Lecture 14 Flashcards
thyroid hormone
what
where
composed of what
key hormone that regulates metabolic rate
butterfly shape on trachea
2 lobes connected by isthmus
follicles = colloid filled = product thyroglobulin
parafollicular cells = located in space in bn follicles = product calcitonin (reg blood Ca levels)
hormones made
Thyroxine = T4 = primary product
- 4 iodines, travels in circ, converted to t3,
doesn’t bind as easily to make as much of an effect
triiodothyronine = more active, T4 is converted to T3
binds more easily to receptors in nucleus to exert an effect
synthesis of thyroid homones
- Iodide is picked up from blood stream and moved into lumen
- thyroglubin is synthesized and moved to lumen
- Iodide is oxidized to from iodine
- Iodine is att to tyrosine in colloid
= tyrosine is a part of the thyroglubin molecule
= can att 1 or 2 Iodine per tyrosine - if two di = T4, if one di/ 1 mono = T3
- picked up by vesicles, fused by lysosomes, chopped thyroglobulin innate T4 or T3
released into circ system = exerts effect
metabolic process reg by thyroid hormone
metabolism, body temp reg, growth, development and tissue maintenance
a. increase basal metabolic rate + body heat production = stimulates glucose oxidation** = calorgenic effect
** stim tissues to breakdown glucose faster = more ATP + more heat = burning calories
b. inc number of NE/E receptors in blood vessels = inc heart rate = maintains bp
c. reg of tissue growth and develpemt
skeletal and NS development and maturation
+ reproductive fn.
transport nad reg of TH
initial response to Thyroid Stimulating hormone is to secrete stored hormone, colloid is then restocked
enough stored hormones in colloid for months
transported in blood bound to thyroxine binding globulin (TBG)
T3 binds better to receptors than t4
peripheral tissues convert t4 to t3 = deiodinase enzymes.f
flow chart of production
hypothalamus secretes TRH that stimulates the anterior pituitary to release TSH
TSH works on the thyroid glands to stimulate TH
TH works on target cells
TH have - feedback, inc in blood = stop producing more.
why is t3 more stable than t4
binds more readily to receptors
if someone was thyroid hormone deficient, would you give t3 ot t4
t4, longer half life, get better binding and tissues can convert to t3 for better response.
hypothyroidism cause
deficits in TSH/TRH secretion, not enough Iodine, Autoimmune thyroiditis (inflammation in thyroid due to immune attack) and removal of thyroid gland
hypothyroidism
symptoms
low BMR =not gen heat, feeling cold
dry skin, puffy eyes, tiredness,
constipation (smooth muscles not working as well)
lack of iodine = result?
hw do we get it ?
3rd world countries?
result = goiter
follicle cells keep making thyroglobulin but can’t iodinate it, TSH keeps stimulating glands,
with Iodine supplementation is reversible
or given TSH/T4 supplements
we get it from table salt = easy way to prevent hypoT.
3rd world = don’t have I in salt
congenital iodine difficientcy syndrome
in infants
can be due to genetic deficiency in fetal thyroid gland or not enough intake of I by mother
- essential for NS and skeletal development
not enough = improper growth and development of CNS*
** imp for myelination of axons, formation of synapses, + int of dendrites = communication - short, disproportionate body and intellectual disability
can be reversed if early w hormone therapy
hyperthyroidism
most common = graves disease
autoimmune disease: hyper functioning thyroid
antibodies bind to TSH receptors on thyroid cells
antibodies mimic TSH, but aren’t under neg. feedback so continuously stim TH prod. = high levels of TH
effect = hot all the time, in heart rate, more nervous bc brain is working harder, weight loss (more calorgenic effect),
buildup behind eyes so they protrude.
goiter = cuz antibody is accumulating TSH, so making thyroglobulin faster than needed.
would need to have thyroid removed/destroyed
calcitonin
hormone from parafolliclar cells of thyroid flands
lowers blood Ca
1. inh bone resorption (stops break down of bone
2. stim Ca uptake and incorporation into bone
inc blood Ca levels = secretion of calcitonin
esp imp in childhood for bone/skeletal development, not so much in adults.
metabolic rate
boys rate of energy expenditure per hour
= total heat produced by all chemical rxns and mechanical work of the body
basal metabolic rate
rate at which energy is epctended by the body per unit time under controlled conditions
E used to maintain only essential activated = energy cost of living
kcal/m^2/hr
influence on BMR
SA, age, gender, stress, hormone
SA = influences the rate of heat loss, major determining factor
inc in SA = inc in BMR
age = inversely proportional to age (growth when young, muscle atrophy in elderly(
higher in makes than females.
reg og metabolic rate
TH = most imp
stimulates all cells to inc O consumption by speeding up use of ATP (with the Na/K pump)
less ATP = resp inc = more ATP made = heat as a by product
hyperthyroidism = high mR = weight loss, hot = muscle atrophy
hypoT = low MR = slow metabolism = obesity = cold
Stress = inc MR
NE and E inc MR by inc fat breakdown
= heat as by product
Fever = assoc w higher MR
TMR
total rate of kcal consumption for all ongoing activies
majority is the BMR
inc in TMR by excerise (work done by muscles)
dietary or food induced thermogenic = eat = E consumed ot digest food = inc in TMR (bc of inc activity of the liver)
fasting/low calorie intake = slows MR = slower breakdownn of food reserves.
energy intake formula
energy intake = total energy output + energy storage
energy intake = E liberated during food oxidation (E released when bonds of complex molecs are broken)
E output = E lost as heat + E to do work (ATP)
E storage = excess stored as fat or glycogen
heat = warms tissues and blood
allows MR to occur efficiently
reg of food intake
when energy intake = output , weight stays stable
body weight can be misleading, musclee is denser than fat tissue
apetite and hunger and satiety
apetite = desire for specific types of foods
dependent on memory and associations, emotional/env conditions
doesn’t reflect bodys caloric needs
hunger = physiological need to eat to maintain E levels
satiety = satisfucntion of hunger = full
reg of eating behaviour overview
not completely understood
neural signals from GI tract
hromones
blood levels of nutrients
Brain stem and hypothalamus = reg eating behaviours
Hunter promotion = neurons of arcuate release NPY and AgRP that stim LHA to release orexin = activate hunger
Satiety promotion = POMC/CART neurons suppress apetite = leasing alpha MSH and CART = work on to sim release of CRH = suppress aptitude
