Kwiminyaka emininzi, kuye kwaba yinto eyinqobo yokuba i- HDL ye-cholesterol yinto ehle "yeyona" ye-cholesterol, ukuba amazinga akho e-HDL aphezulu kakhulu engozini yomzimba wakho, kwaye ukuphakanyiswa kwamazinga e-HDL ye-cholesterol yinto efanelekileyo kakhulu. Kodwa iziphumo ezidakisayo ezivela kwizilingo zamanyango ezinje ziveze ukuba loo mfundiso iyayibuza.
Kutheni i-HDL icatshangelwa "Yilungileyo"
I-cholesterol ye-HDL icingelwa ukuba iqhube i-cholesterol engaphezu kweendonga zemigudu yegazi, ngoko isisuse apho ingaba negalelo kwi- atherosclerosis .
Ngaphezu koko, kwizifundo ze-epidemiological ezibandakanya abantu abangaphezu kwe-100 000, abantu abane-HDL ye-cholesterol amazinga angaphantsi kwe-40 mg / dL babenomngcipheko we-heart high kakhulu kunabo abanamazinga aphezulu e-HDL. Oku kunjalo nangona i- LDL ye-cholesterol ("i-bad" ye-cholesterol) ephantsi. Amazinga e-HDL aphezulu adibaniswe nomngcipheko omncinci webele, i-colon kunye nomdlavuza wamaphaphu.
Ukusuka kwezo zifundo kuvela inkolelo yokuba ukuthatha amanyathelo okunyusa amazinga e-HDL yinto efanelekileyo. Le yinto ebizwa ngokuba yi-HDL hypothesis: iphakamileyo lamazinga akho e-HDL, isichengeni senhliziyo yakho esezantsi.
Amanqanaba angama-HDL anganda njani?
Iinqanaba ze-HDL zibonakala zichithwe kakhulu ngumxube wezinto eziphilayo kunye nemvelo. Abasetyhini banamathuba aphezulu e-HDL kunamadoda (ngo-10 mg / dL).
Abantu abagqithise ngokweqile, abanomdla, okanye abanesifo sikashukela okanye isifo se- metabolic bavame ukuba namazinga aphantsi kwe-HDL.
Utywala lubonakala ukwandisa i-HDL ngemali encinci; Amafutha atshintshe ekudleni adinciphisa.
Izidakamizwa eziqhelekileyo ezisetyenziselwa ukunciphisa i-cholesterol ye-LDL ineempembelelo ezincinci kumazinga e-HDL. Izitatimende , ezona zisetyenziswa kakhulu izidakamizwa zokunciphisa i-cholesterol, zandisa i-HDL kuphela.
I-Fibrates ne- niacin yandisa i-HDL ngesixa esilinganiselweyo.
Ngona nxalenye, kuba akukho ziyobisi ezithembekileyo ezivelisa ukunyuka okuphawulekayo kwi-HDL, iingcebiso ekunyuseni i-cholesterol ye-HDL zijolise ekulawuleni ubunzima kunye nokufumana imithwalo yokuzivocavoca, ngokuchithwa kweziphakamiso zokutya eziphonswe kuyo.
Ukuphosa amanzi kwi-HDL Hypothesis
Ngenxa yokuba ukwandisa amazinga e-HDL kucingelwa ukuba yinto encedo, kwaye ngenxa yokuba akukho ndlela elula okanye ethembekileyo yokwenza njalo, ukuphuhlisa iziyobisi eziphakamisa amanqanaba e-HDL sele yinjongo enkulu kwiinkampani ezininzi zezobisi. Kwaye, ngokwenene, ezi zininzi zezi machiza ziye zaphuhliswa, kwaye zikhokelela kwiimvavanyo zeclini ukubonisa ukhuseleko kunye nokusebenza kwazo.
Okwangoku, ezi zifundo zididekile, ukuba zincinci. Icandelo lokuqala lokugqibela (eligqitywe ngo-2006) kunye ne-CETP yokuqala ye-inhibitor yezilwanyana, i-torcetrapib (ukusuka ePfizer), ayiphumelelanga kuphela ukubonisa ukunciphisa umngcipheko xa i-HDL yonyuka kodwa yenzeni ukwanda kwengozi yomzimba. Olunye uhlolisiso nolunye u-CETP inhibitor - dalcetrapib (ukusuka eRoche) - lugqitywe ngoMeyi 2012 ngenxa yokungahambi kakuhle. Ezi zombini izidakamizwa ezinxulumene kakhulu zandisa amazinga e-HDL, kodwa ukwenza oko akuzange kubangele nayiphi na inzuzo yonyango.
Olunye uphando oludakisayo (i-AIM-HIGH) lushicilelwe ngo-2011, luvavanya inzuzo yokongeza i-niacin (ukwandisa amazinga e-HDL) kwi-anti-statin. Olu phofu aluphumelelanga nje ukubonisa nayiphi na inzuzo ekunyuseni amazinga e-HDL nge-niacin kodwa iphinde icebise ukuba umngcipheko we- stroke wenyuka phakathi kwezigulane ezithatha i-niacin.
Ekugqibeleni, uphando olubonakala kwiLancet ngo-2012 luvavanya inzuzo enokuba nayo enye yeendlela ezahlukahlukeneyo zokuvelisa i-HDL. Abaphandi abazange bakwazi ukubonisa ukuba abantu ababenokuhluka okunjalo banandipha nayiphi na ingcipheko yengozi yomzimba.
Iziphumo zezi zifundo zenza wonke umntu (nokuba izazinzulu ziye zanikela imisebenzi yazo kwi-HDL yophando) zingathandabuzi ukuba i-hypothesis ye-HDL ichanekile.
I-HDL Hypothesis entsha
Okona kuncinci, kubonakala ukuba i-HDL hypothesis elula (ukuba amanqanaba okwandisa "i-cholesterol ye-HDL" yinto enhle yinto enhle) ayichangekanga. Xa i-cholesterol ye-HDL iye yenyuka ngempumelelo yi-CETP-inhibitors, yi-niacin, okanye ngeendidi ezininzi zemfuza, akukho nzuzo iboniswe.
Abaphandi be-HDL basenkqubo yokuhlaziya i-hypothesis yabo elula ye-HDL. Kuvela ukuba xa silinganisa "i-cholesterol ye-HDL," ngokwenene silinganisa iintlobo ezahlukeneyo zeengqungquthela. Kucacile ukuba kukho iindidi ezininzi ze-HDL kunye namancinci, ezimele izigaba ezahlukeneyo ze-HDL metabolism.
Iincinci ze-HDL ezincinci ziquka i- lipoprotein ApoA-1 , engenakho i-cholesterol eninzi. Ngaloo ndlela, iincinci ze-HDL ezincinci zingacatshulwa njenge-lipoproteins "ezingenalutho," ezisendleleni yokukhanda i-cholesterol engaphezu kwamathambo. Ngokwahlukileyo, iindidi ezinkulu ze-HDL ziqukethe i-cholesterol eninzi. Ezi zincinci sele zenze umsebenzi wazo wokukhwabanisa, kwaye zilindele ukuba zibuyiselwe phezulu ngesibindi.
Ngaphantsi kwesi siqonde esitsha, ukwandisa inani leenxalenye ezininzi ze-HDL kuya kubangela amazinga aphezulu e-HDL - kodwa ayinakuphucula "i-cholesterol" yokukhwabanisa amandla. Ngakolunye uhlangothi, ukwandisa iincinci ze-HDL ezincinci kufuneka kuphuculwe ukususwa kwe-cholesterol engaphezu kwegazi zindonga.
Ukuxhasa le ngcamango ehlaziyiweyo kukuba i-CETP inhibitors (iziyobisi ezingaphumeleli kwizilingo zonyango) kubonakala zibangele ukwanda kweengqungquthela ezinkulu ze-HDL, kungekhona ezincinci.
Iithagethi ezintsha ze-HDL unyango
I-hypothesis entsha ye-HDL ibonisa isidingo sokwandisa iincinci ze-HDL ezincinci.
Kule ndlela, iifom zokwenziwa kwe-ApoA-1 ziphuhliswa kwaye zivavanywa ngabantu. Le ndlela, ngelanga, idinga ukunyuswa kwe-ApoA-1 nge-intravenous - ngoko kujoliswe kuyo kwiimeko ezinzima, ezifana ne -coronary syndrome . Izifundo zakuqala zikhuthaze kakhulu, kwaye izilingo zabantu ziqhubekayo.
Kwakhona, isilwanyana sokulinga (okubizwa ngokuba yi-RVX-208 - Resverlogix) siphuhlisiwe esandisa imveliso yomzimba we-ApoA-1. Le myeza yomlomo iphinda ivavanywe kwizilingo zabantu.
Ukongezelela, kwenziwa umsebenzi wokwenza iziyobisi ezikhuthaza i-ABCA1, i-enzyme kwizicubu ezikhuthaza ukudluliselwa kwe-cholesterol kwiindidi ze-HDL.
Ngaloo ndlela, abaphandi baphendukela ekufumaneni iindlela zokunyusa, okanye ukuphucula umsebenzi, iincinci ze-HDL ezincinci (phantsi kwe-hypothesis entsha) zijongene nokunciphisa ingozi yomzimba.
Ngeli xesha
Nangona silindele ukuba izazinzulu zihlele zonke izinto, kwaye ziphucule kwaye zivavanye iindlela ezintsha zokunyusa "uhlobo olulungileyo" lwe-HDL , sonke sinokuqhubeka senza izinto esiziwayo zombili zandisa i-cholesterol ye-HDL kwaye zinciphisa ingozi yomzimba . Zonke ezi zinto zifanelekileyo, zikhuselekile kwaye ziyasebenza.
> Imithombo:
I-BF ebonakalayo, iPloloso GM, Orho-Melander M, et al. I-cholesterol ye-HDL ye-Plasma kunye nomngcipheko we-myocardial infarction: Uphononongo lwe-Mendelian randomisation. Lancet 2012; INGXELO: 10.1016 / S0140-6736 (12) 60312-2.
Roche, Inc. I-Roche inikeza ukuhlaziywa kwiSigaba se-III se-dalcetrapib [release release]. Meyi 12, 2012.
Michos ED, uSibley CT, uBaer JT, et al. Ukunyaniseka kwe-Niacin kunye ne-statin ye-atherosclerosis regression kunye nokukhusela iziganeko zesifo se-cardiovascular disease. J Am Coll Cardiol 2012; INGXELO: 10.1016 / j.jacc.2012.01.045.
I-Vergeer M, iBots ML, van Leuven SI, et al. I-Cholesteryl ester yokudlulisa iproteinyini inhibitor torcetrapib kunye ne-target-target target. Uhlalutyo oluhlanganisiweyo lwe-Atherosclerotic Disease Change by Imaging with a new CETP Inhibitor (RADIANCE). Uhambo luka-2008; INGXENYE: 10.1161 / ICANDELO LE-CIRCULATIONAHA.108.772665.