Obesity Flashcards
how do peroxisomes function in lipid metabolism?
oxidize very long FAs (20+ C) and synthesize phospholipids
how does leptin work?
leptin is released from adipose tissue when E levels are high (lots of TAG deposition)–> acts on hypothalamus–>released neurotrans–>decrease appetite and increase E expenditure–> overall decease in body weight
the more adipose tissue you have, the more leptin you secrete
ya
leptin deficiency in humans is very rare
ya
why wouldn’t leptin injections work in obese individuals?
they already have high levels of leptin–>the receptors in the hypothal don’t respond to leptin, so the same affects of having no leptin are there
what are the stages of adipogenesis?
mesenchymal stem cells–> adipoblasts–>preadipocyte (PPARg levels increase)–>committed pre-adipocytes–>adipocytes
what is the role of PPAR?
master regulator of adipocyte differentiation–>regulates gene expression for lipid and carb metabolism; controls peroxisomal proliferation
what is PPARg?
group of nuclear receptors that are transcription factors
PPARg protein–domains?
DBD and ligand-binding domain
what is PPARg’s ligand?
polyunsat FAs
describe PPARg regulation
PPARg binds polyunsat FA; combines with RXR (which has bound to retinoic acid–all together called PPRE)–>dimerization + cofactor–> induces gene expression of LPL, etc anything to help differentiation of adipocytes
what is the con seq PPARg+PPRE binds to?
AGGTCA N AGGTCA
what is rosiglitazone?
PPARg agonist–>forced differentiation of preadipocytes; lowers BG, insulin sensitizer,
PPARg KO mice?
no differentiation of adipocytes–>no fat storage–>all FAs go to liver–> blood TAG levels very high;
why are obese individuals often diabetic?
lipotoxicity–>excess fats from storage spill ut into other tissues–> liver/muscle–> impaired insulin-stimulated glucose transport
Pancreas–>diminished insulin secretion
