Fat as an Organ Flashcards
Functions of adipose tissue?
-Mechanical cushioning
-Thermal insulation
-Energy store
-Endocrine organ
x2 types of adipose tissue?
-White
-Brown
White adipose tissue?
-Fewer mitochondria
-Unilocular - contains single fat/lipid droplet
-Controlled storage & release of fat
Brown adipose tissue?
-Many mitochondria
-Multilocular - many fat/lipid droplets
-Metabolism - generates heat
-Vital in newborns - as have high SA:body mass ratio
-Not much/any in adults
-Develops from muscle cell progenitors
Brown adipose tissue?
-Many mitochondria
-Multilocular - many fat/lipid droplets
-Metabolism - generates heat
-Vital in newborns - as have high SA:body mass ratio
-Not much/any in adults
-Develops from muscle cell progenitors
What type of fatty acids are mostly in fats (triglycerides)?
Saturated (no double carbon bonds)
O2 consumption of white adipose tissue - high or low?
Low
Purpose of white adipose tissue???
Integral part of whole body carb & fat metabolism
Demonstrate the carb & fat metabolism - white adipose tissue is involved in.
-Liver metabolises fats -> forms FAs
Route of FAs:
-FAs ->(B-oxidation) acetyl CoA -> citric acid cycle - energy
-FAs -> acetyl CoA -> ketone bodies
Acetyl-CoA is converted to ketone bodies instead of using in citric acid cycle if acetyl-CoA exceeds citric acid capacity
-FAs -> triacylglycerols -> store in muscle
-FAs + glycerol -> triacylglycerols -> store in adipose tissue = ANABOLISM - regulated by INSULIN
-Triacylglycerols (TAG) -> FAs in adipose tissue (conversion done by HSL)
HSL = Hormone Sensitive Lipase -> CATABOLISM - regulated by GLUCAGON & ADRENALINE
-Glycerol from adipose tissue can be sent to liver & converted into glycerol - for gluconeogenesis (-> glucose)
-Glucose (may come from glycogen - glycogenolysis) -> pyruvate (glycolysis) -> acetyl CoA… (energy or ketone bodies)
-Glucose (may come from glycogen - glycogenolysis) -> pyruvate (glycolysis) -> acetyl CoA -> FAs -> triacylglycerols (store in muscle or add glyceol to FAs & store in adipose tissue)
-Lactate -> pyruvate -> acetyl-CoA…/glucose
What does muscle generally use for energy supply in fasting state or when doing strenuous exercise?
FAs & ketone bodies - as is glucose preserving (low blood glu so avoid using here)
Pyruvate can be converted to lactate in anaerobic conditions to generate muscle energy
-> lactate then sent to liver - converts it to pyruvate & then to glucose (CORI CYCLE)
What does muscle generally use for energy supply in fed state?
Glucose metabolism -> so converts it to pyruvate & then to acetyl-CoA
How do fat cells develop into mature white adipose tissue?
- Hormonal signals cause differentiation of fibroblast-like precursors -> into adipocytes
- Adipocyte gene expression pattern altered & will begin to accumulate lipid droplets
- Lipid accumulates - droplets merge -> form mature fat cell = triglyceride droplet & nuclei
- Mature fat cell can not now divide
- Mature fat cells hypertrophy & hyperplasia
(is no limit to amount of white adipose tissue that can be stored -> -ve for trying to lose weight)
Thrifty genes?
Genes which enable efficient food utilisation & fat deposition when food is abundant -> increases survival chances in times of famine (scarce food)
–> so these genes allow storage in times of plenty for survival in times of famine
–> an evolutionary advantage
BUT -> these genes are disadvantageous in current times when food is always in abundance & energy rich & high calorie diet & reduced energy expenditure -> leads to fat deposition/storing fat readily & not break down readily -> leads to obesity & diabetes - but means in famine = more likely to survive
Changes in adipocytes in obesity?
- Modest weight gain -> adipocytes increase cell size
- Adipocytes will eventually reach a max. size
- Continued weight gain -> causes recruiting of pre-adipocytes to undergo differentiation
Now - either:
-Continue to gain weight more -> pre-adipocytes grow to max size -> & continue…
or
-Lose weight -> will always have same number of adipocytes -> they will just decrease in cell size
Metabolic intergation?
Metabolism of carbs, lipids, proteins (x3) are coordinated & well regulated to meet bodily requirements -> especially energy need under various conditions
What other peptide hormones do adipocytes (of WAT) produce?
Role of hypothalamus in weight regulation?
*Lateral hypothalamus = ‘hunger centre’ -> animal w/ lesion here lose weight - become anorectic (no appetite!!!)
*Venteromedial hypothalamus = ‘satiety centre’ -> animal w/ lesion here overeat - become obese (no identification of satiety)
Appetite signals other than leptin & hypothalamus?
*Grehlin -> from stomach = hunger
*Glucose, insulin, PPY (pancreatic polypeptide), CCK (cholecystokinin) = fed
*Stored energy -> products of adipose tissue - leptin & RBP4 - produced in proportion to fat content
RBP4 -> reduces tissue insulin sensitivity -> reduce feelings
Pathway of hormones affecting appetite?
- Act on hypothalamus (i.e., ghrelin, NPY, leptin, PYY, insulin)
- Leptin & insulin dec. appetite by inhibitory action on NPY/AgRP neurons
- -> signal satiation
- But when stomach is empty -> ghrelin signals - activates NPY/AgRP neurons
Fat fat cells vs thin fat cells?
Fat - meaning larger & thin meaning smaller -> fat cells
-Fat –> promote insulin resistance & trigger low-grade chronic inflamm -> lead to T2D, high BP, CVD & inc cancer risk
-Thin -> more benignly regulate metabolic interplay between tissues -> release adiponectin = promotes glucose uptake into tissues
Carb metabolism pathways in adipocyte - FED?
*Inc glucose transport - inc insulin => glucose influx via insulin- sensitive transporter
*Inc glycolysis - inc intracellular glucose -> causes enhanced glycolysis -> supplies glycerol phosphate for triglyceride synthesis
*Inc hexose monophosphate pathway (HMP) - metabolism of glucose via HMP produces NADPH - essential for fat synthesis
Fat metabolism pathways in adipocyte - FED?
*Inc FA synthesis - from acetyl-CoA = major FA source in human dipose tissue -> only when re-feeding after a fast.
*Dec triglyceride hydrolysis - inc insulin levels favors the dephosphorylated (inactive) state of hormone-sensitive lipase - preventing TG degradation & promoting storage
Carb metabolism pathways in adipocyte - FAST?
Glucose transport & metabolism are depressed due to low insulin -> causes dec FA & triglyceride synthesis
Fat metabolism pathways in adipocyte - FAST?
*Inc triglyceride hydrolysis - activates hormone-sensitive lipase via phosphorylation -> leads to hydrolysis of stored TG. This activation is enhanced by noradrenaline released from sympathetic nerve endings in adipose tissue
*Inc FA — FA liberated by TG hydrolysis are released into the circulation and transported to other tissues for use as fuel. The glycerol released by TG hydrolysis is used by liver for gluconeogenesis
*Dec FA uptake - in fast state, lipoprotein lipase activity in adipose tissue is low, and lipoprotein TG is not available for TG synthesis in adipose tissue
3 types of body shape?
