Emashumini ambalwa eminyaka, bekuyiqiniso ukuthi i- HDL ye-cholesterol iyinhlobo "enhle" ye-cholesterol, ukuthi izinga eliphezulu le-HDL yakho liyingozi engqondweni yakho, nokuthi ukuphakamisa amazinga e-HDL ye-cholesterol kuwumqondo omuhle kakhulu. Kodwa imiphumela eyadumazayo ngenxa yezilingo eziningana zamuva zokwelashwa ziye zafakaza ukuthi leyo mbono iyabuza.
Kungani i-HDL icatshangwa ukuthi "Kuhle"
I-cholesterol ye-HDL icatshangwa ukuthi idla i-cholesterol engaphezu kwezindonga zemithambo yegazi, ngaleyo ndlela isisuse lapho ingabangela khona ukuqina kwe- atherosclerosis .
Ngaphezu kwalokho, ngezifundo ze-epidemiological ezibandakanya abantu abangaphezu kuka-100,000, abantu abanezifo ze-HDL ze-cholesterol ezingaphansi kuka-40 mg / dL babenengozi enkulu kakhulu yenhliziyo kunabo abanamazinga aphezulu we-HDL. Njalo kunjalo ngisho nalapho ama- cholesterol e-LDL ("ama-bad" we-cholesterol) ephansi. Amazinga e-HDL aphakeme nawo ahlotshaniswa nenengozi enciphise yomdlavuza wesifuba, i-colon ne-lung.
Kusukela kuleso sifundo kufika inkolelo yokuthi ukuthatha izinyathelo zokwandisa amazinga e-HDL kuwumqondo omuhle. Lona okuthiwa i-HDL hypothesis: ephakeme amazinga wakho we-HDL, ukwehlisa ingozi yakho yenhliziyo.
Amanothi we-HDL anganda kanjani?
Amazinga we-HDL abonakala ashukunyiswa kakhulu ngxube yezinto eziphathelene nezakhi zofuzo nezendalo. Abesifazane bavame ukuba namazinga aphezulu e-HDL kunamadoda (ngokulinganiselwa kuka-10 mg / dL).
Abantu abakhuluphele ngokweqile, abahlala phansi, noma abanesifo sikashukela noma isifo se- metabolic bavame ukuba namazinga aphansi we-HDL.
Utshwala lubonakala ukwandisa i-HDL ngemali encane; Amafutha esitokisi ekudleni adinciphisa.
Izidakamizwa ezivame ukusetshenziselwa ukunciphisa i-cholesterol ye-LDL inezimbalwa ezincane kumazinga e-HDL. Izitatimende , izidakamizwa ezinciphisa kakhulu i-cholesterol, ukwandisa i-HDL kuphela kancane.
I-Fibrate ne- niacin yanda i-HDL ngenani elilinganiselwe.
Ngokuyinhloko, ngoba azikho izidakamizwa ezinokwethenjelwa ezikhiqiza ukunyuka okuphawulekayo kwe-HDL, izincomo ekwandiseni i-HDL cholesterol ziye zagxila ekulawuleni isisindo futhi zithola umzimba wokuzivocavoca, ngokunciphisa izincomo zokudla eziphonswe kuyo.
Ukuphonsa Amanzi kwi-HDL Hypothesis
Ngenxa yokuthi ukukhula kwamazinga e-HDL kucatshangwa ukuthi kuyinto enenzuzo, futhi ngenxa yokuthi ayikho indlela elula noma enokwethenjelwa yokwenza kanjalo, ukuthuthukisa izidakamizwa eziphakamisa amazinga e-HDL sekube umgomo omkhulu ezinkampanini eziningana zokwelapha. Futhi ngempela, eziningana zalezi zidakamizwa zakhiwe, futhi zaholela ekuvivinyweni kwemitholampilo ukukhombisa ukuphepha nokusebenza kwazo.
Kuze kube manje, lezi zifundo ziye zadumaza, ukusho okungenani. Isivivinyo sokuqala esiyinhloko (saphetha ngo-2006) ne-CETP yokuqala inhibitor izidakamizwa, torcetrapib (kusuka Pfizer), hhayi kuphela ehluleka ukubonisa ukunciphisa ingozi lapho HDL yanda kodwa empeleni kubonisa ukwanda inhliziyo engozini. Olunye ucwaningo nolunye i-CETP inhibitor - i-dalcetrapib (e-Roche) - laqedwa ngo-May 2012 ngenxa yokungabi namandla. Zombili lezi zidakamizwa ezihlobene zikhulisa kakhulu amazinga e-HDL, kodwa ukwenza kanjalo akuzange kubangele noma iyiphi inzuzo yomtholampilo.
Esinye isifundo esidumazayo (i-AIM-HIGH) sanyatheliswa ngo-2011, sihlola inzuzo yokwengeza i-niacin (ukwandisa amazinga e-HDL) ekwelashweni komthetho. Lolu cwaningo aluphumelelanga kuphela ukubonisa noma yikuphi ukuzuza ekukhuleni amazinga we-HDL nge-niacin kodwa futhi kwaphakamisa ukuthi ingozi yokushaya isifo yanda phakathi kweziguli ezithatha i-niacin.
Okokugcina, uphenyo oluvela eLancet ngo-2012 luhlolisise inzuzo engaba khona yokuba neyinye yezinhlobonhlobo ezihlukahlukene zezofuzo ezandisa amazinga e-HDL. Abacwaningi abakwazi ukukhombisa ukuthi abantu ababenokuhluka okunjalo babejabulela ukunciphisa ingozi yomzimba.
Imiphumela yalezi zifundo inomuntu wonke (ngisho ososayensi abaye bazinikela imisebenzi yabo ku-HDL ucwaningo) bekungabaza ukuthi ngabe i-HDL hypothesis inembile yini.
I-Hypothesis entsha ye-HDL
Okungenani, kubonakala sengathi i-HDL hypothesis elula (lawo mazinga okwanda okuthi "i-HDL cholesterol" njalo into enhle) iye yavinjelwa. Lapho i-HDL i-cholesterol ikhuliswe ngempumelelo yi-CETP-inhibitors, yi-niacin, noma ngezihlukahluka ezihlukahlukene zofuzo, akukho nzuzo eye yaboniswa.
Abacwaningi be-HDL basendleleni yokubuyekeza i-hypothesis yabo elula ye-HDL. Kuvela ukuthi uma sikala "i-cholesterol ye-HDL," empeleni silinganisa izinhlobo eziningana zezinhlayiyana. Ngokuphawulekayo, kunezinhlayiya ze-HDL ezinkulu nezincane, ezimele izigaba ezihlukene ze-HDL metabolism.
I-particle encane ye-HDL iqukethe i- lipoprotein ApoA-1 , ngaphandle kokuningi kwe-cholesterol. Ngakho-ke, izinhlayiyana ze-HDL ezincane zingacatshangwa ngokuthi yi-lipoprotein "ezingenalutho," ezisendleleni yokuyokhipha i-cholesterol engaphezu kwamathambo. Ngokuphambene nalokho, izinhlayiya ze-HDL ezinkulu zine-cholesterol eningi. Lezi zinhlayiya sezivele zenze umsebenzi wazo wokuqhaqhazela, futhi zilindele ukuba zikhuliswe yisibindi.
Ngaphansi kwalokhu kuqonda okusha, ukwandisa inani lezinhlayiyana ze-HDL ezinkulu kungaholela kumazinga aphezulu e-HDL wegazi - kodwa ngeke kuthuthukise "amandla ethu okukhipha amandla e-cholesterol." Ngakolunye uhlangothi, ukwandisa izinhlayiyana ze-HDL ezincane kufanele kuthuthukiswe ukususwa kwe-cholesterol engaphezu kwegazi izindonga zemikhumbi.
Ekusekeleni lokhu kuhlolwa okubuyekeziwe ukuthi i-CETP inhibitors (izidakamizwa ezingaphumeleli ekuvivinyweni kwemitholampilo) kubonakala sengathi zenze ukwanda kwezinhlayiyana ze-HDL ezinkulu, hhayi ezincane.
Izinjongo ezintsha ze-HDL Therapy
I-HDL hypothesis entsha ikhombisa isidingo sokwandisa izinhlayiyana ezincane ze-HDL.
Kuze kube sekugcineni, izinhlobo ze-ApoA-1 zakhiwa zenziwa futhi zihlolwe kubantu. Le ndlela, ngeshwa, idinga ukumnika okungena ngaphakathi kwe-ApoA-1 - ngakho kuhloswe ezimweni eziyingozi, njenge -syndrome eyingozi . Ucwaningo lwasekuqaleni lukhuthaze kakhulu, futhi ukuhlolwa kwabantu kuqhubeka.
Futhi, isidakamizwa sokuhlola (okwamanje esibizwa ngokuthi i-RVX-208 - Resverlogix) sithuthukisiwe okwandisa ukukhiqizwa komzimba we-ApoA-1. Le mithi yomlomo nayo ihlolwe ekuvivinyweni kwabantu.
Ngaphezu kwalokho, kwenziwa umsebenzi wokwakha izidakamizwa ezikhuthaza i-ABCA1, i-enzyme ezinhlakeni ezikhuthaza ukudluliswa kwe-cholesterol kuma-particle we-HDL.
Ngakho-ke, abacwaningi bafuna ukuthola izindlela zokwandisa, noma ukuthuthukisa ukusebenza, izinhlayiyana ze-HDL ezincane (ngaphansi kwe-hypothesis entsha) ezithintekayo ekunciphiseni ingozi yomzimba.
Okwamanje
Njengoba silindele ososayensi ukuba bahlele konke lokhu, futhi ukuthuthukisa nokuhlola izindlela ezintsha zokwandisa "uhlobo olufanele" lwe-HDL , sonke singaqhubeka senza izinto esiziwayo zombili zikhulisa i-cholesterol ye-HDL futhi sinciphise ingozi yomzimba wethu . Zonke lezi zinto zifanelekile, ziphephile futhi ziphumelele.
> Imithombo:
I-Voight BF, uPlososo GM, i-Orho-Melander M, et al. I-cholesterol ye-HDL ye-Plasma kanye nobungozi be-infarction ye-myocardial: Ucwaningo lwe-Mendelian randomization. Lancet 2012; I-DOI: 10.1016 / S0140-6736 (12) 60312-2.
Roche, Inc. Roche inikeza ukubuyekezwa kwesifundo se-Phase III se-dalcetrapib [press release]. Ngo-Meyi 12, 2012.
Michos ED, uSibley CT, uBaer JT, et al. Ukwelashwa kwe-Niacin ne-statin yokuphefumula kwe-atherosclerosis nokuvinjelwa kwezifo zenhliziyo. J Am Coll Cardiol 2012; I-DOI: 10.1016 / j.jacc.2012.01.045.
I-Vergeer M, i-Bots ML, i-van Leuven SI, et al. I-cholesterl ester ukudlulisa amaprotheni inhibitor torcetrapib kanye off-target utshwala. Ukuhlaziywa okuhlanganisiwe kweSifo se-Atherosclerotic Isilinganiselwa Shintsha ngokucabangela ngezilingo ezintsha ze-CETP (RADIANCE). Ukujikeleza ngo-2008; I-DOI: 10.1161 / CIRCULATIONAHA.108.772665.