rest of ch 13

glycogen

stored form of glucose in liver & skeletal muscles

liver glycogen = help maintain blood glucose

muscle glycogen= provides energy for muscle activity

insulin

hormone released by pancreas when blood glucose rises

usually after eating

help cells take up glucose, promote storage, promotes fat storage, supports movement of amino acids into cells

glucagon

hormone released by pancreas when blood glucose is low

signals liver to break down glycogen

helps release glucose into bloodstream

triglycerides

main form of stored fat in adipose cells; 1 glycerol and 3 fatty acids

used for storage when body has excess energy

can be broken down when body needs energy

glycerol

travels to liver & used to make glucose

fatty acids

used as energy source

absorptive phase

after eating; nutrients absorbed from digestive system

glucose & amino acids are available for energy

insulin promotes nutrient uptake & storage

excess energy stored in triglycerides

fasting phase

between meals; nutrients NOT arriving from digestive system

body draws on stored energy

liver glycogen helps maintain blood glucose

fat stores are broken down to supply fatty acids & glycerol

metabolic adaptation

when energy intake falls substantially, body can reduce energy expenditure

reason why its difficult to lose weight

weight change does not always occur in direct proportion to the reduction in food intake

short-term satiety

feeling of fullness that helps bring a meal to an end

duodoenum

first section of small intestine

immediately after the stomach

cholecytoskinin (CCK)

hormone released by small intestine in response to food (fats & proteins)

regulates digestive processes & gallbladder contraction

helps slow aspects of stomach emptying

sends satiety info to brain through the vagus nerve

vagus nerve

carries information between digestive organs and brain

PYY3-36

hormone releases inversely with meal size

helps suppress appetite

leptin

hormone released by fat cells that communicate information about body’s stored energy

helps decrease food intake, inhibit appetite-stimulating neurons in arculate nucleus

increases energy expenditure & metabolic activity

very important in long-term energy balance

endocannabinoids

naturally produced chemical messengers that interact with cannabinoid receptors

act on the same receptors as compounds found in cannabis

2 types (2-AG and AEA)

2-arachidonoylglycerol (2-AG)

involved in signaling in the brain & body

processes including appetite, energy balance, synaptic communication

anandamide (AEA)

naturally occurring signal in body

involved in regulating brain function

trace amounts in chocolate

munchies associated with cannabis

CB1 receptor

major cannabinoid in brain; metabotrophic, G-protein-coupled receptor

when endocannabinoids activate CB1 receptors in feeding-related circuits, they promote eating & influence brain’s response to food

when leptin signaling falls, endocannabinoid signaling….

increases

homeostatic eating

eating to meet body’s energy needs

hedonic eating

eating because food is rewarding or pleasurable

agonist

activates a receptor

antagonist

blocks an agonist from activating a receptor

inverse agonist

reduces a receptor’s baseline activity when that receptor has constitutive eating

can reduce CB1 receptor signaling

hyperphagia

excessive eating/ abnormally increased food intake

lipogenesis

process of making & storing fat

cannabinoid receptors activated trigger this

if CB1 receptors are blocked, it blocks lipogenesis

concerns of CB1

approximately 10% of people taking drug developed a diagnosable disorder

suicide rates went up

behavioral extinction

refers to a reduction in a learned response when the expected outcome no longer follows it

hypothalamus

central part of brain’s regulation of hunger, satiety, metabolism, and body temperature

lateral hypothalamus (LH)

strongly involved in initiating feeding behaviors

2 types of hormones (melanin, orexins)

melanin

peptide NT that can promote feeding

energy balance & can influence food intake

orexins

appetite stimulating; wakefulness & power

orexinogenic = to stimulate eating

ventromedial hypothalamus (VMH)

controls eating in capacity of satiety

rats with damage here tend to overeat

lesion

damage to particular brain region

arculate nucleus (ARC)

near base of hypothalamus

receives information about body’s energy state & contains neurons that can either stimulate or inhibit eating

responds to hormones like leptin, insulin, ghrelin

2 opposing groups of neurons (feeding-promoting pathway and feeding-inhibiting pathway)

feeding-promoting pathway

neurons involving NPY and AgRP encourage eating

feed-inhibiting pathway

neurons involving POMC, a-MSH, and CART that help suppress eating

neuropeptide Y (NPY)

powerful appetite-stimulating NT

stimulates feeding; initially stimulate insulin and glucorticoid secretion, decrease triglyceride breakdown, decrease body temp, reduce energy expenditure

leptin inhibits NPY secreting neurons

agouti-related peptide (AgRP)

works alongside NPY to promote feeding

acts as antagonist at the melanocortin-4 receptor (MC4R)

MC4R

receptor involvd in appetite regulation; normally helps inhibit eating

ghrelin

peptide hormone released by stomach or produced by neurons in brain

rises before meals OR during fasting; helps signal that the body should seek food

opposes PYY3-36

circuit: ghrelin levels increase as stomach empties —> ghrelin promotes activity —> hypothalamus increases drive to eat

cocaine and amphetamine regulated transcript (CART)

peptide NT found in system of arculate nucleus neurons

part of appetite-inhibiting pathway

works with POMC system to help suppress feeling

pro-opiomelanocortin (POMC)

precursor molecule that can process into many biologically active peptides

alpha-melanocyte stimulating hormone (a-MSH)

activates MC4 receptors (help inhibit eating)

type of POMC

POMC neurons —> a-MSH —> MC4R activation —> reduced appetite

opposite of AgRP

paraventricular nucleus (PVN)

hypothalamic nucleus involved in autonomic NS regulation, hormone regulation, feeding-related pathways

receives input from other appetite-regulating neurons

medial pre-frontal cortex

cortical region involved in executive control, planning, decision-making, and regulating behavior

contributes to conscious experience of hunger & decisions about whether to eat

amphetamine

increases signaling involving monoamine NT’s (dopamine & norepinephrine)

increased alertness/ stimulation, reduced appetite, increased energy expenditure

at first, food intake & weight increase

over time, tolerance reduces appetite-suppressing effects

leads to rebound eating & weight gain

tolerance

some dose of a drug produces a reduced effect after repeated exposure

initial appetite suppression may become weaker as body adapts

GLP-1

glucagon-like peptide 1

hormone released by cells in gastrointestinal tract after eating

opposes ghrelin’s hunger-promoting effects & suppresses appetite through pathways involving POMC & CART and nucleus of solitary tract

reduces food intake, increase feelings of fullness, slow stomach emptying

nucleus of solitary tract

brainstem region that receives information from digestive system

semaglutide

long-acting GLP1 receptor agonist (activates receptor)

mimics important effects of body’s natural GLP1 signal

2 brand names (ozempic and wegrovy)

GLP1 activation —> increased influence of appetite-suppressing circuits —> reduced food intake

sleeve gastrectomy

removes large portion of stomach; leaves a narrower, tube-shaped stomach

reduces stomach capacity

reduced ghrelin production (reduces hunger signaling)

NOT reversible

gastric bypass

surgeon creates small stomach pouch connected to section of small intestine

change how much food can be eaten at one time and alters nutrient absorption & gut-hormone signaling

gastrointestinal liner

liner placed inside part of small intestine

acts as barrier between food & intestinal surface

does NOT require removing portion of stomach

anorexia nervosa

originally associated with little to no appetite

can occur alongside depression, anxiety, OCD

bulimia nervosa

recurring episodes of binge eating & compensatory behaviors (excessive exercise, purging, laxatives)

repeated vomiting exposes mouth, teeth, and esophagus to stomach acid