Adipose tissue Flashcards
white adipocytes description
STRUCTURE: large lipid droplet made of TAG, low mitochondria, proteins contained are mainly for the manipulation of TAGS + enzymes for the formation of glycerol3P
FUNCTIONS:
1. main way in which the body accummulates substrates that can be used for energy production - hence STORAGE
brown adipocytes description
STRUCTURE: many small TAG lipid droplets (for faster release), large amount of mitochondria, they express UCP1
FUNCTION: thermogenesis
beige adipocytes description
phenotype inbetween the white and brown, with multiple small droplets of TAGs + more mit than white
pink adipocytes description
present solely in the breasts for milk production
HENCE contain milk granules
REMINDER: milk starts from glucose, then galactose, then lactose and ALSO contains sialyllactose which offers sialic acid to the baby (important for production of glycoproteins and glycoconjugates in mammals)
cell origin of adipocytes
MESENCHYMAL CELLS: give rise to all typs depending on which stimuli they are exposed to
white and beige adipocytes are reversibly able to change into eachother
!! there is also a way DIRECTLY to produce WAT/BAT from endothelial cells and satellite cells in muscles
FACTORS which causes the conversion of precursors into white vs brown adipocytes
WHITE: a high fat diet with high glucose and insulin
BROWN: exposure to low temps (cold) and certain GFs
Effects of increasing WAT (3, with reasons)
- WEIGHT GAIN
- DECREASED GLUC HOMEOSTASIS
- REDUCED INSULIN SENSITIVITY
REASONS:
1. high level of FAs in liver inhibit insulin receptor to recognise insulin and respond
2. high WAT induces the production of TNFalpha. This promotes GM3 synthesis which blocks the insulin receptor. It also creates proinflammatory signals which acts against insulin sensitivity.
Effects of increasing BAT (3, with reasons)
- WEIGHT LOSS
- INCREASED GLUC HOMEOSTASIS
- INCREASED INSULIN SENSITIVITY
REASONS:
1. BAT doesnt release FAs so there are less present in the liver, and there is no inhibition of the insulin receptor
2. having a higher proportion of brown and beige adipose means having a lower proportion of WAT - this means that less pro-inflammatory signals are produced, and less FAs will be released - this has a positive effect on the insulin receptor
localisation of the diff types of adipose tissues
PINK - breasts
BROWN/BEIGE: paravertebral and around clavicle
WHITE: can be either subcutaneous or visceral
what is the diff between subcutaneous or visceral WAT
SC: an excess can have beneficial properties on insulin and glucose homeostasis
VC: an excess is dangerous for insulin and glucose homeostasis, can cause CVD and obesity
REASON FOR THIS OPPOSITE FUNCTION: they receive diff signals from the organs and tissues around them - visceral WAT produces inflammatory cytokines and SC doesnt
glucose entrance and fate in WAT
ENTRANCE: insulin dependent (GLUT4)
immediately phosphorylated and then can be used for 4 processes:
1. glycolysis (produces acetyl coA, pyrivate and ATP)
2. glycerol3P formation through DHAP (there is no glycerol kinase for direct phosphorylation)
3. PPP (NADPH formation for FAS)
4. FAS - since there are fwe mitochondrias the krebs cycle gets saturated fast and acetyl CoA leaves mit as citrate to go into the cytoplasm
what are the conditions necessary for FAS and TAG storage in WAT
INSULIN PRESENT: this ensures we are in fed conditions and have available glucose
if we were instarvation we wouldnt want to uptake glucose and use it up to make TAGs bcos then we would induce hypoglycemia and the brain/RBCs supply would be depleted
3 origins of the FA stores in WAT TAG lipid
- dietary FA transported by chilomycrons
- FAs neosynthesised by liver transported by VLDLs
- FAs biosynthesised from glucose inside the WAT themselves
how are lipids imported into the WATs
LIPOPROTEIN LIPASE expressed on cell membrane
-recognition of chylomicron APOC2
-recognition of VLDL APOB
-degradation of the TAGs contained in these lipoproteins into FAs and glycerol
-the glycerol is mobilised and goes to liver
-the FAs are reformed into TAGs and incorportated into the lipid droplet
how is WAT FA synthesis regulated
SHORT TERM: via acetyl coA carboxylase enzyme (which changes acetyl coa to malonyl coa):
!! this enzyme is active when dephosphorylated.
-insulin activates it
-glucagon inhibits it
-citrate and ATP activate
-acyl Coa chains (ie FAs) inhibit it for -ve feedback
LONG TERM:
-prolonged glycemia and prolonged insulin ACTIVATE it
lipolysis in WAT
HSL - hormone sensitive lipase allows the break down of TAGs (using perilipin) into MAGs and glycerol. the glycerol is released into the blood and FAs release in blood and transported via serum albumin.
activated by glucagon (cAMP/PKA mediated) and inhibited by insulin
function of WATs as secretory organs
ACTIVE IN HOMEOSTASIS: release a large amount of GFs
this can be good for cell proliferation, but bad in excess bcos the prob of mutation increases and it can cause cancers
effects of leptin on WAT
LEPTIN: inhibits hunger and allows satiation
-increases lipolysis and decreases lipogenesis - hence there is decreased food uptake and increased energy expenditure
thermogenesis in WAT
only happens in EXTREME cold conditions
FUTILE CYCLES: the concomitant catabolism AND synthesis of FAs- this process repeated over in a cycle releases energy in the form of heat
describe how BAT produce heat (6 STEPS)
- cold is sensed by SNS
- NE release which has a cAMP/PKA response
- this activates HSL lipolysis BUT the fatty acids mobilised remain within the cell (dont exit)
- FAs undergo beta oxidation for acetyl coa production which then moves to the krebs and ETC
- IN THE ETC: in the IMM there is the UCP1 which forces protons to bypass the ATPsynthase and doesnt allow correct H+ gradient to be established.
- this disruption of the gradient means instead of ATP heat is produced
