Insulin-Zoo li Growth Factor-I

IGF-Kuv yog tus neeg nruab nrab tseem ceeb ntawm GH txoj kev txhawb nqa kev loj hlob, hu ua "kev loj hlob mediator". GH yog tso tawm los ntawm lub caj pas pituitary, uas ua rau lub siab ua kom cov hlwb ua ke thiab tso tawm IGF-I. IGF-Kuv nyob rau hauv kev ncig ntxiv ua rau cov nqaij mos xws li cov pob txha, cov leeg, thiab cov kabmob, ua kom tiav kev sib kis thiab ua tiav cov cim kev loj hlob.
Kev loj hlob ntawm pob txha: IGF-Kuv ncaj qha qhib qhov kev loj hlob thiab kev sib txawv ntawm epiphyseal chondrocytes, txhawb kev ncua ntev ntawm cov pob txha loj hlob daim hlau, thiab yog qhov tseem ceeb ntawm kev loj hlob ntawm cov menyuam yaus; Ib txhij stimulating osteoblast kev ua si, nce pob txha ceev, inhibiting osteoclast pob txha resorption, thiab tswj cov neeg laus cov pob txha homeostasis.

Kev loj hlob ntawm cov nqaij ntshiv: txhawb kev loj hlob thiab kev sib txawv ntawm cov leeg pob txha satellite hlwb (cov leeg pob txha), ua kom cov leeg nqaij fiber ntau hypertrophy; Upregulate amino acid thauj thiab protein synthesis, inhibit nqaij protein degradation, thiab txhim kho cov leeg zoo thiab lub zog.
Kev loj hlob ntawm lub cev: Txhawb kev loj hlob ntawm tes thiab kev ua haujlwm ntawm cov kab mob hauv nruab nrog cev xws li lub plawv, lub siab, lub raum, thiab lub ntsws, ua kom muaj kev loj hlob ntawm tus menyuam hauv plab thiab menyuam yaus.

IGF-Kuv muaj insulin-zoo li kev ua haujlwm (kev siv li ntawm 1/60 ntawm insulin) thiab tswj cov roj metabolism, ua haujlwm tseem ceeb ntawm kev loj hlob thiab cov metabolism.
Kev tswj cov ntshav qabzib: txhawb nqa thiab siv cov piam thaj los ntawm cov leeg pob txha thiab cov ntaub so ntswg adipose, accelerates glycogen synthesis; inhibits hepatic gluconeogenesis, txo cov piam thaj hauv siab, txhim kho insulin rhiab heev, thiab pab tswj cov ntshav qabzib.

Cov metabolism hauv rog: txhawb kev rog rog thiab txo cov rog rog; inhibiting qhov kev loj hlob thiab kev sib txawv ntawm adipocytes, txo qhov feem pua ​​​​ntawm cov rog hauv lub cev, tshwj xeeb tshaj yog txo cov roj visceral deposition, thiab txo cov kev pheej hmoo ntawm metabolic syndrome.
Lub zog tshuav nyiaj li cas: tswj qhov chaw hypothalamic qab los noj mov thiab cuam tshuam rau kev noj zaub mov noj; Optimize zog metabolism efficiency los ntawm regulating mitochondrial muaj nuj nqi hauv hlwb.

IGF-Kuv tswj hwm lub voj voog ntawm tes, txhawb nqa kev loj hlob thiab kev sib txawv, inhibits apoptosis, thiab tuav cov ntaub so ntswg ruaj khov ntawm tes los ntawm kev ua kom muaj cov cim qhia tseem ceeb xws li PI3K/Akt thiab MAPK/ERK.
Cell proliferation: stimulates cell faib nyob rau hauv cov ntaub so ntswg xws li daim tawv nqaij, plab hnyuv mucosa, thiab vascular endothelium, txhawb cov ntaub so ntswg loj hlob thiab rov ua dua tshiab.

Anti apoptosis: Txhim kho qhov kev qhia ntawm cov tshuaj tiv thaiv apoptotic protein (Bcl-2), txo qis kev ua haujlwm ntawm pro apoptotic protein (Bax), txo cov cell apoptosis vim yog oxidative kev nyuaj siab, o, ischemia thiab lwm yam kev raug mob, thiab tiv thaiv cov ntaub so ntswg ncaj ncees.
Kev cai sib txawv: Inducing stem cells kom sib txawv rau hauv cov cell tshwj xeeb xws li cov leeg, paj hlwb, thiab cov pob txha, thiab koom nrog cov ntaub so ntswg kho thiab rov tsim dua tshiab.

Insulin-Zoo li Growth Factor-Iyog ib qho tseem ceeb neurotrophic uas plays lub luag hauj lwm irreplaceable nyob rau hauv txoj kev loj hlob, kho, thiab ua hauj lwm kev cai ntawm lub hauv paus thiab peripheral paj hlwb.
Neurodevelopment: txhawb kev loj hlob, kev tsiv teb tsaws, thiab kev sib txawv ntawm embryonic neurons, induces tsim thiab kev sib txuas ntawm neural synapses, thiab tsim neural networks; Ua kom lub cev loj hlob ntawm oligodendrocytes, txhawb nqa myelin synthesis, thiab xyuas kom muaj kev sib kis tau zoo ntawm cov teeb liab neural.

Neuroprotection: Inhibit neuronal apoptosis, alleviate oxidative kev nyuaj siab, glutamate toxicity, thiab o puas rau neurons; Txhawb nqa cerebral ntshav txaus, txhim kho cov khoom noj khoom haus rau lub hlwb, thiab tiv thaiv ischemic thiab hypoxic hlwb raug mob.
Kev paub txog kev ua haujlwm: Txhim kho cov yas ntawm hippocampal neurons, txhawb kev qhia txog kev kawm thiab kev nco txog cov noob, thiab txhim kho kev txawj ntse; Kev ncua kev loj hlob ntawm cov kab mob neurodegenerative xws li senile dementia thiab Parkinson's disease.

Kev loj hlob hormone deficiency (GHD)
Cov menyuam yaus uas muaj GHD tau txo cov kab mob siab IGF-Kuv synthesis vim tsis txaus pituitary GH secretion, ua rau kev loj hlob qeeb, luv luv, thiab ncua hnub nyoog ntawm pob txha.
Diagnostic tus nqi: Txo cov ntshav IGF-I qib yog cov cim qhia biochemical tseem ceeb ntawm GHD, thiab ua ke nrog GH stimulation test tuaj yeem txhim kho qhov tseeb ntawm kev kuaj mob.
Lwm txoj kev kho: Recombinant human IGF-I (rhIGF-I) tuaj yeem txhawb nqa pob txha loj hlob thiab txhim kho qhov siab ntawm cov menyuam yaus uas muaj GH insensitive syndrome (Laron syndrome) thiab GHD uas tsis teb rau rhGH kho.

Idiopathic dwarfism (ISS)
Cov menyuam yaus uas muaj ISS ​​uas tsis muaj GH tsis txaus tab sis muaj cov ntshav IGF qis-Kuv qib lossis tsis txaus ua haujlwm lom neeg yog ib qho ua rau cov menyuam yaus luv.
Kev kuaj mob thiab tus nqi kho mob: Tshawb xyuas IGF-I qib tuaj yeem pab txiav txim siab txog etiology ntawm ISS; RhIGF-Kuv txoj kev kho mob tuaj yeem txhim kho tus nqi loj hlob ntawm cov neeg mob me thiab ua rau cov neeg laus qhov siab.

Cov neeg laus loj hlob hormone deficiency (AGHD)
Cov neeg laus AGHD feem ntau tshwm sim los ntawm cov qog pituitary, phais pituitary, lossis kev kho hluav taws xob, thiab yog tus cwj pwm los ntawm cov nqaij ntshiv, rog rog, osteoporosis, qaug zog, thiab kev txawj ntse poob. Cov kab mob tseem ceeb yog qhov txo qis hauv IGF-I qib.
Kev kuaj mob thiab kev saib xyuas: Serum IGF-Kuv yog qhov zoo tshaj qhov taw qhia rau AGHD kev tshuaj ntsuam xyuas thiab kev saib xyuas kev ua tau zoo, nrog rau qib txo qis txhawb kev kuaj mob.
Lwm txoj kev kho mob: rhGH hloov kho tuaj yeem ua kom cov leeg nqaij, txo cov roj visceral, txhim kho pob txha ceev, thiab txhim kho lub neej zoo los ntawm kev nce IGF-I qib.

Osteoporosis (postmenopausal, senile osteoporosis)
Lub hauv paus ntawm osteoporosis yog txo cov pob txha tsim thiab nce pob txha resorption. IGF-Kuv, raws li qhov tseem ceeb ntawm kev tswj hwm ntawm cov pob txha metabolism, txo qis nrog hnub nyoog thiab muaj feem cuam tshuam rau qhov pib ntawm pob txha.
Pathogenesis koom haum: Txo IGF-Kuv ua rau txo qis kev ua haujlwm ntawm osteoblast, overactivation ntawm osteoclasts, txo cov pob txha ntom, thiab muaj kev pheej hmoo ntawm pob txha.
Therapeutic potential: rhIGF-I combined with calcium supplements and vitamin D can promote bone formation, increase bone density, and reduce the risk of vertebral and non vertebral fractures, especially for elderly osteoporosis.

Alzheimer's Disease (AD)
Qib ntawm IGF-Kuv nyob rau hauv cov ntaub so ntswg ntawm lub hlwb ntawm cov neeg mob AD tau txo qis, uas yog txuam nrog neuronal apoptosis, synaptic poob, thiab kev txawj ntse poob.
Kev tshawb fawb kho mob: Exogenous IGF-Kuv tuaj yeem txo - amyloid deposition, inhibit Tau protein hyperphosphorylation, alleviate neuroinflammation, thiab txhim kho kev kawm thiab kev nco muaj peev xwm, ua rau nws muaj peev xwm kho lub hom phiaj rau AD.
Parkinson tus kab mob (PD)
Lub apoptosis ntawm dopaminergic neurons nyob rau hauv substantia nigra ntawm PD muaj feem xyuam rau tsis txaus IGF-I, uas tuaj yeem tiv thaiv dopaminergic neurons thiab txhawb kev kho paj hlwb.

Kev tshawb nrhiav kev kho mob: IGF-Kuv txoj kev kho mob tuaj yeem ncua qhov kev poob qis ntawm PD lub cev muaj zog, txhim kho cov tsos mob xws li tshee thiab nqaij tawv, thiab ua ke nrog levodopa tuaj yeem txhim kho kev ua tau zoo.
Ischemic mob stroke
Upregulation ntawm IGF-Kuv qhia tom qab cerebral ischemia yog ib qho endogenous neuroprotective mechanism; Exogenous supplementation yuav alleviate hlwb edema, inhibit neuronal apoptosis, txhawb angiogenesis thiab paj hlwb regeneration, thiab txhim kho neurological deficits.

Cov neeg mob uas muaj cov kab mob metabolic (kev rog, ntshav siab, hyperglycemia, hyperlipidemia) feem ntau txo qis ntawm IGF-I thiab insulin tsis kam, thiab IGF-Kuv koom nrog qhov tshwm sim thiab txhim kho cov piam thaj thiab lipid metabolism.
Pathological mechanism: Tsis txaus IGF-Kuv ua rau txo qis insulin rhiab heev thiab nce cov ntshav qabzib; Txo cov rog rog, tsub zuj zuj ntawm visceral rog, thiab exacerbation ntawm metabolic ntshawv siab.
Kev cuam tshuam tus nqi: nce IGF-I qib tuaj yeem txhim kho insulin tsis kam, txo cov ntshav qab zib thiab cov rog hauv lub cev, muab kev cuam tshuam tshiab rau cov kab mob metabolic thiab hom 2 mob ntshav qab zib.

Hlawv thiab mob ntev
Lub xeev metabolic siab ntawm lub cev tom qab kub hnyiab ua rau txo qis hauv IGF-I qib, ncua kev kho ntawm daim tawv nqaij, thiab muaj kev pheej hmoo kis mob.
Daim ntawv thov kev kho mob: Hauv zos lossis kev siv lub cev ntawm rhIGF-Kuv tuaj yeem txhawb kev loj hlob ntawm daim tawv nqaij fibroblasts, collagen synthesis, ua kom lub qhov txhab zoo, thiab txo qis kev tsim caws pliav.

Nqaij atrophy
Kev pw tsaug zog ntev, kev phais immobilization, cov neeg laus tsis muaj zog, qog nqaij hlav cachexia, thiab lwm yam. ua rau txo qis hauv IGF-I qib, ntau dua cov leeg nqaij protein ntau dua li kev sib txuas, txo cov leeg nqaij, thiab txo cov leeg nqaij.
Kev cuam tshuam cuam tshuam: IGF-Kuv tuaj yeem thim rov qab cov leeg nqaij atrophy, nce cov leeg nqaij thiab lub zog, txhim kho cov ceg tawv, thiab txhim kho tus kheej- kev saib xyuas muaj peev xwm ntawm cov neeg laus cov neeg laus uas tsis muaj zog.

Cov qog nqaij hlav ntsig txog (kev pabcuam kuaj mob, kev soj ntsuam kuaj mob, cov hom phiaj kho mob)
Kev ua kom tsis zoo ntawm IGF-Kuv txoj kev taw qhia muaj feem cuam tshuam nrog qhov tshwm sim, cuam tshuam, thiab metastasis ntawm ntau cov qog nqaij hlav, thiab cov ntshav siab IGF-Kuv qib yog cov kab mob qog nqaij hlav.
Kev kuaj mob pab: Cov ntshav IGF-Kuv theem ntawm mob ntsws cancer, mob qog noj ntshav mis, mob qog nqaij hlav prostate, mob qog noj ntshav thiab lwm tus neeg mob tau nce zuj zus, uas tuaj yeem siv los ua qhov ntsuas pab rau kev kuaj mob qog noj ntshav.

Kev soj ntsuam kev soj ntsuam: Siab IGF-Kuv qib qhia tias muaj mob qog noj ntshav siab, muaj kev pheej hmoo siab ntawm metastasis, thiab qhov tsis zoo ntawm cov qog.
Cov hom phiaj kho mob: inhibiting IGF-I/IGF-1R txoj kev taw qhia (xws li IGF-1R monoclonal antibodies) tuaj yeem thaiv cov qog cell proliferation thiab induce apoptosis, ua rau nws yog ib qho tseem ceeb rau kev kho mob qog noj ntshav.