Cov khoom

Kev rog rog, hom 2 mob ntshav qab zib mellitus thiab hyperlipidemia feem ntau sib koom ua ke thiab cuam tshuam nrog kev mob hnyav thiab kev tuag.Kev noj cov carbohydrate refined thiab tshwj xeeb tshaj yog fructose tau nce ntau nyob rau hauv xyoo tas los no thiab tau ua rau muaj kev nce ntxiv ntawm kev rog thiab ntshav qab zib.Kev tshawb fawb ntawm tib neeg thiab tsiaj txhu tau pom tias kev noj zaub mov ntau ntawm fructose tau zoo cuam tshuam nrog nce dyslipidemia, insulin tsis kam, thiab kub siab.Metabolism ntawm fructose tshwm sim feem ntau hauv daim siab thiab siab fructose flux ua rau txhim kho hepatic triglyceride tsub zuj zuj (hepatic steatosis).Qhov no ua rau muaj kev cuam tshuam cov piam thaj thiab lipid metabolism thiab nce proinflammatory cytokine qhia.Ntawm no peb qhia tau hais tias fructose hloov cov piam thaj-stimulated qhia ntawm activated acetyl CoA carboxylase (ACC), pSer hormone rhiab heev lipase (pSerHSL) thiab adipose triglyceride lipase (ATGL) nyob rau hauv hepatic HepG2 los yog thawj kab mob siab hauv vitro.Qhov no tau cuam tshuam nrog kev nce de novo triglyceride synthesis hauv vitro thiab hepatic steatosis hauv vivo hauv fructose- piv rau cov piam thaj-piv thiab cov zaub mov noj zaub mov.Cov kev tshawb fawb no muab kev nkag siab tshiab rau hauv cov txheej txheem koom nrog hauv fructose-mediated hepatic hypertriglyceridemia thiab txheeb xyuas fructose-uptake raws li lub hom phiaj kho mob tshiab rau cov kab mob lipid.