Ukwanda okuqhubekayo kwesibalo seziguli ezinesifo sikashukela sohlobo 2 kanye nezinkinga zaso ezigcina sekwemithambo, zibeka lesi sifo njengenkinga yomhlaba wonke.
Isifo sikashukela i-mellitus asisizi amazwe athuthukile futhi nengqalasizinda noma amazwe athuthukile. I-WHO ilinganisela ukuthi kunabantu abacishe babe yizigidi eziyi-150 abanesifo sikashukela emhlabeni wonke. Futhi ukwanda kwalesi sifo ngonyaka kungu-5-10%.
E-Russia namuhla iziguli ezingaba yizigidi ezingama-2,5 ezinesifo sikashukela zibhalisiwe. Kepha lesi sibalo asisiwona owokugcina, ngoba isibalo samacala angakhonjwanga acishe alingane nezigidi eziyi-8. Kalula nje, i-5% yabantu baseRussia baneSifo sikashukela. Kulaba, 90% banesifo sikashukela sohlobo 2.
Izinkinga ezivame kakhulu zesifo sikashukela yizifo zenhliziyo, okuthi emaphathini angama-70% aholele emiphumeleni yenhlekelele engenakuphikwa. Ngalesi sizathu, i-American Association of Cardiology yabeka lesi sifo njengesifo senhliziyo.
Izici zobungozi
I-Postprandial hyperglycemia ingaphezu koshukela wegazi we-10 mmol / L noma ngaphezulu ngemuva kokudla okujwayelekile okujwayelekile. Ukubaluleka kwe-hypprlycemia yangemuva nangemuva kokuqina kwezinkinga ezifika sekwephuzile kwesifo sikashukela sezinzwa kuphezulu kakhulu. Ukuphazamiseka kwemetaboliki ngohlobo lwesifo sikashukela sohlobo 2 kukwenza izici eziningi zobungozi zemithambo yegazi nenhliziyo, kufaka phakathi:
- Ukukhuluphala ngokweqile
- Umfutho wegazi ophezulu we-Arterial.
- Amazinga aphezulu we-inhibitor 1 esebenzayo ye-fibrinogen ne-plasminogen.
- Hyperinsulinemia.
- I-Dyslipidemia, ebonakala ikakhulukazi nge-cholesterol ephansi ye-HDL (lipdrinsins ephezulu) ne-hypertriglyceridemia.
- Ukumelana ne-insulin.
Ukufa kwabantu ngenxa yesifo senhliziyo nesibalo sokubonakaliswa okungelona iqiniso kwalesi sifo ezigulini ezinesifo sikashukela kuphakama izikhathi ezingama-3-4 kunabantu abaneminyaka efanayo kodwa abanaso isifo sikashukela.
Ngakho-ke, izici zobungozi ezingabonakali kanye nezici ezibonisa uhlobo lwesifo sikashukela sohlobo 2, kufaka phakathi ukumelana ne-insulin ne-hyperglycemia, kufanele zibe nesibopho sokuthuthuka okusheshayo kwe-vasher atherosulinosis kulezi ziguli.
Izinkomba ezijwayelekile zokulawulwa kukashukela okuphezulu (i-glycated hemoglobin, glycemia esheshayo) ayichazi ngokuphelele ingozi eyengeziwe yezinkinga zenhliziyo ezigulini ezinesifo sikashukela sohlobo 2. Izici zobungozi ezifakazelwe zifaka phakathi:
- Umfutho wegazi ophezulu we-Arterial.
- Isisulu sokuqothuka.
- Ubulili (amadoda atholakala kalula).
- I-Dyslipidemia.
- Iminyaka.
- Ukubhema.
I-postprandial glucose
Kodwa, njengoba imiphumela yocwaningo olunzulu ikhombisile, i-postprandial glycemia idlala indima ebaluleke ngokulinganayo ekwakhiweni kwesifo senhliziyo nesifo sokuqina kwemithambo yegazi. Ucwaningo lomtholampilo lwe-DECODE oluhlola ubungozi bokushona ezinhlotsheni ezahlukahlukene ze-hyperglycemia luveze ukuthi ukucwaswa kwe-glucose ye-postprandial kuyisici esizimele sobungozi esibikezela ukwedlula i-hemoglobin ye-glycated.
Lolu cwaningo luqinisekisile ukuthi lapho kuhlolwa ubungozi bomphumela omubi wenhliziyo onesifo sikashukela sohlobo 2, umuntu akufanele acabangele izinkomba zokuzila ngokushesha kwe-glycemia HbA1c, kodwa futhi nezinga le-glucose egazini amahora ama-2 ngemuva kokudla.
Kubalulekile! Ukuxhumana phakathi kwe-glycemia yokuzila ukudla ne-postprandial ngokuqinisekile kukhona. Umzimba awukwazi ngaso sonke isikhathi ukubhekana ngempumelelo nenani lama-carbohydrate atholakala ngesikhathi sokudla, okuholela ekuqokeleleni noma ekutholeni kancane kwe-glucose. Ngenxa yalokhu, izinga le-glycemia landa kakhulu ngokushesha ngemuva kokudla, alihle phakathi nosuku futhi ngisho nomkhuba wokuzila ushukela wegazi uyagcinwa.
Kunombono wokuthi, ekuhlolweni kwengozi yezifo zesistimu yezinhliziyo, izinga lokuphakama kweshukela egazini ku-mellitus yesifo sikashukela elihlobene ngqo nokudla kokudla kubaluleke kakhulu kunokuzila ushukela.
Uma isiguli sinezimpawu zokuphazamiseka kwesifo sikashukela kanye ne-microcirculatory ngesifo sikashukela sohlobo 2, lokhu kukhombisa ukuthi i-postprandial hyperglycemia yenzeka kudala ngaphambi kokuba kutholakale nezimpawu zesifo sikashukela, futhi nengozi yezinkinga eziphezulu ibe khona isikhathi eside.
Eminyakeni embalwa edlule, kunombono oqinile mayelana nezinqubo okusolwa ngazo isifo sikashukela mellitus. Izimbangela zesifo sikashukela sohlobo 2 zingukutholwa kokuvikelwa kwe-insulin nokungahambisani ne-insulin, ukuthuthukiswa kwako kuncike ekuhlanganisweni kwezinto ezitholakele noma ezizalwe kabusha.
Isibonelo, kutholakale ukuthi inqubo ye-homeostasis incike ohlelweni lokuphendula kusibindi esiyinkimbinkimbi - izicubu ezisusiwe - amaseli we-pancreatic beta. Kwi-pathogenesis yesifo sikashukela i-mellitus, ukungabikho kwesigaba sokuqala secretion ye-insulin kubaluleke kakhulu.
Akuyona imfihlo ukuthi i-glycemia iyaguquguquka phakathi nosuku futhi ifinyelela amazinga aphezulu ngemuva kokudla. Umshini wokukhishwa kwe-insulin kubantu abanempilo usungulwe kahle, kufaka nokuphendula ukubukeka nephunga lokudla, elinomthelela ekukhutshweni kweglucose egazini.
Isibonelo, kubantu abangenakho ukubekezelela ushukela (i-NTG) noma isifo sikashukela, ukugcwaliswa kabusha kwe-glucose kuholela ekutholeni kokuqala kwe-insulin, okuthi ngemuva kwemizuzu eyi-10 ifinyelele inani layo eliphakeme. Ngemuva kwalokhu kulandela isigaba sesibili, isibalo sazo senzeka ngemizuzu engama-20.
Ezigulini ezinesifo sikashukela sohlobo 2 kanye ne-NTG, ukwehluleka kwenzeka kulolu hlelo. Impendulo ye-insulin ayikho ngokuphelele noma ngokwengxenye (isigaba sokuqala secretion se-insulin), isb. Ayanele noma ibambezelekile. Ngokuya kobunzima besifo, isigaba sesibili singaphazamiseka noma sigcinwe. Imvamisa, kuyalingana ekuvumelaneni kwe-glucose, futhi ngasikhathi sinye ukungabekezelelwa kweglucose.
Nakani! Isigaba sokuqala secretion ye-insulin sinomthelela ekuhlelweni kwezicubu ezixakile yi-glucose yesikhathi esetshenziswa kanye nokunqoba ukumelana ne-insulin.
Ngaphezu kwalokho, ngenxa yesigaba sokuqala, ukukhiqizwa kwe-glucose ngesibindi kuyacindezelwa, okwenza sikwazi ukuvimbela i-postprandial glycemia.
I-hyperglycemia engapheli
Lapho lesi sifo sikhula, lapho indima ehamba phambili idlalwa yi-hyperglycemia, amangqamuzana e-beta alahlekelwa ukusebenza kwawo namaseli we-pulse abhujiswe, isimo se-pulse secretion siyaphazamiseka, futhi lokhu kukhulisa i-glycemia.
Njengomphumela walezi zinguquko ze-pathological, izinkinga zanda ngokushesha. Ngokuvela kwe-angiopathy yesifo sikashukela yibambe iqhaza:
- Ukucindezelwa kwe-Oxidative.
- I-non-enzymatic glycation yamaprotheni.
- I-Autooxidation ye-glucose.
I-Hyperglycemia ithatha umsebenzi oyinhloko ngezindlela zokubonakala kwalezi zinqubo. Kufakazelwe ukuthi noma ngaphambi kokuthola i-hyperglycemia yokuzila okukhulu, ama-75% amaseli we-beta alahlekelwa umsebenzi wawo. Ngenhlanhla, le nqubo iyaphenduka.
Ososayensi bathole ukuthi amaseli we-pancreatic beta asesimweni esiguqukayo, okungukuthi, avuselelwa njalo futhi ama-beta-cell mass adts ahlangabezana nezidingo zomzimba ze-hormone insulin.
Kepha nge-hyperglycemia engapheli engapheli, amandla okusinda kwamangqamuzana e-beta aphendule ngokwanele nge-insulin ukuvusa ushukela obukhulu ancishiswa kakhulu. Ukungabikho kwalokhu kuphendula kokulayishwa kwe-glucose kugcwele ukwephulwa kwesigaba se-1 nelesi-2 secretion ye-insulin. Ngaso leso sikhathi, i-hyperglycemia engamahlalakhona ibanga umphumela wama-amino acid kumaseli we-beta.
Ubuthi be-glucose
Ukukhiqizwa kwe-insulin ephazamisekile ku-hyperglycemia engapheli kuyinqubo eguqukayo, inqobo nje uma i-carbohydrate metabolism ijwayelekile. Amandla we-hyperglycemia engapheli yokuphazamisa ukukhiqizwa kwe-insulin ibizwa ngokuthi ubuthi be-glucose.
Le pathology, eyaqhamuka ngemuva kwesizinda se-hyperglycemia, ingenye yezimbangela eziphambili zokuphikiswa kwe-insulin yesibili. Ngaphezu kwalokho ubuthi be-glucose bubangela ukudana kwamaseli we-beta, okuboniswa ukwehla komsebenzi wabo wokubhala.
Ngesikhathi esifanayo, amanye ama-amino acid, ngokwesibonelo, i-glutamine, asithinta kakhulu isenzo se-insulin, siguqula ukumuncwa kweglucose. Ezimweni ezinjalo, i-desensitization etholakele ingumphumela wokuqalwa kwemikhiqizo ye-metabolic - i-hexosamines (hexosamine shunt).
Ngokusekelwe kulokhu, kusobala ukuthi i-hyperinsulinemia ne-hyperglycemia ngokuqinisekile ingasebenza njengezinto ezizimele zobungozi zezifo zenhliziyo. I-hypprlycemia ye-postprandial kanye neyangemuva ibangela izindlela eziningi ze-pathological ezibandakanyekile ekuthuthukisweni kwezinkinga zesifo sikashukela.
I-hyperglycemia engapheli ifaka ukwakheka okukhulu kwama-radicals mahhala, okwaziyo ukubopha kumangqamuzana e-lipid futhi kuvuse ukukhula kokuqala kwe-atherosclerosis.
Ukubopha kwe-NO molecule (nitric oxide), eyi-vasodilator enamandla egcinwe yi-endothelium, kuthuthukisa ukungasebenzi kahle kwe-endothelial dysfunction futhi kusheshise ukukhula kwe-macroangiopathy.
Inani elithile lama-radicals mahhala lakhiwa njalo emzimbeni we-vivo. Ngaso leso sikhathi, kugcinwa ibhalansi phakathi komsebenzi wokuvikelwa kwe-antioxidant kanye nezinga lama-oxidants (yama-radicals wamahhala).
Kepha ngaphansi kwezimo ezithile, ukwakheka kwamakhompiyutha ajikelezayo akhula, okuholela ekucindezelekeni oku-oxidative, okuhambisana nokungalingani phakathi kwalezi zinhlelo ngokwanda kwenani lama-oxidants okuholela ekunqotshweni kwama-molecule we-biological cellular.
Lezi zinhlayiya ezilimele zimpawu zokucindezela kwe-oxidative. Ukwakheka okuphezulu kwama-radicals kwamahhala kwenzeka ngenxa ye-hyperglycemia, ukwanda kwe-autooxidation ye-glucose nokubamba iqhaza kwayo ezinhlelweni ze-protein glycation.
Inani elikhulu lama-radicals wamahhala yi-cytotoxic lapho ukwakheka kwawo sekuwedlulele. Bafuna ukuthatha i-elektroni yesibili noma eyengeziwe kwamanye ama-molecule, ngaleyo ndlela babangele ukuphazamiseka kwabo noma alimaze isakhiwo samaseli, izicubu, izitho zomzimba.
Sekutholwe ukuthi esimweni sokuthuthukisa i-mellitus nesifo sokuqina kwesifo sikashukela, kunguku ngqo kwama-radicals wamahhala nokucindezela kwe-oxidative okubandakanya, okulandelayo:
- kuhambisana nokuntuleka kwe-insulin;
- kuholela ku-hyperglycemia.
I-Hyperglycemia ingaba uphawu oluphambili lomsebenzi we-endothelial wemikhumbi ye-coronary.
Ukwelashwa kwe-postprandial hyperglycemia
Ukuthola isinxephezelo se-carbohydrate metabolism, kunengqondo ukusebenzisa iqoqo lezinyathelo ezibandakanya:
- ekudleni okulinganiselayo;
- ekusebenzeni ngokomzimba;
- ekwelashweni kwezidakamizwa.
Nakani! Isici esibalulekile ekwelashweni ngempumelelo kwesifo sikashukela kungukudla okune-kilojoule kanye nokusebenza ngokomzimba okwanele. Ukudla kufanele kuhloswe ekuvinjelweni jikelele kwama-carbohydrate futhi ikakhulukazi ahlanjululwayo. Lezi zinyathelo ziphazamisa ukukhula kwe-postprandial hyperglycemia futhi zithinte ukuqina kwaso usuku lonke.
Ukudla kanye nokuzivocavoca kukodwa, njengomthetho, akukwazi ukubhekana nokukhiqizwa kukashukela okuphezulu ebusuku ngesibindi, okuholela kokuzila ukudla okuphezulu kanye ne-postprandial glycemia.
Njengoba i-hyperglycemia isixhumanisi esiyinhloko esithinta ukucwaswa kwe-insulin, kuphakama umbuzo wezokwelapha izidakamizwa zohlobo 2 lwesifo sikashukela. Imvamisa, okususelwa ku-sulfonylurea kusetshenziselwa lokhu.
Izidakamizwa kuleli qembu zithuthukisa i-insulin secretion futhi zinciphise ukushesha kwe-glycemia. Kepha banethonya elincane kwi-postprandial hyperglycemia.
Ubudlelwano obusondelene phakathi kwezinkinga ezibulala inhliziyo zenhliziyo kanye ne-postprandial hyperglycemia buletha odokotela kanye nesiguli, ngakolunye uhlangothi, umsebenzi wokubheka njalo kwe-postprandial hyperglycemia, ngakolunye uhlangothi, ukusetshenziswa kwabalawuli be-prandial ukulungisa i-glycemia.
Ukuvimbela i-postprandial hyperglycemia ngaphandle kokukhushulwa kokuqashelwa kwe-inso native hormone insulin kungazuzwa ngokukhawulela i-adsorption yamakhabhohayidi emathunjini amancane kusetshenziswa i-acarbose.
Ukuncika kudatha yokucwaninga eqinisekisa iqhaza elibalulekile lama-amino acid (ngaphandle kweglucose) ohlelweni lokuvikelwa kwe-insulin ngamaseli e-beta kwinqubo yokudla, ucwaningo luqale ngemiphumela enciphisa ushukela yokufana kwe-benzoic acid, phenylalanine, okufika ekugcineni kokuhlanganiswa kwe-repaglinide ne-nateglinide.
Ukuvikelwa kwe-insulin okuvuswa ngabo kusondele ekucasheleni kwayo kwemvelo kokuqala kubantu abanempilo ngemuva kokudla. Lokhu kuholela ekwehleni okusebenzayo kwamanani aphezulu eglucose esikhathini se-postprandial. Le mishanguzo inomphumela omfushane, kepha osheshayo, ngenxa yokuthi ungavimba ukwanda okubukhali koshukela ngemuva kokudla.
Muva nje, izinkomba zokujova kwe-insulin ezigulini ezinesifo sikashukela sohlobo 2 zikhuphuke kakhulu. Ngokwesilinganiso esilinganiselwe kakhulu, cishe i-40% yeziguli ezinesifo sikashukela sohlobo 2 zidinga ukwelashwa kwe-insulin. Kodwa-ke, i-hormone empeleni ithola okungaphansi kwe-10%.
Ukuqala ukwelashwa kwe-insulin kwesifo sikashukela sohlobo 2, izinkomba zendabuko yile:
- izinkinga ezinkulu zesifo sikashukela;
- imisebenzi yokuhlinzwa;
- ingozi ye-cerebrovascular eyingozi;
- i-infarction ye-myocardial eyingozi kakhulu;
- ukukhulelwa
- izifo.
Namuhla, odokotela bayazi ngokuphelele isidingo zemijovo ye-insulin ukuze banciphise ubuthi be-glucose futhi babuye nomsebenzi we-beta-cell ku-hyperglycemia engapheli.
Ukwehliswa okusebenzayo kokukhiqizwa kweshukela ushukela ngohlobo 2 sikashukela kudinga ukwenziwa kusebenze kwezinqubo ezimbili:
- I-Glycogenolysis.
- I-Gluconeogenesis.
Njengoba ukwelashwa kwe-insulin kusiza ukunciphisa i-gluconeogeneis, i-glycogenolysis esibindini futhi ithuthukise ukuzwela okuphathelene ne-insulin, lokhu kungalungisa izindlela ze-pathogenetic zesifo sikashukela i-mellitus.
Imiphumela emihle yokwelashwa kwe-insulin yesifo sikashukela ifaka:
- ukwehla kokuzila ukudla kwe-hyperglycemia nangemva kokudla;
- kunciphisa ukukhiqizwa kwe-glucose yesibindi kanye ne-gluconeogeneis;
- ukukhiqizwa kwe-insulin okuphezulu njengempendulo yokuvuselela ushukela noma ukudla;
- kusebenze kwezinguquko ze-antiatherogenic kuphrofayela ye-lipoproteins kanye ne-lipids;
- ukuphuculwa kwe-anaerobic ne-aerobic glycolysis;
- ukwehla kwe-glycation kwama-lipoprotein namaprotheni.
