What is the most important hallmark of homeostasis?

it is maintained through a negative feedback loop

As we lose water and use up energy, how does our body know to seek out water and food?

hormones

What fraction of the average mammal is water?

What % range is body water content in humans?

What do cells require water for?

Water serves as a solvent for which 7 things?

What fraction of the average mammal is water?

What % range is body water content in humans?

What do cells require water for?

Water serves as a solvent for which 7 things?

-  2/3

-  45% to 70%

-  for all processes

-  Na+,  Cl-,  K+,  sugars,  amino acids,  proteins,  & vitamins

What 4 ways is water continuously lost?

- perspiration

- respiration

- urination

- defecation

What about the fluid in the extracellular compartment can vary?

What requirement does intracellular fluid have?

How is this requirement met?

What is another term for the extracellular compartment?

What about the fluid in the extracellular compartment can vary?

What requirement does intracellular fluid have?

How is this requirement met?

What is another term for the extracellular compartment?

- the amount and concentration

- the amount must remain stable

- it is tightly regulated

- interstitial fluid

What % of the body's fluid compartments are each of the following:

Plasma -

Intracellular fluids -

Interstitial fluid -

What % of the body's fluid compartments are each of the following:

Plasma - 8%

Intracellular fluids - 64%

Interstitial fluid - 25%

What causes osmotic thirst?  Give an example of when this would occur.

What occurs in response to osmotic thirst?

What does this do?

What causes osmotic thirst?  Give an example of when this would occur.

What occurs in response to osmotic thirst?

What does this do?

increased extracellular salt concentrations (eg, after a meal).

in response, thirst kicks in --> dilutes the extracellular salt concentrations w/o depleting the cells of water

What about cell membranes makes osmotic thirst possible?

They are semipermeable and let some molecules through (such as H2O) but not others (such as salts)

What tendency of molecules makes it possible for increased extracellular salt concentrations to draw water ouf of cells?

- tendency to distribute evenly

Does water enter or leave the cell under hypertonic conditions?

it leaves the cell

(when you're hyper, you lose weight)

What salt concentrations result in hyper/hypotonic conditions?

[salt] higher than 0.9% NaCl = hypertonic

lower than... = hypotonic

What is hypovolemic thirst? What is the % change that causes it?  What are 3 things that could cause that % change?

- reduced volume thirst; if blood volume (which is extracellular) drops by more than 8%.

- could be from an injury, perspiration, diarrhea

What are baroreceptors?  Where are they?

After they relay info to the brain, what responses does the brain have?

What are baroreceptors?  Where are they?

After they relay info to the brain, what responses does the brain have?

They are a specific type of neuron in the blood vessels that detect fluid depletion in hypovolemic thirst.

The brain tries to restore blood pressure by vasoconstriciton & replenish body's water supply by water retention & thirst

What is one other possible cause of hypovolemic thirst?

surgery that blocks water from entering the stomach

What spontaneous mutation do Brattleboro rats have?  What is the consequence of this?

How can their condition be normalized?

What spontaneous mutation do Brattleboro rats have?  What is the consequence of this?

How can their condition be normalized?

- spontaneous mutation in the AVP gene

- all the water they drink is excreted rapidly so they must drink constantly to maintain proper hydration.

- by treatment with AVP

What is diabetes insipidus?  What 2 species does the name apply to?  What are the 2 main symptoms?

- failure to produce or respond to AVP

- rats and humans

- 1) extreme thirst

2) excretion of excessive volume of dilute urine

Name and describe the 3 types of diabetes insipidus.

1) Central DI:  disruption in normal production, storage and release of AVP

2) Nephrogenic DI:  defect in kidney tubules, unable to properly respond to AVP

3) Gestational DI:  enzyme made by the placenta destroys AVP

Treatment for the 3 types of diabetes insipidus?

Central DI:  synthetic hormone desmopressin

Gestational is usually desmo. too.

Nephrogenic DI:  low salt diet; sometimes a diuretic that acts as an anti-diuretic in these individuals

What is food needed for in warm-blooded animals?

- primarily to maintain body temperature

- only a small fraction of it is needed for nutrition

What happens to nutrients after feeding?

- some are made available in the body immediately after feeding

- excess nutrients are stored as glycogen and fat

What does it mean that feeding has to happen proactively and what are the implications of this?

- the animal must physically obtain the food and eat it, both acts which require some energy/nutrients, so feeding must occur before nutrient levels become dangerously low.

- implications: animal must have a way of monitoring nutrient supplies & anticipate future nutrient needs

Where is glucagon made?  What process does it stimulate?

- in the alpha cells of the pancreas

- conversion of glycogen to glucose

(providing ready energy)

Where is insulin made?  What are its effects?

- beta cells of the pancreas

- conversion of glucose to glycogen and fat

(fat is generally for longer-term storage)

- activates glucose transporters to take glucose to cells that need it (ie, if some cells need some glucose/energy, they get it delivered first, then whatever is leftover is what gets stored as glycogen)

What is the definition of diabetes mellitus?  What are its effects?

- insulin production slows or stops (or cells become unresponsive to it)

- glucose can't enter cells so body starves (even tho food/nutrients available)

- excess glucose builds up in body & damages:  kidneys, retina, peripheral nerves, cardiovasc. sys.

- The brain can still use glucose even w/o insulin

Type I diabetes is also known as these 2 other names.

Type II diabetes is also known as __ .

Type I diabetes is also known as these 2 other names.

Type II diabetes is also known as __ .

type I = insulin dependent OR juvenile diabetes

type II = non-insulin-dependent

What happens in type I diabetes?  What is the treatment for it and how does it work?  Why is it not a perfect treatment?

- the pancreas fails to produce insulin.

- can be treated with insulin administration, which directs glucose out of circulation and to tissues in need.

- not perfect bcz cannot mimic the amount and timing of secretions from the pancreas

What is type II diabetes?  What do these conditions lead to?  What is type-II diabetes mainly a result of?  Describe the treatment for it.

- pancreas & insulin release intact but cells have become insensitive to insulin.

- leads to high levels of insulin

- mainly result of obesity

- treated thru weight loss && oral drugs that increase the sensitivity of insulin receptors

What is gestational diabetes?  What are the 3 effects of it on the baby?  How is it diagnosed?  What 3 measures can be taken to treat it?

- hormones from the placenta block the action of the mother's insulin

- 1) macrosomia ('fat' baby);  2) low blood glucose levels at birth;  3) higher risk of breathing problems

- diagnosed by blood tests

- special diet, exercise, & insulin injections

What/when kind of experiment was the precursor to the study of leptin's role in body weight?

When was leptin discovered?

What effect does it have?

Where is it secreted from?

What/when kind of experiment was the precursor to the study of leptin's role in body weight?

When was leptin discovered?

What effect does it have?

Where is it secreted from?

- parabiosis experiment / 1973

- discovered 1994

- potently reduces food intake

- secreted by fat cells

With regard to leptin, what is meant by ob/ob and db/db?  What is the main characteristic of mice with these alleles?

ob/ob = lack leptin gene

db/db = lack leptin receptor

- mice lacking either the gene or the receptor are extremely obese

What is the result of leptin microinjections in the brain?

- it reduces food intake and body weight in ob/ob animals

Why can't we treat obesity with leptin?

obese individuals have more leptin in circulation than non-obese individuals, but they seem insensitive to it

How does estrogen affect food intake and activity?

How does OVX affect rat food consumption & activity?    Effect of E given to OVX hamsters?

How does estrogen affect food intake and activity?

How does OVX affect rat food consumption & activity?    Effect of E given to OVX hamsters?

- decreases food intake / increases activity

- food consumption increases 20%, activity decreases (as would be expected!)

- E to ovx hamsters = increased wheel-running

What does E cause in OVX rats?

What does subsequent P treatment cause?

What is the purpose of this function?

What does E cause in OVX rats?

What does subsequent P treatment cause?

What is the purpose of this function?

- causes fat cells to produce progesterone (P) receptors

- activates P receptors and enhances uptake of fat by adipocytes

- to increase fat stores during pregnancy

With regard to feeding/weight, what does castration do to adult rats?

- lack of T causes them to gain weight more slowly

Feeding/weight:  what are effects of central administration of T (but not DHT) on adult rats?

Via what mechanism?

Feeding/weight:  what are effects of central administration of T (but not DHT) on adult rats?

Via what mechanism?

- T (but not DHT) reduces feeding,

most likely via its conversion to estradiol

Feeding/weight:  Effects of peripheral T administration on adult rats?

- anabolic effects:

- muscles, which have androgen receptors, increase their uptake of amino acids in the presence of testosterone