Regulation of Appetite and Body weight Flashcards

1
Q

Thermodynamic model of energy balance (what is it)

Define (in the context of the model): weight gain, weight loss

A

Energy storage/balance: difference between energy coming in and energy going out

Weight gain: in > out

Weight loss: out > in; in < out

Long term changes are more sustained, daily changes are variable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Components of energy intake

What impacts nutrient availability?

Energy content of major foods

A

Main component of energy intake is the digestible energy

What we get out of food depends on how it’s been cooked (raw prolly got more nutrients) and gut factors (things like surgery)

Energy content of most foods: carbs, proteins, fats, alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Components of energy output

A

REE (resting energy expenditure)

NREE (non resting energy expenditure)

TEF (thermodynamic effect of food)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Resting energy expenditure definition

When is the value collected for a test?

Depends on __? What’s the strongest determinant of REE?

Why is REE higher in obese pts?

A

(usually collected following an overnight fast)

Energy required at rest to carry out essential functions (about 60-70% of total Eo); used for heat generation, maintaining essential functions (e.g. breathing, heart beating etc)

Depends a lot on body composition

Fat free mass/lean muscle massstrongest determinant of REE (higher in obese pts because they have greater NET mass, (FFM + fat mass, but I don’t understand how obese individuals can have a more FFM??)

Brown adipose tissue, being the more metabolically active fat may also contribute to REE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Non resting energy expenditure

Definition (+ what % of Eo)

exercise vs non exercise activity thermogenesis

A

Non resting energy expenditure (energy used when you’re doing stuff); 20 - 30% of Eo

exercise activity thermogenesis: intentional movement

Exercise can impact REE for up to 24 hours, may be a feed forward effect, depends on exercise intensity**

Non exercise = standing, shivering, movement that’s not at the level of exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Thermic effect of food (TEF)

What is it, what % of Eo and what does it depend on?

A

Thermic effect of food: energy required to digest food we eat (10% of Eo)

protein requires more energy to digest compared to carbs or fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Components of stored energy

A

Triglycerides

Protein

Glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Triglycerides

T/F: they’re the major fuel reserve of the body and have a potentially unlimited capacity

What happens to adipocytes as we gain weight?

Associate w/ water or naw?

A

True dat; Most energy formed as triglycerides

As we gain weight, our adipocytes get larger and increase in number

Them are hydrophobic so naw

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Proteins

Where are they stored? What are they manily used for?

Associate w/ water or naw?

A

Proteins: stored in muscle, mainly for structural purposes

aa’s can be used for energy if we’re depleted;

Kinda but apparently at a lower volume/gram than carbohydrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Glycogen

Why’s it efficient at storing energy? Hydrophilic or naw?

What’s the capacity (finite or unlimited and why?)

What’s the capacity in liver vs muscle? T/F: trained athletes can double their capacity

A

Glycogen – very hydrophilic;

Efficient energy storage b/c its branched chains so that allows for quick cleavage of glucose moieties

Capacity is finite (less than one day’s worth of glycogen storage) because it traps a ton of water; liver = 120grams/500kcal; muscle = 400 grams/1600 kcal; trained athletes can apparently double this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Weight loss is usually loss of what kinda weight?

Long term weight loss is loss of what?

A

Changes in body weight = changes in water weight usually;

long term – changes in adipocyte/fat mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Energy storage is net __ from conception onwards

Energy needs of babies vs adults

Temporal changes in stored energy:

What happens over 24 hrs (net positive/negative?)

Changes to body mass (do you maintain constant, does it vary, what does age have to do with anything?)

A

From conception onwards, energy storage is net positive

Babies have larger Ei compared to Eo coz they’re growing (baby = 50-60 kcal; infant/child = 80-110 kcal)

Avg adult intake = 30ish kcal/day

In 24 hr period, you’ll be net positive; energy balance is only when averaged over time

In general, you maintain a constant body mass

With aging, you lose muscle mass and gain fat mass

Changes in body mass also trigger changes in energy expenditure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is this concept of adaptive thermogenesis?

A

Adaptive thermogenesis: change in energy expenditure that’s observed with change in weight; observed change in energy expenditure is out of proportion to change in weight (there’s about a 400-500 calorie difference in energy expenditure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

BMI calculation (metric and US)

BMI classifications

A

BMI: proportion of weight to height

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Set point hypothesis

How does this hypothesis explain what happens with obese patients?

A

Body is programmed to function optimally within a certain range and it uses active mechanisms to control that

There might be some dysfunction/dysregulation in the system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Settling point hypothesis

A

Depending on what’s happening at the time, your body’s set point might change and it tries to maintain that new set point via passive mechanisms

17
Q

Classic theories of food intake regulation. Which ones refers to short term vs long term regulation?

A

Glucostatic vs lipostatic

Glucostatic: short term

Lipostatic: long term

18
Q

Glucostatic theory vs Lipostatic theory

A

Glucostatic theory: Basically glucose levels determine hunger/satiety mechanisms

Lipostatic theory: Similar to glucostatic except its body fat (talks about long term regulation)

19
Q

Where are hypothalamic nutrient sensors?

The __ nucleas has 2 clusters of 1st order neurons that regulate apppetite. Clusters are __ and __. Which one is stimulated by presence of nutrients and is anorexigenic? Which one is activated by ghrelin and is orexigenic?

1st order neurons stimulate 2nd order neurons in the __ and __, which control appetite and satiation

A

At the blood-brain barrier

arcuate; Melanocortin secreting neurons, and Neuropeptide Y secreting neurons.

Melanocortin stimulating neurons = anorexigenic and stimulated by presence of food; in charge of satiety

Neuropeptide Y secreting neurons: in charge of hunger (activated by ghrelin)

Lateral nuclei and Medial nuclei

20
Q

Appetite center is made up of __ and __ (lah-fah)

A lesion in the appetite center leads to __

Satiety center is made up of __, ___ and __ (pvn and Van Damme)

A lesion in the satiety center causes__

A

LHA and PFA

Anorexia

PVN, VMN, DMN

Obesity

21
Q

Sensorineural input types (+ examples)

A

External environment; basically visual cues, temperature, light/circadian patterns?, food palatability

Internal environment: blood pressure, nutrient status, blood osmolarity, gut stretch, memory

22
Q

Hormonal input examples (all the “ins” from the gut” plus sugar, sex and iodine)

A

Leptin

Ghrelin

Gut peptides

Glucocorticoids, thyroid hormones, sex steroids

23
Q

Metabolic output (affected areas)

What’s the main driver of energy balance?

A

Ant and post pituitary

Limbic system

CNS and ANS

Hypothalamic output to the autonomic nervous system

24
Q

Who produces leptin?

What are the GI tract factors that stimulate energy intake? Inhibit it?

Main determinant of REE

Impact of exercise

A

Adipose tissue (mainly) and stomach (a little bit)

Stimulatory GI factors: ghrelin – release stimulated by absence of food in the stomach

Inhibitory GI factors: incretins (GLP1,CCK, PYY) - release stimulated by presence of food in stomach

Fat mass will be the main determinant of REE and will feed back to hypothalamus about drive to eat; this happens via Leptin, the hormone that controls satiety

Exercise will affect body composition and heat production

25
Q

Describe the leptin pathway (both pathways, leading up to appetite suppression and inhibition of food intake)

A

Leptin binds to its receptor on the POMC neurons in the arcuate nucleus, which will then stimulate 2nd order neurons (MC4R – melanocortin 4 receptor) and the signal = inhibition of food intake

Leptin also binds to the NPY secreting neurons to the MC3R and inhibit appetite stimulation

26
Q

Relationship between leptin and fat mass. This is suggestive of what problem that explains why leptin replacement doesn’t work for weight loss in obese patients?

A

There’s a linear relationship between increasing BMI (therefore increasing adipose tissue) and leptin levels

There’s probably some leptin resistance; obese pts were given leptin replacement; it didn’t help with weight loss

27
Q

Congenital leptin deficiency (what is it and how do you treat it? What are the patient’s symptoms?

A

Pts can’t make leptin at all so they have no inhibitory signal to the hypothalamus

When given recombinant leptin, observed decrease in weight

28
Q

Hypothalamic hypogonadism (what is it, how does it manifest?)

A

In severe food deficiency states (like anorexia) or when Leptin levels are otherwise really low (e.g. congenital Leptin deficiency), the body minimizes the chance of reproduction as a means of biological conservation and there’s insulin resistance to maintain blood glucose levels

29
Q

Signal transdusction between ENS and CNS

(which neurons sent what signals to the NTS? Which 3 brain areas are affected? who relays the signals back to the ENS and what is the ENS response?

A

Between gut and CNS, nutrients cross blood brain barrier and impact brain directly

Signals are transmitted via the vagus nerve to the NTS, which activates mechanoreceptors (stretch), chemoreceptors, and gut hormones

Vagal efferents relay info back to gut ENS

ENS responds by either promoting or inhibiting digestion

30
Q

Give the following for GIP and CCK

Source (where they come from)

Release stimulated by

Effect on appetite

Physiologic effects

A

GIP and CCK:

GIP - Duodenum (K cells), CCK (+ jejunum; I cells)

GIP - Carbohydrate and fat, CCK (fat and protein)

Decrease

GIP -↓ gastric acid, ↑ insulin

CCK -↑ pancreatic enzymes and bile
Satiety

31
Q

GLP1, PYY and OXM

A

GLP1 - Distal ilium (L cells); PYY - ileum, colon, brainstem; OXM - ileum and colon

GLP1 - Carbohydrate, fat and bile acids; PYY - fat + bile acids; OXM - fat and carbohydrate

Decrease

GLP1 - ↑ insulin, delays gastric emptying, ↓ glucagon

PYY - Satiety (eating pie makes you full)

OXM - ↓ gastric acid, ↓ ghrelin

32
Q

Give the source, stimulus for release, effect on appetite and physiologic effects for:

Insulin

Ghrelin

A

Insulin:

Beta cell / Pancreas

Carbohydrate >> protein

Decrease

Glucose homeostasis

Ghrelin:

Stomach

Lack of food/stretch

Increase

↑ GH, ↓ EE, ↓ thermogenesis

33
Q

what’s the whole idea of the satiety cascade?

factors that will impact satiety (basically 3 big categories)

A

Over time, satiety levels are decreasing after having eaten a meal

Meal quality, meal quantity, nutrition status

34
Q

What’s non-shivering thermogenesis?

what upregulates BAT? (when you SNS, you prolly got a cold and u need to take T3)

why’s it a big deal?/how does it do its job?

3 proteins involved, where are they located/how are the activated (one is cold, 2 eats too much, 3’s got gains)

between white and brown adipose tissue, who’s the more metabolically active?

A

Upregulated by cold, T3 and sympathetic nervous system

heat is generated in BAT by uncoupling oxidative phosphorylation from the ETC;

Uncoupling proteins increase membrane permeability to protons

UCP1 is induced by cold

UCP2 – induced by diet; expressed kind of everywhere

UCP3 – mainly in skeletal muscle

***BAT is the more metabolically active adipose tissue

35
Q

Brown fat locations

(Chimdiya would massage Matthew’s __ w/ a blade; the other name for your collar bone; biggest artery in body and where it sits on; location of adrenal gland (ie what else was it called?))

A

Neck

Supraclavicular

Para aortic

Para vertebral

Suprarenal

36
Q

what’s beige adipose tissue? and how’s it different from BAT and WAT?

how would you make beige adipose tissue?

A

Beige adipose tissues :

basically white adipose tissue in which mitochondria have been upregulated and those uncoupling proteins have been upregulated so there’s smaller lipid droplets and slightly more heat generation (it’s somewhere in between BAT and WAT)

Some signal would have to trigger browning of adipose tissue like adrenergic and thyroid stimuli

37
Q

metabolic response to cold stimulus in obese patients

A

Obese and overweight people don’t have the typical metabolic response to cold stimulation (no heat generation, no increase in BAT)

38
Q

effect of beta adrenergic agonist in brown fat activity

A

B adrenergic agonist: mirabegron – upregulate sympathetic activity and upregulate brown fat activity; REE also upregulated