requirements. For higher energy density feeds, we expect that the animal would have to eat less to reach their energy requirements.

In reality, an animal will eat to reach its energy requirements unless it can’t. For instance, low energy density feeds like hay are harder to break down and digest in the rumen since it must be broken down until it’s small enough. The rumen fills up and stretch receptors signal the brain to stop eating. As such, the animal is trying to eat to a certain energy requirement but cannot because the feed is so low in energy density.

In contrast, high density feeds see the animal decrease its intake because its body senses the high energy content can meet its requirements.

Question 11

What are stretch receptors?

Answer 11

Nerves around the stomach that signal the brain to stop eating once the stomach begins to stretch

Question 12

Describe the concept of quantity of feed consumed and energy needs.

Answer 12

Animals normally eat the quantity of food required to meet their energy needs. They will eat less than this requirement if their stomach becomes full before consuming enough energy.

Question 13

Describe how need drives intake.

Answer 13

Need normally drives intake in the following ways:
- genetics, physiology, health, etc. dictate growth rate
- growth rate determines energy requirement
- animal then eats to energy requirement

Question 14

What are the two interpretations concerning energy requirements and need?

Answer 14

1. An animal that produces more has a higher energy requirement so they eat more to reach this requirement.
2. If an animal eats more, it has more energy available, so it can produce more.

The first interpretation is the one we use. Making an animal eat more does not improve performance if they can eat as much as they want. Production is largely based on hormones and genetics.

Question 15

What type of controls regulate intake?

Answer 15

Short term and long term controls

Short term: controls size and frequency of meals within a day.

Long term: regulates intake over several days or weeks

Both types of controls are integrated in the brain and other body systems.

Question 16

What is daily intake?

Answer 16

Daily intake = number of meals x average meal size

meals are based on hunger and satiety

Question 17

How can daily intake be increased and decreased?

Answer 17

To increase daily intake, increase meal size or number of meals per day.

To decrease daily intake, decrease meal size or number of meals.

Question 18

What are the long term regulation controls of intake based on?

Answer 18

They are based on energy balance.

The goal is to maintain ideal body weight.

Question 19

What critical points in the body help regulate energy balance?

Answer 19

Brain, liver, stomach, pancreas, small intestine

blood, fat

The use of multiple systems and tissues show how this is a redundant system

Question 20

What is the metabolic set point?

Answer 20

The point we are trying to meet by gaining or losing weight.

Question 21

Describe the path to meet energy balance.

Answer 21

Gut, liver, and CNS sense the status of the body and send signals to the hypothalamic centers. These centers integrate the signals and tell whether or not the number or size of meals should change. This leads into energy intake plus or minus, which directly relates back to energy balance.

Question 22

Where are the CNS intake control centers? What are they?

Answer 22

These centers are in the hypothalamus

They are the lateral hypothalamus and the ventromedial nucleus (VMN)

Question 23

What is the role of the lateral hypothalamus?

Answer 23

Feeding and hunger center

Question 24

What is the role of the ventromedial nucleus (VMN)?

Answer 24

satiety centers

Question 25

What do CNS centers regulate?

Answer 25

They regulate the beginning and end of each meal, and determine meal size and frequency.

The faster a satiety center is turned on during a meal, the smaller the meal will be. The sooner the hunger center is turned on after a meal, the more meals will be consumed per day.

These centers maintain long-term nutrient intake at a level determined by other factors.

“thresholds”

ex. and underweight animal would take longer for its satiety control to kick in

Question 26

What might lesions of the VMN cause? (like those seen in mice)

Answer 26

Loss of satiety center, animal will eat until obesity and not know when to stop

Question 27

How does sensory stimulation regulate intake?

Answer 27

Factors sensed in the process of locating and consuming food include sight, smell, taste, texture, temperature, sound, etc.

1. Food characteristics
   - palatability
2. Other external stimuli
   - other animals, “feeding time”
   - social pressures
3. Environmental discomfort
   - hot, muddy, stress, lack of space, etc.

Question 28

Describe appetite.

Answer 28

Appetite is the level of desire for food.

It is a balance of hunger and satiety, and is determined by the integration of many signals

Question 29

What environmental or physiological factors regulate intake?

Answer 29

• stress
• disease (animal would have to expend energy for digestion, runs the risk of catching foodborne illness, etc.)

Question 30

What signals communicate the availability of nutrients?

Answer 30

1. Physical signals
   - gut fill
2. Chemical signals
   - blood glucose
   - rumen VFA
   - digesta pH
   - digesta osmolarity
3. Endocrine/Neuroendocrine signals
   - blood and CNS
   - hormones (e.g. insulin and gut hormones)

Question 31

What are stretch receptors?

Answer 31

These are nerves located in the gut wall the send a signal to the brain when activated. This is a mechanical regulation that indicates physical fill.

Question 32

What is gut fill dependent on?

Answer 32

1. Gut capacity
   - not well correlated with body weight
   - dependent on other things in the body
   - can stretch or shrink
2. Rate and extent of digestion
3. Rate and passage of feed

Physical fill can be used to limit intake; ex. fiber in companion animals

As a side note, pregnancy can also decrease gut capacity.

Question 33

Describe chemostatic controls regulating intake.

Answer 33

Nutrient concentrations are sensed by chemoreceptors like the gut, blood, or brain. As a result signals are sent to the hypothalamus intake centers.

• low blood glucose in non-ruminants
• high VFA in the rumen and blood
• high dissolved compounds in the duodenum
• imbalanced blood AA
• high plasma free fatty acids (non-esterified)
• signal to the brain either by second endocrine hormone or nerve impulse (afferent signal)

Question 34

Describe glucose.

Answer 34

Glucose is a nutrient and the main absorbed metabolite in non-ruminants. Glucose stimulates insulin secretion from the pancreas.

Question 35

Describe insulin

Answer 35

Insulin is a hormone secreted by the pancreas when blood glucose (BG) increases. It decreases plasma glucose and is a short term regulator important in the liver, adipose, and muscle.

Its functions are largely anabolic:
- inc. glucose uptake
- inc. glycogen synthesis
- inc. lipid synthesis
- inc. protein synthesis

Generally, insulin works by binding to an insulin receptor on a cell, which activates intracellular signals to stimulate uptake.

High insulin and low glucagon after a meal stimulates satiety centrally; short term insulin creates satiety.

Low blood glucose stimulates hunger. High insulin can result in increased intake in the long run because blood glucose drops and the animal becomes hungry sooner.

Question 36

What does a glycemic index measure?

Answer 36

It measures blood glucose after a test meal.

It is a carbohydrate-insulin model of obesity.

High glycemic index foods stimulate insulin, resulting in increased fat synthesis and storage, as well as increased intake because the animal becomes hungry sooner after a meal.

The glycemic index can be changed with processing.

Question 37

Describe type II diabetes.

Answer 37

This is insulin resistant diabetes.

The cell fails to respond to insulin because their is some sort of disruption of insulin signaling such as …
1. no receptor
2. failure to activate intracellular signal

Insulin is available to the animal and is being made by the pancreas, but either it cannot bind to the cell receptor or cannot cause the signal pathway. Insulin cannot be given to help this.

Question 38

Describe type I diabetes.

Answer 38

This is often referred to as juvenile diabetes. It is rarely seen in animals.

In this type of diabetes, the pancreas does NOT produce insulin. It is an autoimmune disease which kill the pancreatic beta cells, the site of insulin secretion.

Question 39

When does insulin resistance occur?

Answer 39

• during inflammation and disease (want E from glucose directed to recovery)
• during fasting and early lactation (when we do not want all of the glucose going to adipose; want it to be used for E)
• in obese animals

Question 40

What does insulin resistance result in?

Answer 40

High BG, fatty liver, and fat in muscle tissue. This can cause tissue damage, and liver failure.

Question 41

How can we test for insulin resistance?

Answer 41

• random plasma glucose: only catches bad cases
• fasting plasma glucose: even when fasted T2D animals will still have high BG
• Glucose tolerance test (GTT): the best test; involves giving an oral dose of glucose and insulin (in a normal response, insulin prevents BG from going to high; insulin resistant response see BG rise to high levels)

Question 42

Describe glucagon.

Answer 42

Glucagon is the opposite of insulin. It is secreted by the pancreatic alpha cells.

Its secretion is increased by the presence of amino acids, propionate, and butyrate.

Its secretion is decreased by the presence of glucose, ketones, and fatty acids.

Its actions are largely catabolic:
- dec. glucose use by many cells
- inc. glycogen breakdown
- dec. glycogen synthesis
- inc. gluconeogenesis from AA

Question 43

Describe how the gut hormones help regulate intake.

Answer 43

The major gut hormones are CCK (cholecystokinin) and GLP1 (glucagon like peptide 1).

They are secreted by the intestine in response to fat and protein. They induce satiety in the brain. They are not as well stimulated by carbs (ex. bacon and eggs fills you up more than cereal)

Question 44

What is ghrelin?

Answer 44

A hormone secreted by the stomach before a meal. It stimulates hunger.

It also stimulates secretion of growth hormone.

Question 45

How do gut hormones help regulate metabolism?

Answer 45

CCK, GIP (glucose inhibitory peptide or glucose-dependent insulinotropic peptide), GLP-1 play a role in regulating metabolism.

They increase insulin secretion by lowering the plasma glucose concentration required to stimulate insulin secretion.

If you IV glucose, sometimes you also need to give insulin because there will not be a large enough insulin response.

Question 46

In the long-term, how is intake matched with nutrient requirements to maintain a metabolic set point?

Answer 46

Important factors include

1. Pull of nutrients (nutrient demand)
2. amount of body fat
3. internal stresses (fever or disease)
4. environment (temp. or day length)

Question 47

What happens if input > output?

Answer 47

positive energy balance (gaining weight)

Question 48

What happens in input < output?

Answer 48

negative energy balance (losing weight)

Question 49

What effect does pull of nutrients from peripheral blood have?

Answer 49

This increases intake depending on the physiological state of the animal (ex. lactating vs. not lactating), genetics, and productivity.

Question 50

What is leptin?

Answer 50

Leptin is a hormone synthesized and secreted by adipose tissue. More of it is present when the fat cells are larger (more fat stored).

Leptin decreases feed intake and increases energy expenditure.

Question 51

Describe the lipostatic theory of intake regulation.

Answer 51

Leptin from adipose tissue enters the bloodstream, reaching the hypothalamus and causing intake to decrease and energy expenditure to increase.

Question 52

How is leptin disrupted?

Answer 52

No leptin or no leptin receptor

Question 53

Describe the ob/ob mouse.

Answer 53

similar to T1D
- defect is the leptin gene (ob gene, aka the obesity gene)
- biologically active leptin is not secreted
- no feedback with increased fat in adipose tissue, and the animal continues to eat

Question 54

Describe the db/db mouse.

Answer 54

Similar to T2D

• defect in the leptin receptor (db gene)
• plenty of leptin is secreted, but the cells and animal lack the ability to respond to it

Question 55

What would happen is leptin was given to the ob/ob mouse? To the db/db mouse?

Answer 55

Giving leptin to the ob/ob mouse would see a decrease in intake. This is because they do not produce leptin, and with leptin present, the brain would be signaled to stop eating.

If given to the db/db mouse, there would be no effect since they lack working receptors for leptin.

Question 56

Do defects in ob and db genes in humans cause obesity.

Answer 56

Obesity and intake regulation in people and other animals is more complex and is a polygenic trait, i.e. it is controlled by many genes not working well together.

Human food intake behavior also has substantial cultural, social, and psychological influences.

Question 57

What is the hepatic oxidation theory of intake regulation?

Answer 57

Blood from the gut goes to the liver, which is extensively involved in metabolism.

The theory proposes that the energy state of the liver is sensed (ratio of ATP to ADP) and a signal is sent to the brain by the hepatic vagus nerve

i.e. feed intake controlled by oxidation of fuel in the liver

Question 58

Why does the system sometimes not work, resulting in an overweight animal?

Answer 58

Consumption of high energy foods stimulates brain pleasure systems. This creates a strong reward for consumption of energy, sugar, and fat that was useful to living in the wild when food was not always reliably available.

The current environment is different from the environment the original system was built for. For many domestic animals, there is no long, cold, hungry winters.

Therefore, the carbohydrate insulin model is out of date for modern times.
- high glycemic index foods stimulate insulin secretion resulting in increased fat synthesis and storage
- the system did not see these until modern times