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30 Cards in this Set

  • Front
  • Back
how are fats transported, stored, absorbed?
released bile salts..
lipases
fats packed into chylomicrons- transported out to any tissue
in liver they are made into VLDLs


in adipose tissue they're stored as triglycerides
transported as fatty acids bound to albumin
how is SREBP regulated? what does it regulate? how do dietary fats play into this regulation?
Gene dealing with fatty acid synthhesis
overexpression of this gene increases triglyceride content in the liver

transcription factor involved in lipogenesis
turned on by insulin
inhibited by polyunsaturated fatty acids
polyunsaturated fats inhibit the expression of SREBP
what is stearoyl-CoA desaturase?
why is this an important enzyme?
how is it effected by dietary fat??
enzyme determining if fat is going to be stored or metabolized
takes saturated fat and turns it into monounsaturated fat so it can be stored in a triglyceride

polyunsaturated FA inhibit expression of stearoyl-CoA desaturase (has sterol response element in it)
name the different PPARS
PPAR alpha- important in liver
PPAR beta- important in muscle
PPAR gamma- important in adipocytes

increased expression of genes involved in transporting fats from blood into cells
lipoprotein lipase gets turned on
translocase gets turned on

alpha, beta- get into cell genes that oxidized get turned on, controls lipoprotein lipase
gamma- genes that have to do with storing fat get turned on
why is PPARgamma important in diabetes?
you get increased differentiation of fat cells that are more insulin sensitive
increased expression of adiponectin
decreased expression of resistan
increased expression of glucose transporter
what are the health benefits of omega 3 and omega 6?
n-3: reduced inflammation
n-6: decreased amount of LDL cholesterol
why are trans fats detrimental to human health?
(cholesterol effect, inflammation, diabetes)
increases LDL doesnt increase HDL
increased inflammation
why is vit C important in biology?
the main antioxidant
it can be regenerated
it doenst become an oxidant itself in the body
humans cant synthesize it
why is vit C an ideal antioxidant? what are some benefits associated with vit C as an antioxidant?
vit C is transported by GSH (glutathione) which is inheritantly low in plasma

helps fight UV radiation

helps down regulate inflammatory agents
what transcription factors can vit C influence? what pathways are influenced?
inhibits expression of c-Jun and c-Fos
which are the factors that constitute the AP-1 complex

NF-kB
ICAM

important in cellular transformation and and progression of cancer
what is the function of biotin?
it is a cofactor responsible for carbon dioxide transfer in several carboxylase enzymes involved in energy metabolism
what genes involved in energy metabolism are effected by biotin? what is the consequence of this regulation?
biotin is like insulin in that induces the same genes that make glucokinase
and neg induces enzymes that help gluconeogensis (decreases effect of PEPCK)

been found that diabetics have had low levels of biotin

it increases glycolysis
how is biotin involved in the histone code?
existence of biotinylated histones: H1, H2A, H2B, H3, H4
10 lysine residues on specific histones are targets for biotinylation
some of these lysine sites are also sites for acetylation/methylation

acetylation of lysine can effect biotinylation of adjacent lysine residues
what is the biological function of B6?
PLP is the active form of B6 and is an important cofactor in amino acid metabolism (transamination, deamination)

can clear homocysteine to cysteine
B6 can influence regulation of what class of receptors?
it can bind to steroid receptors thus disallowing steroids to bind
what role does B6 play in homocysteine metabolism, why is this important?
helps in metabolism of homocysteine.
lots of homocysteine in the blood has connections to increased CVD and stroke

heart disease went down with women who ingested more vit B6
what are the significant forms of dietary vit A - what forms are relevant to regulation of gene expression?
butter, liver, carrots, broccoli, tomatoes

we can get preformed vit A from animal sources and we can convert alpha and beta

retinoic acid
retinol, retinal, retinoic acid, and related compounds are known as retinoids
vit A turns on many genes, many of these genes are associated with what?
cell differentiation
know the pathway of retinoic acid receptors, vit A, and effects on chromatin/gene expression
refer to paper
what is the beta-carotene/cancer story?
beta-carotene was once thought to be a big fighter against cancer
however, in smokers it increased their risk for cancer
later discovered that the smoke inside the lungs leading to oxidative stress caused a change in beta-carotene metabolism which can increase the mutagenicity of tobacco carcinogens
what is the lycopene/cancer story?
helps in prostate cancer
what factors influence the lycopene content of foods?
when its picked- vine ripened
how its grown
if its processed
what carotenoids have been studied in relation to macular degeneration? and why?
is there good evidence for protection?
zeroan
lutein

evidence not great
where do our gut microflora come from? where is the primary location of most?
come when were born

our environment, mothers milk

colon
what are some phenotypic features of gnotobiotic mice
big bellies
serious immune system problems
antibody deficiency
higher susceptibility to infections
reduced number of peyer's patches
reduced number of CD4 T cells critical for immune response
what are some factors that can change microbiotia populations in humans?
host genotype
host environment
host lifestyle
host pathobiology
host physiological status
what is the general difference in the gut microbiotia of lean/obese people?
microbiotia of obese people is more efficient at extracting energy from food than lean microbiotia

there is changes in relative abundance of bacteriodetes and firmicutes- more firmicutes in obese and less bacteriodetes
what are some ways the microbiotia can effect obesity?
-it is more efficient in obese people
-fermentation of polysaccharides that cannot be digested by host
-subsequent absorption of monosaccharides and short chain fatty acids and their conversion to more complex lipids in liver
-microbial regulation of host genes that promote deposition of lipids adipocytes
-
how is diet/gut microbiotia related to disease, inflammation, type 2 diabetes?
fat enriched diet-> increased concentrations of LPS in plasma ->metabolic endotoxemia

during high fat feeding -> increased gram neg to gram positive ratio --> aka more LPS (gram neg) type bacteria

translocation of LPS in gut may be involved in metabolic disease leading to inflammation

dietary fibers can reduce effect of high fat diet, and bring gram pos/neg ratio back to normal and plasma endotoxemia

thus intestinal microbiotia could be responsible for changes of metabolic endoxtemia and for the onset of the corresponding diseases
what is clostridium difficile infection? how is it being treated?
infection caused by disruption in the microflora- causes diarrhea, death

it can be treated by taking metronidazole or vancomycin
or FECAL TRANSPLANT