homeostasis (pt.2)

brain

major consumer of and needs substantial energy (glucose or ketones) to function

continous

fluctuates

never

the need for energy is BLANK, but energy acquistion is episodic and BLANK; energy acquistion and energy expenditure are BLANK completely balanced.

post-prandial 

post-absorptive

two phases of energy-balance well fed state; after eating a meal, these are the two phases of energy utilization and storage:

post-prandial

occurs immediately after ingestion; food is broken down into metabolic fuels which enter the blood stream

post-absorptive

excess energy from a meal is stored; done by INSULIN

insulin

released from pancreas (beta cells)

• lowers blood glucose levels

functions of insulin

1. facilitates uptake of glucose into tissues for oxidation

2. converts glucose to glycogen for storage; only responsible for energy storage

3. necessary for storage of fat in adipose tissue

glycogenesis

conversion of glucose into glycogen (energy storage)

lipogenesis

storage of fat into adipose tissue

cephalic

GI phase

two phases of insulin release from pancreas

cephalic

occurs as a result of sensory stimuli associated with food intake; even before nutrients have arrived in the digestive system, insulin-induced reduction in blood levels of metabolic fuels may increase hunger

GI phase

storage of excess nutrients occur when insulin is released to absorption of nutrients from the gut 

fasting state

influx of energy no longer exceeds body’s energy usage; the body must shift from putting energy into storage into getting it out of storage

• glucagon

glucagon

released from pancreas (alpha cells)

• facilitate glycogenolysis, lipolysis, gluconeogenesis and ketogenesis

• generate metabolic fuels for energy expenditure - increase blood glucose levels 

glycogenolysis

breakdown of glycogen stored in the liver to glucose to power the brain

lipolysis

breakdown to adipose tissue into free fatty acids and glycerol to fuel peripheral tissues

gluconeogenesis

back up system used in fasting; amino acids in liver converted to glucose - leads to production of ketone bodies as a side reaction

ketone bodies

generated via ketogenesis; power the brain when glucose levels are low 

diabetes

trouble moving surplus glucose out of the blood; result in symptoms such as elevated appetite, increased thirst/urination and high blood glucose

hyperglycemia

high blood glucose; toxic and can lead to serious health problems such as neuropathy, heart disease, stroke, blindness and kidney failure

type 1 diabetes

insulin dependent mellitus; autoimmune disorder in which beta cells of the pancreas are destroyed by the immune system

type 2 diabetes

tissue develops a resistance/insensitivity to insulin; incresed insulin secretion

hemoglobin A1c

diabetes diagnosis; measures average amount of sugar in blood over the past three months

glucose tolerance test

diabetes diagnosis; measures how well your body processes glucose 

anti-body test

type 1 diabetes diagnosis only; immune system makes antibodies that act against the cells in the pancreas that make insulin and these antibodies can be detected in blood

type 1 treatment

montioring glucose levels with glucometer and replacement of missing insulin via injection; diet/exercise

type 2 treatment

early stages can be controlled by diet/exercise; if left uncontrolled the pancreas can stop producing insulin and thus requiring exogenous insulin treatment

arcuate nucleus of hypothalamus

portion of the hypothalamus that controls food intake and feeding behaviors

two circuits

1. feeding stimulatory circuit

2. feeding inhibitory circuit

feeding simulatory circuit

anabolic; produces two orexigenic peptides that stimulate food intake; reduce metabolism and promote weight gain

NPY and AgRP

orexigenic peptides produced by feeding stimulatory circuit 

feeding inhibitory circuit

catabolic; produces two anorexigenic signaling molecules that inhibit food intake, increases metabolism and promotes weight loss

POMC

CART

two anorexigenic signaling molecules produced in feeding inhibitory circuit

insulin and leptin

both circuits of the ARC are modulated by these peripheral adiposity signals that cross or are transported across the blood brain barrier and convey information about the body’s energy reserves 

• low when underfed and high levels when well-fed

well-fed state

high insulin and leptin; decrease in feeding behavior by inhibiting NRY and AgRP and activating CART and POMC

underfed state

low insulin and leptin; increases feeding behavior by activating NPY and AgRP while inhibiting POMC and CART

ghrelin

hunger hormone produced in stomach; acts in opposition of leptin and stimulates feeding by activating NPY and AgRP neurons in ARC

NTS

nucleus of solitary tract; receives and integrates andiposity information from ARC with peripheral satiety signals

OVX

leads to increased food intake/body mass - due to low levels of estrogen

estrogen

prevents increased food intake/body mass

• increase enzyme activity in fat tissue and this leads to less fat storage

progesterone

does not prevent effects of OVX and induces increased body mass

• decrease enzyme activity in fat tissue and leads to more fat storage