Ukungahambi kahle kwe-lipid metabolism ku-mellitus yesifo sikashukela: umphumela we-insulin

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I-insulin ibandakanyeka kulawulo lwe-metabolism, ukuhanjiswa kwe-transmembrane kwama-ion, ama-amino acid. Umphumela we-insulini kuma-carbohydrate metabolism kunzima ukuwuthatha ngokweqile. Abantu abanesifo sikashukela futhi bakhombisa izimpawu zokulimala kwemetabolism.

Isifo sikashukela mellitus sitholakale kakhulu muva nje. Izifo zidala ukuphazamiseka okuhlukahlukene kwe-metabolic. Isifo sikashukela i-mellitus, i-pathological physiology engahluka kakhulu, isendaweni yesithathu ngemuva kwezifo ze-oncology nezifo zenhliziyo. Kunabantu abacishe babe yizigidi eziyi-100 abanesifo sikashukela emhlabeni. Njalo eminyakeni eyi-10, inani labanesifo sikashukela liba ngaphezu kwezikhathi ezi-2.

Abantu abavela emazweni asathuthuka kanye nezinto ezingathathelwa ndawo emazweni athuthukile basengozini enkulu yokugula. Ukuphazamiseka kwemetabolic ku-mellitus yesifo sikashukela kuholela kuma-pathologies ahlukahlukene. Isifo sikashukela sohlobo 2 sivame ukuthinta abantu ngemuva kweminyaka engama-45.

I-Mechanism yesenzo se-insulin

Ngo-1869, abakwaLangerhans bathola iziqhingi kuma-pancreas kamuva aqanjwa ngaye. Kwaziwa ukuthi isifo sikashukela singabonakala ngemuva kokususwa kwesibindi.

I-insulin iprotheni, okungukuthi, i-polypeptide equkethe amaketanga ka-A no-B. Baxhunywe ngamabhuloho amabili angenasisekelo. Kuyaziwa manje ukuthi i-insulin iyakhiwa futhi igcinwe amaseli e-beta. I-insulin iphazanyiswa ama-enzymes abuyisa izibopho ze-disulfide futhi abizwa nge- "insulinase." Ngaphezu kwalokho, ama-enzyme e-proteinolytic abandakanyeka ku-hydrolysis yamaketanga ezingxenyeni eziphansi zamangqamuzana.

Kukholelwa ukuthi i-inhibitor eyinhloko ye-insulin secretion yi-insulin egazini ngokwayo, kanye namahomoni e-hyperglycemic:

  • adrenaline
  • ACTH,
  • i-cortisol.

I-TSH, i-catecholamines, i-ACTH, i-STH kanye ne-glucagon ngezindlela ezahlukahlukene yenza kusebenze i-adenylcyclase kulwelwesi lweseli. Lesi sakamuva sakha ukwakheka kwe-cyclic 3,5 adenosine monophosphate, sisebenzisa enye into - iprotein kinase, sisebenzisa imicrotubules ye-beta-Island, okuholela ekunciphiseni kokukhishwa kwe-insulin.

Ama-microtubules luhlaka lwe-beta-cell lapho i-insulin eyakhiwe khona ngaphambili ihamba ngamaseli kuya kulolwelwesi lweseli.

Isikhuthazo esinamandla kakhulu sokwakheka kwe-insulin i-glucose yegazi.

Indlela yokusebenza kwe-insulin nayo ilele ebudlelwaneni bokuphikisana nabalamuli be-intracellular 3,5 - GMF kanye ne-3,5 AMP.

Umshini we-carbohydrate metabolism

I-insulin ithinta umzimba we-carbohydrate kushukela. Isixhumanisi esiyisihluthulelo salesi sifo ukuntuleka kwale nto. I-insulin inethonya elihle kuma-carbohydrate metabolism, kanye nezinye izinhlobo zemetabolism, ngoba ukugcinwa kwe-insulin kuyancipha, umsebenzi wayo uyancipha, noma ukwamukelwa kwezicubu ezixhomekeke kumsulin ngamaseli kuyaphazamiseka.

Ngenxa yokwephulwa kwe-carbohydrate metabolism ku-mellitus yesifo sikashukela, umsebenzi wokuthathwa kwe-glucose ungene kumaseli uyancipha, umthamo wawo egazini uyanda, nezindlela zokusebenzisa ushukela ezizimele ze-insulin ziyasebenza.

I-Sorbitol shunt yisimo lapho i-glucose incishiselwa i-sorbitol, bese i-oxidised to fructose. Kodwa i-oxidation ikhawulelwe i-enzyme encike ku-insulin. Lapho i-polyol shunt icushiwe, i-sorbitol iqongelela izicubu, lokhu kunomthelela ekubonakala:

  • i-neuropathy
  • katarayta
  • ama-microangiopathies.

Kukhona ukwakheka kwangaphakathi kwe-glucose kusuka kumaprotheni kanye ne-glycogen, kepha ngisho nalolu hlobo lwe-goiukosis aluthwa amaseli, ngoba kunokuntuleka kwe-insulin. I-Aerobic glycolysis ne-pentose phosphate shunt iyacindezelwa, kuvela i-cell hypoxia kanye nokuntuleka kwamandla. Umthamo we-hemoglobin ye-glycated uyakhuphuka, akuyona into ethwala umoya-mpilo, ekhulisa i-hypoxia.

Iprotein metabolism kushukela ingathikamezeka:

  1. i-hyperazotemia (inani elikhulayo le-nitrogen eseleyo),
  2. i-hyperazotemia (ukukhuphuka kwevolumu yamakhemikhali e-nitrogen egazini).

Imvelo yamaprotheni nitrogen ingu-0.86 mmol / L, futhi i-nitrogen ephelele kufanele ibe ngu-0.87 mmol / L.

Izimbangela ze-pathophysiology yilezi:

  • ukwanda kwamaprotheni
  • kusebenze kokuqanjwa kwama-amino acid esibindini,
  • initrogen eseleyo.

I-nitrogen engamaprotheni yi-nitrogen:

  1. ama-amino acid
  2. urea
  3. i-ammonia
  4. i-creatinine.

Lokhu kungenxa yokunyuka kokubhujiswa kwamaprotheni, ikakhulukazi esibindini nasemisipha.

Ngomchamo onesifo sikashukela, umthamo wamakhompiyutha we-nitrogen uyakhuphuka. I-Azoturia inezizathu ezilandelayo:

  • ukukhuphuka kwenqwaba yemikhiqizo ene-nitrogen esegazini, ukucekeka kwabo emchameni,
  • ukungasebenzi kahle kwama-metabolism abonakala nge-ketonemia, i-hyperlipidemia, i-ketonuria.

Esikhathini sikashukela, i-hyperlipidemia iyakhula, okuwukukhuphuka kwegazi lamazinga e-lipid. Inani labo lingaphezu kokujwayelekile, okungukuthi ngaphezulu kwama-8 g / l. I-hyperlipidemia elandelayo ikhona:

  1. ukuvuselelwa kwezicubu ze-lipolysis,
  2. ukuvimbela kokubhujiswa kwe-lipid ngamaseli,
  3. ukwanda kwe-cholesterol,
  4. ukunqandwa kokulethwa kwamafutha aphezulu kumaseli,
  5. umsebenzi wehlile we-LPLase,
  6. ketonemia - ukwanda kwevolumu yemizimba ye-ketone egazini.

Eqenjini lezidumbu ze-ketone:

  • i-acetone
  • i-acetoacetic acid
  • i-p-hydroxymalic acid.

Umthamo ophelele wezidumbu ze-ketone esegazini ungaphezulu kuka-30-50 mg%. Kunezizathu zalokhu:

  1. ukusebenza kwe-lipolysis,
  2. ukukhuphuka kwe-oxidation kumaseli amaningi aphezulu,
  3. ukumiswa kokuqanjwa kwe-lipid,
  4. ukwehla kwe-oxidation ye-acetyl - i-CoA kuma-hepatocytes ngokwakhiwa kwezidumbu ze-ketone,

Ukwabiwa kwemizimba ye-ketone kanye nomchamo kuwukubonakaliswa kwesifo sikashukela esibonisa inkambo engemihle.

Imbangela ye ketonuria:

  • imizimba eminingi ye-ketone ehlungiwe ezinso,
  • ukuphazamiseka kokudla kwamanzi kushukela, kuboniswa yi-polydipsia ne-polyuria,

I-Polyuria iyindlela yokusebenza ekhonjiswa ekwakhiweni nasekuchazeni komchamo ngevolumu edlula amanani ajwayelekile. Ngaphansi kwezimo ezijwayelekile, kusuka ku-1000 kuye ku-1200 ml kukhishwa ngosuku olulodwa.

Isifo sikashukela, i-diuresis yansuku zonke ingu-4000-10 000 ml. Izizathu yilezi:

  1. I-Hyperosmia yomchamo, eyenzeka ngenxa yokususwa kwe-glucose eyeqile, i-ion, i-CT ne-nitrogen compounds. Ngakho-ke, ukuhlunga koketshezi ku-glomeruli kuyashukunyiswa futhi kuvimbela ukuphinda kubuye,
  2. Ukwephulwa kokuphindukuzalwa kanye ne-excretion, okubangelwa i-neuropathy yesifo sikashukela,
  3. I-Polydipsia.

I-insulin ne-fat metabolism

Ngaphansi kwethonya le-insulin, isibindi singagcina inani elithile le-glycogen. I-glucose ethe xaxa engena esibindini iqala ukwenza i-phosphorylate futhi ngaleyo ndlela igcinwe esitokisini, kodwa bese iguqulwa iba ngamafutha, kunokuba i-glycogen.

Lokhu kuguqulwa kube ngamafutha kungumphumela wokuvezwa ngokuqondile kwe-insulin, futhi igazi elakheka phakathi nenqubo yamafutha acid lihanjiswa ngezicubu ze-adipose. Egazini, amafutha ayingxenye ye-lipoprotein, edlala indima enkulu ekwakhiweni kwe-atherossteosis. Ngenxa yale pathology, ingaqala:

  • embolism
  • ukushaya kwenhliziyo.

Isenzo se-insulin kumaseli we-adipose izicubu ziyafana nomphumela wazo kumaseli wesibindi, kepha ukwakheka kwamafutha acid esibindini kuyasebenza ngokwengeziwe, ngakho-ke kudluliswa kusuka kuwo kuya kwezicubu ze-adipose. Amafutha acid kumaseli agcinwa njenge-triglycerides.

Ngaphansi kwethonya le-insulin, ukwephulwa kwe-triglycerides kwezicubu ze-adipose kuncishiswa ngenxa yokuvinjwa kwe-lipase. Ngaphezu kwalokho, i-insulin isebenze ekuqukeni kwamafutha acid ngamangqamuzana futhi ibandakanyeka ekunikezelweni kwawo nge-glycerol, edingekayo ekwakhiweni kwe-triglycerides. Ngakho-ke, ngokuqhubeka kwesikhathi, amafutha aqongelela, kufaka phakathi i-physiology yesifo sikashukela mellitus.

Umphumela we-insulin kuma-metabolism wamafutha ungahle uguqulwe, ngezinga lawo eliphansi, ama-triglycerides aphinda ahlukaniswe ngama-acid acid kanye ne-glycerol. Lokhu kungenxa yokuthi i-insulin inhibits lipase ne-lipolysis isebenza lapho ivolumu yayo incishisiwe.

Ama-acid acids amahhala, akhiwa ngesikhathi i-hydrolysis ye-triglycerides, ngasikhathi sinye ingena egazini futhi isetshenziswa njengomthombo wamandla wezicubu. I-oxidation yalawa ma-asidi ingaba kuwo wonke amaseli, ngaphandle kwamaseli wezinzwa.

Inani elikhulu kakhulu lama-asidi anamafutha akhululwa lapho kunokuntuleka kwe-insulin emabhulokeni amafutha abuye athelwe yisibindi. Amaseli wesibindi angakwazi ukuhlanganisa ama-triglycerides noma kungekho i-insulin. Ngokuntuleka kwalokhu, ama-acid anamafutha akhululwa emabhulokheni aqoqwa esibindini ngendlela ye-triglyceride.

Ngalesi sizathu, abantu abanokuntuleka kwe-insulin, naphezu kokuthambekela okujwayelekile kokunciphisa umzimba, bakhulisa ukukhuluphala esibindini.

I-lipid engasebenzi kahle ne-carbohydrate metabolism

Esikhathini sikashukela, inkomba ye-insulin glucagon yehliswa. Lokhu kungenxa yokwehla kwe-insulin secretion, kanye nokwanda kokukhiqizwa kwe-glucagon.

Ukuphazamiseka kwe-lipid metabolism ku-mellitus yesifo sikashukela kuvezwa ekukhuthazeni okubuthakathaka kokulondolozwa nokukhushulwa okwandayo kokugqugquzelwa kwezindawo ezigcinwe ezitolo. Ngemuva kokudla, esifundeni se-postabsorption yile:

  1. isibindi
  2. umsipha
  3. izicubu ze-adipose.

Imikhiqizo yokugaya nama-metabolites ayo, esikhundleni sokugcinwa njengamafutha nama-glycogen, ajikeleza egazini. Izinqubo ze-cyclic nazo zivela ngezinga elithile, ngokwesibonelo, izinqubo ezifanayo ezenzeka nge-gluconeogeneis ne-glycolysis, kanye nenqubo yokuqhekeka kwamafutha nokwakheka.

Zonke izinhlobo zikashukela zibonakaliswa ukubekezelela ushukela omncane, okungukuthi, i-hyperglucoseemia ngemuva kokudla noma ngisho nesisu esingenalutho.

Izimbangela eziphambili ze-hyperglucoseemia yilezi:

  • ukusetshenziswa kwezicubu ze-adipose nezicubu zomkhawulo kukhawulelwe, ngoba lapho kungekho i-insulin HLBT-4 ayivezwa ngaphezu kwe-adipocytes nama-myocyte. I-glucose ayikwazi ukulondolozwa njenge-glycogen,
  • i-glucose esibindini ayisetshenziselwa ukugcinwa ngendlela ye-glycogen, ngoba ngevolumu ephezulu ye-insulin kanye ne-glucagon ephezulu, i-glycogen synthase ayisebenzi,
  • i-glucose yesibindi ayisetshenziselwa ukwakheka kwamafutha. Ama-enzymes we-glycolysis kanye ne-pyruvate dehydrogenase asesimweni esivumelanayo. Ukuguqulwa kweglucose ibe yi-acetyl-CoA, okudingekayo ekuhlanganisweni kwamafutha acid, kuvinjelwe,
  • indlela ye-gluconeogenesis icushiwe ekuqoqweni okuphansi kwe-insulin kanye ne-glucagon ephezulu kanye nokwakheka kweglue kusuka ku-glycerol kanye nama-amino acid.

Okunye ukubonakaliswa kwesifo sikashukela kuyizinga elikhulayo lama-lipoproteins, imizimba ye-ketone namafutha asimahla wamafutha egazini. Amafutha adliwayo awafakwa kwezicubu ze-adipose ngoba i-adipocyte lipase isesimweni esisebenzayo.

Kuqukethwe okuqukethwe okuphezulu kwamafutha acid egazini. Amafutha acid adonswa yisibindi, amanye awo aguqulwa aba ngama-triacylglycerols, angena egazini njengengxenye ye-VLDL. Inani elithile lama-acid angena ku-β-oxidation ku-mitochondria yesibindi, bese i-acetyl-CoA esetshenzisiwe isetshenziselwa ukwakheka kwezidumbu ze-ketone.

Umphumela we-insulin kumetabolism ubuye eqinisweni lokuthi ngokufakwa kwe-insulin kwezicubu ezihlukile zomzimba, ukwakheka kwamafutha nokuqhekeka kwe-triglyceride lipids kuyasheshiswa. I-metabolidi ye-lipid engasebenzi kahle ukugcinwa kwamafutha, okusebenza ukwanelisa izidingo zamandla ezimweni ezingezinhle.

Ukubonakala ngokweqile kwe-cAMP kuholela ekunciphiseni kokuhlanganiswa kwamaprotheni kanye nokwehla kwe-HDL ne-VLDL. Njengomphumela wokwehla kwe-HDL, ukuphuma kwe-cholesterol kusuka kuma-membrane amaseli kuya kwi-plasma yegazi kuyehla. I-cholesterol iqala ukufakwa ezindongeni zemikhumbi emincane, okuholela ekwakhekeni kwe-angiopathy yesifo sikashukela kanye ne-atherossteosis.

Ngenxa yokuncipha kwe-VLDL - amanqwabelana aqongelela esibindini, kuvame ukuthululwa njengengxenye ye-VLDL. I-Protein synthesis iyacindezelwa, okubangela ukwehla kokwakhiwa kwama-antibody, bese-ke, iziguli zesifo sikashukela ezinganele ezifweni ezithathelwanayo. Kuyaziwa ukuthi abantu abanenkinga yamaprotheni metabolism bahlushwa i-furunculosis.

Izinkinga ezingaba khona

I-Microangiopathy iyi-glomerulonephritis yesifo sikashukela. Ngenxa ye-retinopathy yesifo sikashukela, abantu abanesifo sikashukela balahlekelwa umbono wabo ngamacala angama-70-90%. Ikakhulu, abanesifo sikashukela bahlakulela ikati.

Ngenxa yokuntuleka kwe-HDL, i-cholesterol eyeqile ivela kulwelwesi lweseli. Ngakho-ke, izifo zenhliziyo ezi-coronary noma i-endarteritis eqothulayo zingavela. Kanye nalokhu, kwakheka i-microangiopathy ene-nephritis

Esikhathini sikashukela, isifo se-periodontal sakhiwa nge-gingivitis - periodontitis - isifo se-periodontal. Ku-diabetes, izakhiwo zamazinyo ziyaphazamiseka futhi izicubu ezisekelwayo ziyathinteka.

Izimbangela zenkambiso yama-microvessels kulezi zimo, ngokunokwenzeka, ukwakheka kokuxhunyaniswa kwe-glucose okungenakuphikiswa namaprotheni odongeni lwe-vascular. Kulokhu, ama-platelets afaka isici esivusa ukukhula kwezakhi zomzimba ezibushelelezi odongeni lwe-vascular.

Ukuphazamiseka kwe-metabol metabolism nakho kuvezwa ngeqiniso lokuthi ukungena kwamafutha kwesibindi kuyanda esibindini, i-lipid resynthesis. Imvamisa, zenziwa zisesimweni se-VLDL, ukwakheka kwazo kuncike kumthamo wamaprotheni. Kulokhu, abanikeli beqembu le-CHZ, okungukuthi, i-choline noma i-methionine, bayadingeka.

I-Choline synthesis ivuselela i-lipocaine, ekhiqizwa yi-pancreatic duct epithelium. Ukuntuleka kwalo kuholela ekukhuluphaleni kwesibindi kanye nokwakheka kwezinhlobo zesifo sikashukela kanye nesishukela esiphelele.

Ukushoda kwe-insulin kuholela ekumelaneni okuphansi kwezifo ezithathelwanayo. Ngakho-ke, i-furunculosis iyakhiwa.

Ividiyo ekulesi sihloko izokhuluma ngemiphumela ye-insulin emzimbeni.

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