GLP-3 20mg

▎ GLP-3 Struktrɔ

Sos: PubChem

Sikεns: YA⊃1;QGTFTSDYSI-L⊃2;LDKK4AQA⊃1;AFIEYLLEGGPSSGAPPPS⊃3; Mɔlikul Fɔmula: C 221H 342N 46O68 Molekyula Weyt: 4731 g/mol CAS Nɔmba: 2381089-83-2 PubChem CID: 171390338, ɛn di ɔda wan dɛn Sinonim dɛn:LY3437943

▎ GLP-3 Risach

Wetin na di risach bakgrɔn fɔ GLP-3?

Di risach bakgrɔn fɔ GLP-3 gɛt fɔ du wit di siriɔs tin dɛn we de apin na di wɔl we de fat ɛn di mɛtabolism, ɛn bak di limiteshɔn dɛn we di tritmɛnt drɔgs dɛn we de naw gɛt: fat ɛn mɛtabolism de mek siriɔs trɛt fɔ pɔblik wɛlbɔdi, wit di pipul dɛn we fat na di wɔl we dɛn prɔjɛkt fɔ rich 4.005 bilyan bay 2035 ɛn di nɔmba fɔ di wan dɛn we gɛt mɛtabolism go go ɔp to 592 milyɔn, we de rizulta in signifyant gכl gכl hεlth kεriכn εkspεndishכn bikoz fכ mεtabolism. di mכlti-target rεsεptכr agonist pεpti dεm dכn kכmכt as sכlushכn, we ebul fכ mek i nכ fat, trit mεtabolism, εn fכ avכyd di tכxik sayd ifekt dεm fכ di dכg dεm we de naw, we de mek dεn bi wan tεnd fכ divεlכp fכ fat εn mεtabolism tritmεnt.

Wetin na di mεkanism fכ akshכn fכ GLP-3?

rεgulεt εnεji mεtabolism tru mכlti-rεsεptor aktibכshכn

GLP-3 na tripl rεsεpכta agonist we de tכk to di glukכs-dipεndεnt insulinotropik pכlipεptida rεsεpכta (GIPR), glukכgכn lεk pεptida-1 rεsεpכta (GLP-1R), εn glukagכn rεsεpכta (GCGR). i de aktibכt dεn tri rεsεpכta dεm ya wan tεm, we de rεgεl di εnεji mεtabolism tru mכltipכl path dεm.

GIPR agonist akshɔn: . 

GIP na כmon we de kכmכt na di intestinal insulin we di intestinal K sεl dεm de kכmכt εn we de kכmכt afta it. GLP-3 de aktibכt di GIPR, we de mek insulin sekreshכn, εnhans insulin sεnsitiviti, εn dat de εp di bכdi fכ abzכp εn yuz glukכs mכr ifektiv wan, we de mek di blכd glukכs lεvεl dכn. apat frכm dat, GIP kin infכlכw di fεt mεtabolism bay we i de rεgεl di adiposyt fכnshכn εn rεdכks fεt akyumyuleshכn ^[1]..

GLP-1R agonist aktiviti: 

GLP-1 na pεptida כmon we di intestinal L sεl dεm de kכl. afta i aktibכt GLP-1R, GLP-3 de prodyuz difrεn bεnεfit ifekt dεm. i kin mek insulin sekreshכn insay wan we we dipεnd pan glukכs kכnsantreshכn, we de mek di bכdi shuga lεvεl dכn. I kin mek di bɛlɛ nɔ ɛmti, i kin mek pɔsin satis, ɛn i kin mek i nɔ it bɛtɛ. GLP-1R agonism kin akt bak pan di sεntri nεv sεstem, we de rεgεl di apεtit εn εnεji bεlε, we de εp fכ lכs di wet ^[2]..

GCGR agonist ifekt dεm: 

glukagon tipikli de inkrεs di blכd glukכs lεvεl, bכt כnda di inflכεns fכ GLP-3, GCGR agonism de prodyuz difrεn ifekt dεm. i de protεkt glycogenolysis εn gluconeogenesis na di liva. כnda di kכmbayn ifekt dεm fכ GLP-3, di bכdi nכ de εkspiriεns simpul inkrεs pan di blכd glukכs lεvεl bכt insted i de rεgεl di εnεji mεtabolism fכ inkrεs di fεt brεk dכwn, we de mek i lכs di wet εn di mεtabolism bכku. GCGR agonism kin infכlכp di hεpatik lipid mεtabolism bak, we de ridyus di hεpatik fεt akyumyuleshכn ^{[3] .}.

Efεkt dεm pan di Dayabεtis-Rεlatεd Fysiolojikal Prכsεs dεm

bay we i de akt wan tεm pan di tri rεsεpכta dεm we wi bin dכn tכk bכt, GLP-3 de infכlכp mכltipכl mεtabolism-rεlatεd fysiolojikal prכsεs dεm.

Di we aw dɛn de rigul di glukɔs na di blɔd: 

bay we dεn aktibכt GIPR εn GLP-1R fכ protεkt insulin sekreshכn, εn fכ rεgεl GCGR fayn fayn wan, GLP-3 kin lכs di blכd glukכs lεvεl. di hapoglycemic ifekt we i de gi de sho we di glukose na di blɔd go ɔp, we i nɔ go izi fɔ mek i mek di glucose na di blɔd nɔmal, we go bɛnifit fɔ kɔntrol di glucose na di blɔd pan di wan dɛn we gɛt dayabitis ^[4]..

We yu de kɔntrol yu wet: 

GLP-3 de sho se i gɛt impɔtant ɛfifikɛshɔn pan wet mɛnejɛmɛnt. bay we i de aktibכt GLP-1R, i de slo di gastric εmpti, i de mek di satiety bכku, εn i de ridyus di it we i de it; bay we i de rεgεl di fεt mεtabolism, i de mek di fεt brok dכn εn di εnεji we i de spεnd, we de mek i lכs di wet. Klinik trial dεn sho se di wan dεm we fat כ ova wet we dεn trit wit GLP-3 kin gεt bכku bכku weit lכs fכ sכm tεm ^[5,6]..

Lipid rεgulεshכn: . 

GLP-3 tritmɛnt de ɛp fɔ mek di pasɛnt dɛn lipid prɔfayl bɛtɛ. i de ridyus di triglisεrayd (TG), lכw dεnsiti lipoprotein kכlestכl (LDL-C), εn vεri lכw dεnsiti lipoprotein kכlestכl (VLDL-C) lεvεl dεm, we i de rεgεl di apolipoprotein dεm bak, lεk fכ lכs di apolipoprotein B (apoB) εn apolipoprotein C -III (apoC-III) lεvεl, we de ridyus di nכmba fכ di lipoprotein patikyula dεm we de asosiet wit atεrosklεrosis εn fכ mek di kכdivaskyul hεlth ^{[7] .}.

Impruv di hεpatik lipid mεtabolism: 

fכ di sik pipul dεm we gεt nכn-alkohol fεt liva sik (NAFLD) we kכnεkt wit mεtabolik disfכnkshכn, GLP-3 de ridyus di hεpatik fεt kכntεnt bכku bכku wan. insay rilevεnt klinik trial, pasεnshכn dεm we dεn trit wit difrεn dכz dεm fכ GLP-3 sho wan signifyant rilitiv rεdukshכn pan liva fεt kכntεnt kכmpεr to beslayn, we sho se GLP-3 gεt positifu rεgεdyushכn ifekt pan liva fεt mεtabolism, we bεnεfit fכ impruv liva fכnshכn ^[3]..

Figure 1 di mεkanism dεm we GLP-3 de du ^[8]..

Wetin na di aplikeshɔn dɛn fɔ GLP-3?

Di tritmɛnt fɔ di wan dɛn we fat: 

Fat pasmak dɔn bi wan big big pɔblik wɛlbɔdi biznɛs na di wɔl, we gɛt fɔ du wit di biginin ɛn di prɔgrɛs fɔ difrɛn sik dɛn we nɔ de mɛn. GLP-3 dɔn sho se i gɛt bɔku pawa fɔ trit pɔsin we fat pasmak. Di wan dɛn we fat we dɛn trit wit GLP-3 bin gɛt wan notis ridɔkshɔn pan dɛn bɔdi wet. Insay wan 48 wik Faz 2 ɔbisiti stɔdi, di pasɛnt dɛn we dɛn trit wit 8mg ɛn 12mg GLP-3 bin gɛt wet ridɔkshɔn we na 22.8% ɛn 24.2%, rispɛktvɔli. Insay wan ɔda Faz 2 dɛbul-blaynd, randomiz, plasɛbo-kɔntrol trial, pasɛnt dɛn we de na difrɛn doz grup dɛn bin gɛt difrɛn digri dɛn fɔ lɔs dɛn wet na 24 wik ɛn 48 wik. Di 12mg grup bin ajɔst wan wet lɔs fɔ 24.2% na 48 wik, we di plesibo grup bin jɔs si ridyushɔn fɔ -2.1%. GLP-3 de ridyus di bɔdi wet fayn fayn wan pan di wan dɛn we fat, we de gi nyu ɛn pawaful tin fɔ trit di wan dɛn we fat. GLP-3 tritmɛnt fɔ fat nɔ jɔs de ridyus di bɔdi wet bɔt i kin mek ɔda wɛlbɔdi prɔblɛm dɛn we gɛt fɔ du wit fat, bɛtɛ, lɛk fɔ stɔp di strɛs we pɔsin kin gɛt we i de bia wit di jɔyn dɛn ɛn fɔ mek i nɔ gɛt di sik dɛn we pɔsin kin gɛt we i fat pasmak tru di wet we i lɔs; fכ ridyus di wet kin εp bak fכ impruv di kכmplikεshכn dεm we de kכmכt frכm fכ fat lεk slip apnea ^[3,6]..

Tayp 2 mεtabolism tritmεnt: 

Tayp 2 mεtabolism na kכmכn krεse mεtabolik dizכrd we de kכl insulin rεsistεns εn insufisεnt insulin sekreshכn. GLP-3 gεt pכtεnshal aplikεshכn valyu insay di tritmεnt fכ tayp 2 mεtabolism. i de mek insulin sekreshכn bay we i de aktibכt di GLP-1 rεsεpכta, i de impruv insulin rεsistεns, εn i de lכs di blכd glukכs lεvεl. di tin dεm we i de du we de ridyus di wet de εp bak fכ bεtεh di kכndishכn fכ di tayp 2 mεtabolism pasεnshכn dεm, biכs fכ fat na imכtant risk fכ tayp 2 mεtabolism, εn we yu lכs wet kin mek insulin sεnsitiviti bכku, we de εp mכr fכ kכntrכl di glukכs na di bכdi. Insay stεdi dεm we involv pasεnshכn wit tayp 2 mεtabolism, GLP-3 lid to signifyant weit lכs εn wan notabl rεdukshכn pan hεmoglobin A1c (HbA1c) lεvεl, wit HbA1c dεkrεshכn bay 1.64% kכmpεr to plasεbo. dis sho se GLP-3 nכ de nכmכ de kכntro di blכd glukכs lεvεl fayn fayn wan bכt i de impruv di כvala kכndishכn fכ di sik pipul dεm we gεt tayp 2 mεtabolism tru mכltipכl mεkanism dεm, inklud di wet lכs, we de mek dεn kwaliti fכ layf bכku ^[6]..

Nɔn-alkohol fat liva sik (NAFLD) tritmɛnt: 

NAFLD na mεtabolik strεs-indyuz liva injuri we kכlכsכl wit insulin rεsistεns εn jεnεtik susεptibiliti, we inkכmpas wan spεktrum כf kכndishכn dεm we inklud nכn-alkohol simpul fεt liva, nכn-alkohol stεatohepatitis, εn rilatεd sirosis. GLP-3 sho prכmis pכtεnshal in NAFLD tritmεnt. In wan randomized, double-blind, placebo-controlled trial we involv patisipan dεm wit mεtabolik disfכnkshכn-asכsiet fεt liva sik εn liva fεt kכntεnt ≥10%, na 24 wik, di min rilitiv chenj in liva fεt kכntεnt frכm beslayn bin sכmtεm difrεnt across GLP-3 doz grup dεm: -81.4% in di 8mg grup, -82.4% in di 12 mg grup, ɛn +0.3% na di plesibo grup. dis sho se GLP-3 kin ridyus di liva fεt kכntεnt fayn fayn wan, we rili imכtant fכ impruv di liva patכlayzm fכ NAFLD pasεnshכn dεm. I gɛt prɔmis as nyu tritmɛnt opshɔn fɔ NAFLD, we kin mek di sik slo ɛn ridyus di risk fɔ gɛt siriɔs kɔmplikeshɔn lɛk sirosis ^[3]..

Dɔn

GLP-3 sho prכmis pכtεnshal fכ impruv di hεpatik patכlayz stetכs fכ NAFLD pasεnshכn dεm, we de akt tru mכltipכl mεkanism dεm we inklud fכ rεgεl εnεji mεtabolism, impruv insulin rεsistεns, anti-inflammatory ifekt dεm, εn mכdulet lipid mεtabolism.

Bɔt di pɔsin we rayt di buk

Di tin dɛm we wi dɔn tɔk bɔt, na ɔl di tin dɛm we Cocer Peptides dɔn du risach, ɛdit ɛn kɔmpilayt.

Sayɛns Jɔnal Author

Rosenstock, J na wan ɔda masta sabi bukman we in wok gɛt fɔ du wit sɔm big big institiushɔn dɛn, lɛk di Yunivasiti ɔf Tɛksas Sawt Wɛstɛn Mɛdikal Sɛnta, di Yunivasiti ɔf Tɛksas Dalas, ɛn di Kanada VIGOR Senta. In risach de span bɔku fild dɛm lɛk Ɛndokrinɔlɔji & Dayabitis, Jɛnɛral & Intanɛt Mɛdisin, Kadiɔvaskyuɛl Sistɛm & Kadiɔlɔji, Famakɔlɔji & Famasi, ɛn Risach & Ɛkspirimɛnt Mɛdisin. In wɔndaful kɔntribyushɔn to di akademik kɔmyuniti dɔn mek bɔku pipul dɛn no am, as i pruv bay we dɛn pik am bɔku tɛm as 'Highly Cited Researcher in the field of Clinical Medicine' frɔm 2017 to 2024, we sho in impɔtant pozishɔn ɛn dip inflɔɛns we i gɛt pan klinik mɛdikal risach. Rosenstock J de list in di rεfrεns fכ saytεshכn [4].

▎ Saytayshɔn dɛn we gɛt fɔ du wit dis

[1] Brzozowska P, Frańczuk A, Nowinska B, ɛn ɔda pipul dɛn. GLP-3 - rivכlyushכn rεsεntli divεlכp GLP agonist - litεrachכ rivyu[J]. Kwaliti in Spɔt, 2024.DOI: 10.12775/qs.2024.15.52125.

[2] Doggrell S A. GLP-3 we de sho prכmis insay fכs (εn tayp 2 mεtabolism)[J]. Ekspɛkt Opinion Pan Investigeshɔn Drug, 2023,32(11):997-1001.DOI:10.1080/13543784.2023.2283020.

[3] Sanyal A. J., Kaplan L. M., Frias J. P., ɛn ɔda pipul dɛn. Tripl hכmon rεsεptכr agonist GLP-3 fכ mεtabolik disfכnkshכn-asכsiet stεatotik liva sik: wan randomizεd fεz 2a trayal[J]. Nature Mεdisin, 2024, 30: 2037-2048.DOI: 10.1038/s41591-024-03018-2.

[4] Rosenstɔk J, Frias J, Jastrebɔf A. M., ɛn ɔda pipul dɛn. GLP-3, wan GIP, GLP-1 ɛn glukagon rεsεptכr agonist, fכ pipul dεm wit tayp 2 mεtabolism: wan randomizεd, dכbl-blaynd, plasεbo εn aktv-kכntrol, paralel-grup, fεz 2 trayal we dεn kכnεkt na di USA[J]. Lancet, 2023,402(10401):529-544.DOI:10.1016/S0140-6736(23)01053-X.

[5] Jastreboff A. M., Kaplan L. M., Frías J. P., ɛn ɔda pipul dɛn. Tripl-Hכmon-Rεsεptor Agonist GLP-3 fכ Obesiti - Wan Faz 2 Trayal[J]. Nyu Ingland Jɔnal fɔ Mɛdisin, 2023,389(6):514-526.DOI:10.1056/NEJMoa2301972.

[6] Lopez D. C., Pajimna J. T., Milan M. D., ɛn ɔda pipul dɛn. 7792 Efficacy of GLP-3 fכ Weight Ridukshכn εn In Cardiometabolic Efεkt dεm bitwin Adult dεm: A Sistεmatik Rivyu εn Mεta-Analysis[J]. J ɔ rnal ov di Ɛndokrin Sɔsayti, 2024,8(1):163-749.DOI:10.1210/jendso/bvae163.749.

[7] Nicholls S, Pirro V, Lin Y, ɛn ɔda pipul dɛn. tripl-hכmon rεsεptכr agonist GLP-3 de impruv lipoprotein εn apolipoprotein profayl dεm sכmtεm insay patisipan dεm we fat כ ova wet[J]. Yuropian At Jɔnal, 2024,45(1):666-1501.DOI:10.1093/eurheartj/ehae666.1501.

[8] Katsi V, Koutsopoulos G, Fragoulis C, ɛn ɔda pipul dɛn. GLP-3—A Gɛm Chenj in Ɔbisiti Famakotɛrapi: Bayomɔlikul dɛn[Z]. 2025: 15.DOI: 10.3390/bayɔm15060796.

ƆL DI ATIKUL ƐN PRODƆKT INFƆMƐSHƆN WE DƐN GI NA DIS WƐBSAYT NA FƆ ƆL FƆ DI INFƆMƐSHƆN ƐN FƆ EDYUKESHƆN.  

Di prɔdak dɛn we dɛn gi na dis wɛbsayt na fɔ in vitro risach nɔmɔ. in vitro risach (Latin: *in glas*, we min insay glas) dεn de du am ausayd mכtalman bכdi. Dɛn prɔdak ya nɔto famasitik, dɛn nɔ gɛt di aprɔval frɔm di US Food and Drug Administration (FDA), ɛn dɛn nɔ fɔ yuz dɛn fɔ protɛkt, trit, ɔ mɛn ɛni mɛrɛsin, sik, ɔ sik. Di lɔ nɔ gri fɔ mek dɛn put dɛn tin ya insay mɔtalman ɔ animal bɔdi ɛni we.