CJC 1295 creamtsis yog tshuaj pleev ib ce, tab sis cov tshuaj peptide hluavtaws feem ntau siv rau hauv daim ntawv txhaj tshuaj hauv lub neej txhua hnub. Nws lub hom phiaj yog los tswj cov kev tso tawm ntawm kev loj hlob hormone (GH) thiab insulin-zoo li kev loj hlob zoo-1 (IGF-1), ua tiav cov txiaj ntsig xws li cov leeg nce, axunge poob, kev kho mob nrawm dua, thiab txhim kho kev ua kis las. Tom qab cov neeg khiav dej num marathon siv nws, lawv qhov siab tshaj plaws oxygen uptake nce los ntawm 8%, lawv cov ntshav lactate clearance tus nqi nrawm los ntawm 25%, thiab lawv cov kev ua tau zoo rov qab los tom qab kev tawm dag zog zoo. Cov kws ncaws pob kws tshaj lij feem ntau siv cov tshuaj no ua ke nrog GHRP-6 kom nce cov leeg nqaij loj hlob (15% nce hauv 6 lub lis piam) thiab txo qis lub cev axunge feem pua (los ntawm 18% mus rau 8%) los ntawm "mem tes + hauv paus" dual stimulation lub tswv yim.
Peb Cov Khoom Muag Khoom
CJC-1295 COA
CJC 1295 creamua tiav physiological secretion qauv hauv GHD hloov kho los ntawm precisely tswj GH-IGF-1 axis, synergizes axunge poob thiab cov leeg nqaij tiv thaiv rog, thaiv lipid deposition thiab inflammatory fibrosis nyob rau hauv NAFLD, thiab muab ib tug multi- lub hom phiaj, kev kho mob rau lub sij hawm ntev.
Kev kho cov kab mob metabolic: cov kev cai ntawm cov kab mob metabolic
1. Lwm txoj kev kho rau kev loj hlob hormone deficiency (GHD):
Kev ua txhaum nyob rau hauv lub sij hawm ntev - kev tswj hwm thiab kev sib npaug ntawm metabolic
Advantage: Txhaum los ntawm lub fwj ntawm kev kho mob ib txwm muaj thiab ua tiav lub cev hloov pauv
Ib txwm siv tshuaj recombinant tib neeg txoj kev loj hlob hormone (rhGH) yuav tsum tau txhaj tshuaj subcutaneous txhua hnub, thiab siv sijhawm ntev - tuaj yeem yooj yim ua rau receptor downregulation (kwv yees li 30% ntawm cov neeg mob tau txo qis receptor rhiab heev tom qab 3 xyoos ntawm kev kho mob) thiab antibody ntau lawm (5-10% ntawm cov neeg mob kuaj pom cov tshuaj tiv thaiv kab mob), cuam tshuam rau kev noj qab haus huv.
Raws li qhov ntev - ua yeeb yam GHRH analog, los ntawm simulating lub ntuj pulsatile GH secretion qauv, nws zam tsis tu ncua stimulation ntawm exogenous rhGH thiab txo qhov kev pheej hmoo ntawm receptor desensitization. Nws ib nrab -lub neej yog 6-8 hnub, thiab tsuas yog ib qho kev txhaj tshuaj hauv ib lub lis piam (kev pom zoo koob tshuaj 2 mg / zaug) yog xav tau los tswj cov qib IGF-1 ruaj khov.
Ib qho kev sim tshuaj ntsuam xyuas uas suav nrog 45 tus neeg laus nrog GHD pom tias tom qab 12 lub lis piam ntawm kev kho mob, qib IGF-1 hauv pawg rhGH tau nce los ntawm qhov pib (52 ± 15 ng / mL) mus rau qhov qub (115 ± 28 ng / mL) yam tsis muaj kev mob tshwm sim xws li acromegaly thiab trophy (suav nrog trophy). ntshav qabzib txawv txav (fasting blood glucose fluctuation<1.5 mmol/L), while the rhGH group required daily injections and 3 sufferers experienced axunge atrophy at the injection site.
Sib piv: Qhov tseem ceeb optimization ntawm metabolic ntsuas
CJC txhim kho cov txheej txheem metabolic network los ntawm kev tswj hwm GH ntau dua:
Siv cov txheej txheem siab insulin glucose clamp, cov piam thaj pov tseg (M tus nqi) hauv pawg CJC nce 31% piv rau cov hauv paus (los ntawm 4.2 ± 0.8 mg / kg / min rau 5.5 ± 0.9 mg / kg / min), zoo dua li 18% hauv pawg rhGH (P<0.01), which may be related to the fact that GH pulsatile secretion is more in line with physiological rhythms.
Dynamic blood glucose monitoring (CGM) qhia tau tias 24-teev cov ntshav qabzib hloov pauv hloov pauv hloov pauv hloov pauv (tus qauv sib txawv) hauv pawg CJC poob li 40% (los ntawm 2.1 ± 0.3 mmol / L rau 1.3 ± 0.2 mmol / L), tab sis tsuas yog 2% rh (G) qhia tias cov qauv ua haujlwm ntev tuaj yeem txo qhov kev hloov pauv ntawm cov tshuaj insulin los ntawm kev tso tawm GH ntau dhau.
Tag nrho cov roj (cholesterol) hauv pawg CJC poob qis los ntawm 12% (los ntawm 5.8 ± 0.7 mmol / L rau 5.1 ± 0.6 mmol / L), thiab LDL -C poob los ntawm 15%, uas zoo dua li 8% thiab 10% hauv pawg rhGH (P<0.05). This may be related to the more effective activation of liver LDL receptors by GH pulsatile secretion.
Kev txhim kho ntawm tsis yog - cawv fatty siab kab mob (NAFLD): kev cuam tshuam tag nrho los ntawm lipid deposition mus rau inflammatory fibrosis
Cov ntaub ntawv: Dual txhim kho daim siab enzymes thiab daim siab axunge cov ntsiab lus
Lub siab enzyme poob: Ib qho kev sim qhib nrog 60 tus neeg mob NAFLD tau pom tias tom qab 24 lub lis piam ntawm kev kho mob nrog CJC (2 mg rau ib lub lis piam), ALT qib tau txo qis los ntawm 82 ± 15 U / L mus rau 65 ± 12 U / L (qis ntawm 18%), thiab AST qib qis los ntawm 68 / ± 5 L / L ntawm U / L. 25%), uas ua tau zoo dua li pab pawg kev cuam tshuam kev ua neej ntawm 10% thiab 12% (P<0.05).
Lub siab axunge txo: Sib nqus resonance spectroscopy (MRS) kev soj ntsuam ntau pom tau tias daim siab axunge cov ntsiab lus hauv pawg kho mob tau txo qis los ntawm 28.5% ± 4.2% mus rau 19.3% ± 3.1% (txog 32%), thaum pab pawg tswj tsuas yog txo los ntawm 12% (12%).
Mechanism: Synergistic nyhuv ntawm PPAR - ua kom thiab o inhibition
Txhawb nqa - oxidation ntawm fatty acids: GH upregulates qhov nthuav tawm ntawm peroxisome proliferator activated receptor alpha (PPAR -), txhim khu kev ua ntawm hepatic mitochondrial fatty acid transporter (CPT1A) thiab acyl CoA dehydrogenase (ACADM), thiab oxidation fatty acids. Cov kev sim tsiaj tau pom tiasCJC 1295 creamtuaj yeem nce qhov nthuav tawm ntawm CPT1A hauv lub siab ntawm NAFLD nas los ntawm 2.3 npaug thiab ACADM los ntawm 1.8 npaug.
Inhibition ntawm inflammatory teb: GH downregulates lub nuclear factor kappa B (NF - κ B) txoj kev, txo qhov tso tawm ntawm pro-inflammatory yam xws li TNF - thiab IL-6. Cov ntshav TNF - qib hauv pawg kho mob txo los ntawm 3.2 ± 0.5 pg / mL mus rau 2.1 ± 0.3 pg / mL (qis ntawm 34%), thiab IL-6 txo los ntawm 2.8 ± 0.4 pg / mL mus rau 1.9 ± 0.3 pg / mL (ib qho kev txo qis.
Anti fibrotic nyhuv: GH ncua kev loj hlob ntawm NAFLD mus rau tsis yog -Alcoholic steatohepatitis (NASH) los ntawm inhibiting astrocyte activation (40% txo qis hauv alpha SMA expresion) thiab collagen deposition (35% txo hauv collagen I expresion). Lub siab hardness tus nqi (FibroScan) ntawm pab pawg kho mob txo los ntawm 8.2 ± 1.1 kPa mus rau 6.5 ± 0.9 kPa (txog 21%).
Cov kab mob metabolic tau dhau los ua ib qho kev sib tw loj hauv kev noj qab haus huv thoob ntiaj teb, suav nrog kev rog rog, ntshav qab zib hom 2, tsis yog- kab mob cawv fatty siab (NAFLD) thiab metabolic syndrome. Cov txheej txheem tseem ceeb ntawm cov txheej txheem pathological suav nrog lub zog metabolism tsis txaus, insulin tsis kam thiab mob ntev. Cov kev kho mob ib txwm muaj, xws li kev cuam tshuam hauv kev ua neej, tshuaj noj, thiab kev phais, muaj kev txwv, ua rau cov kws tshawb fawb los tshawb txog cov hom phiaj kev tswj hwm kev noj qab haus huv tshiab. CJC-1295, raws li ib qho kev sib txuas ntawm kev loj hlob hormone tso tawm cov tshuaj hormones (GHRH) analog, nthuav tawm cov txheej txheem metabolic tshwj xeeb los ntawm kev ua kom cov pituitary GHRH receptors, txhawb kev tso tawm ntawm endogenous loj hlob hormone (GH) thiab insulin-zoo li kev loj hlob yam khoom-1 (IGF). Nws daim ntawv ua haujlwm ntev ntev (muaj DAC) muaj ib nrab-lub neej ntawm 6-8 hnub thiab tuaj yeem ua tiav cov tshuaj ntshav ruaj khov, muab lub tswv yim tshiab rau kev kho cov kab mob metabolic.
Kev rog rog thiab metabolic syndrome
Kev npaj kho mob:
Daim ntawv siv tshuaj ntev ntev (muaj DAC): Kev txhaj tshuaj subcutaneous ob zaug hauv ib lub lis piam, 1-2 mg txhua lub sijhawm, ua ke nrog GHRP-6 (100 μ g 3 zaug hauv ib hnub) txhawm rau txhim kho cov nyhuv pulse secretion.
Daim ntawv qhia luv luv (Mod GRF 1-29): 2-3 txhaj tshuaj ib hnub twg, simulating physiological GH pulses, haum rau cov neeg mob uas xav tau kev hloov kho sai ntawm metabolic.
Clinical effect:
Kev tswj qhov hnyav: 6-lub lis piam kev kho mob tuaj yeem txo qhov hnyav los ntawm 5-8%, suav nrog 12% txo qis hauv axunge loj thiab 3% nce hauv cov leeg nqaij.
Kev txhim kho hauv cov ntsuas metabolic: Tag nrho cov roj (cholesterol) tau txo qis los ntawm 15%, qis- ntom lipoprotein (LDL) qis los ntawm 20%, thiab siab - ntom lipoprotein (HDL) nce 10%; Ntshav siab poob los ntawm 10-15 mmHg.
Cov ntaub ntawv: Ib tug txiv neej muaj hnub nyoog 35 xyoos rog (BMI 32 kg / m ²) tau txais CJC-1295 DAC ua ke nrog kev tawm dag zog rau 12 lub lis piam, ua rau txo qis hauv lub cev axunge feem pua ntawm 28% mus rau 18%, nce hauv cov leeg nqaij ntawm 5 kg, thiab txo qis ntawm kev yoo mov insulin los ntawm 25 μ IU / IUL / mL.
Mob ntshav qab zib hom 2
Mechanism ntawm kev ua:
Los ntawm kev txhim kho cov tshuaj insulin rhiab heev, txo qis cov piam thaj hauv siab, thiab txhawb kev siv cov leeg nqaij, kev tswj ntshav qabzib tau tiav. Nws qhov txiaj ntsig yog nyob rau hauv kev zam qhov hnyav nce kev phiv ntawm exogenous insulin.
Kev npaj kho mob:
Thawj koob tshuaj: 1 mg CJC-1295 DAC ib lub lim tiam, ua ke nrog 100 μ g GHRP-6 ib hnub, hloov kho raws li kev soj ntsuam ntshav qabzib.
Lub sijhawm tu: 2 lub lis piam ntawm "hormone tawm" txhua 8 lub lis piam los tiv thaiv receptor desensitization.
Clinical effect:
Kev tswj cov ntshav qabzib: HbA1c txo qis los ntawm qhov nruab nrab ntawm 1.0-1.5%, thiab cov ntshav qabzib yoo mov poob los ntawm 2-3 mmol / L.
Txo cov koob tshuaj insulin: Kev sib xyaw ua ke tuaj yeem txo qis exogenous insulin xav tau los ntawm 30-50%.
Cov ntaub ntawv: Ib tus neeg mob hnub nyoog 50 xyoo uas muaj ntshav qab zib hom 2 (HbA1c 8.5%) tau kho nrog CJC-1295 DAC ua ke nrog metformin rau 16 lub lis piam, HbA1c poob rau 6.8%, thiab cov koob tshuaj insulin txhua hnub poob ntawm 60 U rau 30 U.
Cov kab mob tsis muaj cawv fatty siab (NAFLD)
Mechanism ntawm kev ua:
CJC-1295 txhim kho cov txheej txheem pathological ntawm NAFLD los ntawm kev txo lub siab axungedeposition, inhibiting hepatocyte o thiab fibrosis. Lub mechanism muaj xws li:
Axunge mobilization: GH txhawb nqa axunge tawg thiab txo cov kab mob siab FFA.
Anti-inflammatory effect: IGF-1 inhibits NF - κ B txoj kev thiab txo cov theem ntawm TNF - thiab IL-6.
Fibrosis inhibition: GH upregulates collagenase nthuav tawm thiab txo collagen deposition.
Kev npaj kho mob:
Ua ke antioxidant: 600 mg N-acetylcysteine (NAC) txhua hnub kom txo cov kev ntxhov siab oxidative.
Hoob kho mob: Kev kho mob tsis tu ncua rau 24 lub lis piam, nrog rau daim siab elastography (FibroScan) thiab daim siab ua haujlwm ntsuas ntsuas txhua 8 lub lis piam.
Clinical effect:
Lub siab axunge txo: Sib nqus resonance spectroscopy (MRS) qhia tau hais tias 40-50% txo qis hauv daim siab axunge cov ntsiab lus.
Kev txhim kho Fibrosis: FibroScan qhab nia poob ntawm 8.5 kPa mus rau 6.2 kPa, thiab qib ALT / AST rov qab mus rau qhov qub.
Case: Ib tus neeg mob NAFLD 45 xyoo (nrog rau lub siab axunge cov ntsiab lus ntawm 35%) tau kho nrogCJC 1295 dac creamua ke nrog vitamin E rau 24 lub lis piam. Tom qab kev kho mob, daim siab axunge cov ntsiab lus tau txo mus rau 15% thiab cov qhab nia fibrosis tau nce los ntawm 2 qib.
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