TY  - JOUR
AU  - Dobutović, Branislava
AU  - Sudar, Emina
AU  - Soskić, Sanja S.
AU  - Obradović, Milan M.
AU  - Nikolić, Dragana
AU  - Gluvić, Zoran
AU  - Stokić, Edita
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10323
AB  - Gojaznost se danas smatra bolešću savremenog društva i njena zastupljenost u svetu ima karakter epidemije. Istraživanja usmerena na razumevanje biologije adipocitne ćelije i adipoznog tkiva, značajno doprinose rasvetljavanju mnogih aspekata različitih metaboličkih poremećaja koji prate pojavu gojaznosti tj. prekomerenog prisustva adipoznog tkiva. Gojaznost je posledica dugotrajnog pozitivnog energetskog balansa, neprimerenog stilu života savremenog čoveka. Danas je utemeljena činjenica da je adipozno tkivo endokrini organ u kojem se sintetiše i eksprimira više od 60 različitih faktora - adipokina, sa snažnim uticajem na veliki broj metaboličkih procesa u organizmu. Adipokini mogu imati pro-inflamatorno ili anti-inflamatorno dejstvo. Mnogobrojna istraživanja jasno ukazuju na uzročnu vezu gojaznosti i hronične inflamacije slabog inteziteta, koja vodi razvoju poremećaja vezanih za prisustvo gojaznosti, naročito metaboličkih poremećaja koji znatno umanjuju kvalitet života. Svojom endokrinom funkcijom, adipocitne ćelije reflektuju metabolički status i prenose informaciju na druge organe, tkiva kao i centralni nervni sistem.
AB  - Obesity is a disease of the modern society and considering the number of obese people it has character of the worldwide epidemic. Understanding the biology of adipocytes and the events occurring in adipose tissue contributes to clarification of many aspects of the various metabolic disorders associated with obesity and excessive presence of adipose tissue. Overweight in individuals is the result of a long-term positive energy balance inappropriate to life style of the modern man. Today, it is well accepted that adipose tissue is an endocrine organ in which more than 60 of adipokines are synthesized and are expressed with strong influence on a great number of metabolic processes in organism. Adipokines have pro-inflammatory or anti-inflammatory effects. Increasing evidence indicates that obesity is causally linked to a chronic low-grade inflammatory state, and contributes to the development of obesity-linked disorders, in particular to metabolic dysfunction which significantly reduces the quality of life. Adipocytes, with their endocrine function, reflect metabolic status and transport information into organs, tissues and central nervous system, too.
T2  - Medicinska istraživanja
T1  - Patofiziologija gojaznosti
T1  - Pathophysiology of obesity
VL  - 46
IS  - 1
SP  - 43
EP  - 54
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10323
ER  - 

@article{
author = "Dobutović, Branislava and Sudar, Emina and Soskić, Sanja S. and Obradović, Milan M. and Nikolić, Dragana and Gluvić, Zoran and Stokić, Edita and Radak, Đorđe J. and Isenović, Esma R.",
year = "2012",
abstract = "Gojaznost se danas smatra bolešću savremenog društva i njena zastupljenost u svetu ima karakter epidemije. Istraživanja usmerena na razumevanje biologije adipocitne ćelije i adipoznog tkiva, značajno doprinose rasvetljavanju mnogih aspekata različitih metaboličkih poremećaja koji prate pojavu gojaznosti tj. prekomerenog prisustva adipoznog tkiva. Gojaznost je posledica dugotrajnog pozitivnog energetskog balansa, neprimerenog stilu života savremenog čoveka. Danas je utemeljena činjenica da je adipozno tkivo endokrini organ u kojem se sintetiše i eksprimira više od 60 različitih faktora - adipokina, sa snažnim uticajem na veliki broj metaboličkih procesa u organizmu. Adipokini mogu imati pro-inflamatorno ili anti-inflamatorno dejstvo. Mnogobrojna istraživanja jasno ukazuju na uzročnu vezu gojaznosti i hronične inflamacije slabog inteziteta, koja vodi razvoju poremećaja vezanih za prisustvo gojaznosti, naročito metaboličkih poremećaja koji znatno umanjuju kvalitet života. Svojom endokrinom funkcijom, adipocitne ćelije reflektuju metabolički status i prenose informaciju na druge organe, tkiva kao i centralni nervni sistem., Obesity is a disease of the modern society and considering the number of obese people it has character of the worldwide epidemic. Understanding the biology of adipocytes and the events occurring in adipose tissue contributes to clarification of many aspects of the various metabolic disorders associated with obesity and excessive presence of adipose tissue. Overweight in individuals is the result of a long-term positive energy balance inappropriate to life style of the modern man. Today, it is well accepted that adipose tissue is an endocrine organ in which more than 60 of adipokines are synthesized and are expressed with strong influence on a great number of metabolic processes in organism. Adipokines have pro-inflammatory or anti-inflammatory effects. Increasing evidence indicates that obesity is causally linked to a chronic low-grade inflammatory state, and contributes to the development of obesity-linked disorders, in particular to metabolic dysfunction which significantly reduces the quality of life. Adipocytes, with their endocrine function, reflect metabolic status and transport information into organs, tissues and central nervous system, too.",
journal = "Medicinska istraživanja",
title = "Patofiziologija gojaznosti, Pathophysiology of obesity",
volume = "46",
number = "1",
pages = "43-54",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10323"
}

Dobutović, B., Sudar, E., Soskić, S. S., Obradović, M. M., Nikolić, D., Gluvić, Z., Stokić, E., Radak, Đ. J.,& Isenović, E. R.. (2012). Patofiziologija gojaznosti. in Medicinska istraživanja, 46(1), 43-54.
https://hdl.handle.net/21.15107/rcub_vinar_10323

Dobutović B, Sudar E, Soskić SS, Obradović MM, Nikolić D, Gluvić Z, Stokić E, Radak ĐJ, Isenović ER. Patofiziologija gojaznosti. in Medicinska istraživanja. 2012;46(1):43-54.
https://hdl.handle.net/21.15107/rcub_vinar_10323 .

Dobutović, Branislava, Sudar, Emina, Soskić, Sanja S., Obradović, Milan M., Nikolić, Dragana, Gluvić, Zoran, Stokić, Edita, Radak, Đorđe J., Isenović, Esma R., "Patofiziologija gojaznosti" in Medicinska istraživanja, 46, no. 1 (2012):43-54,
https://hdl.handle.net/21.15107/rcub_vinar_10323 .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Nikolić, Dragana
AU  - Dobutović, Branislava
AU  - Sudar, Emina
AU  - Soskić, Sanja S.
AU  - Tanasković, Slobodan
AU  - Boljević, Miljana
AU  - Mušicki, Biljana
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10325
AB  - Ateroskleroza se manifestuje kao bolest koronarnih, perifernih i cerebrovaskularnih arterija. Aterosklerotične promene dovode do sužavanja prečnika arterija što dovodi do ishemije u mnogobrojnim organima, čime je poremećeno normalno funkcionisanje kako organa tako i organizma u celini. Centralnu ulogu u patogenezi ateroskleroze zauzima aterogena dislipidemija. Razvoj ateroskleroze počinje malim oštećenjima endotela izazvanim različitim činiocima, koji mogu uticati na povećanje ekspresije adhezivnih molekula. Disfunkcionalni endotel je mesto gde dolazi do infiltracije i akumulacije lipoproteina male gustine (LDL) u vaskularnom zidu. LDL tada podleže oksidativnoj modifikaciji, a kao krajnji produkt nastaje oksidovani LDL (oxLDL). Mnogobrojna eksperimentalna istraživanja ukazuju da su male guste LDL-čestice mnogo aterogenije u poređenju sa većim i lakšim LDL česticama. LDL podleže različitom stepenu oksidacije. Minimalno oksidovani LDL (LDL( - )) pokazuje svoj aterogeni potencijal time što stimuliše vaskularne endotelne ćelije na lučenje velikog broja proinflamatornih molekula kao što su adhezivni molekuli, hemotaktni proteini i faktori rasta. Za razliku od LDL(-), potpuno oksidovani LDL nema sposobnost preuzimanja putem LDL receptora već ga prepoznaju recptori 'hvatači', što dovodi do formiranja makrofag penastih ćelija a u nastavku i stvaranja ateroma. Prisustvo oxLDL u cirkulaciji kod ljudi predstavlja jedan od glavnih faktora rizika od kardiovaskularnih bolesti i ateroskleroze. Buduće studije imaju zadatak da izuče šta se dešava sa oxLDL- om in vivo, kao i da li je i u kojoj meri oksidacija LDL koja igra ključnu ulogu u nastanku penastih ćelija, značajna u kasnijim fazama stvaranja plaka.U okviru ovog preglednog člana, izloženi su najnoviji podaci iz litearture o uticaju oxLDL-a u patogenezi arteroskleroze.
AB  - Atherosclerosis is manifested as a disease of coronary, cerebrovascular and peripheral arteries. Atherosclerotic changes lead to narrowing of the diameter of the arteries leading to ischemia in various organs, which disturbes the normal functioning of both organs and organism as a whole. Atherogenic dyslipidemia has a central role in the pathogenesis of atherosclerosis. Development of atherosclerosis begins with endothelial damage caused by variety of factors, which may cause an increase in expression of adhesion molecules. Dysfunctional endothelium is the place where infiltration and accumulation of low density lipoprotein (LDL) in the vascular wall occurs. LDL undergoes oxidative modification and the final product produced is oxidized LDL (oxLDL). Numerous experimental studies sug- gest that small dense LDL particles are particularly atherogenic compared with larger and lighter LDL particles. LDL is subject to varying degrees of oxidation. Minimally oxidized LDL (LDL(- )) exhibits its atherogenic potential by stimulating vascular endothelial cells to secrete a large number of proinflammatory molecules, such as adhesion molecules, chemotactic proteins, and growth factors. Unlike the LDL(-), fully oxidized LDL cannot bind the LDL receptors, but is recognized by scavenger receptors, which leads to the formation of macrophage foam cells and eventually atheroma. The presence of oxLDL in the circulation in humans is a major risk factor for cardiovascular disease and atherosclerosis. Future studies are warranted to elucidate the role of oxLDL in vivo, and whether and to what extent oxidation of LDL, which plays a key role in the development of foam cells, is critical for later stages in creating the plaque. In this review article, we present current knowledge of the impact of oxLDL in the pathogenesis of arteriosclerosis.
T2  - Medicinska istraživanja
T1  - Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze
T1  - Aterosclerosis and effect of oxidation low density lipoprotein in patogenesis of aterosclerosis
VL  - 45
IS  - 4
SP  - 66
EP  - 71
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10325
ER  - 

@article{
author = "Obradović, Milan M. and Nikolić, Dragana and Dobutović, Branislava and Sudar, Emina and Soskić, Sanja S. and Tanasković, Slobodan and Boljević, Miljana and Mušicki, Biljana and Radak, Đorđe J. and Isenović, Esma R.",
year = "2011",
abstract = "Ateroskleroza se manifestuje kao bolest koronarnih, perifernih i cerebrovaskularnih arterija. Aterosklerotične promene dovode do sužavanja prečnika arterija što dovodi do ishemije u mnogobrojnim organima, čime je poremećeno normalno funkcionisanje kako organa tako i organizma u celini. Centralnu ulogu u patogenezi ateroskleroze zauzima aterogena dislipidemija. Razvoj ateroskleroze počinje malim oštećenjima endotela izazvanim različitim činiocima, koji mogu uticati na povećanje ekspresije adhezivnih molekula. Disfunkcionalni endotel je mesto gde dolazi do infiltracije i akumulacije lipoproteina male gustine (LDL) u vaskularnom zidu. LDL tada podleže oksidativnoj modifikaciji, a kao krajnji produkt nastaje oksidovani LDL (oxLDL). Mnogobrojna eksperimentalna istraživanja ukazuju da su male guste LDL-čestice mnogo aterogenije u poređenju sa većim i lakšim LDL česticama. LDL podleže različitom stepenu oksidacije. Minimalno oksidovani LDL (LDL( - )) pokazuje svoj aterogeni potencijal time što stimuliše vaskularne endotelne ćelije na lučenje velikog broja proinflamatornih molekula kao što su adhezivni molekuli, hemotaktni proteini i faktori rasta. Za razliku od LDL(-), potpuno oksidovani LDL nema sposobnost preuzimanja putem LDL receptora već ga prepoznaju recptori 'hvatači', što dovodi do formiranja makrofag penastih ćelija a u nastavku i stvaranja ateroma. Prisustvo oxLDL u cirkulaciji kod ljudi predstavlja jedan od glavnih faktora rizika od kardiovaskularnih bolesti i ateroskleroze. Buduće studije imaju zadatak da izuče šta se dešava sa oxLDL- om in vivo, kao i da li je i u kojoj meri oksidacija LDL koja igra ključnu ulogu u nastanku penastih ćelija, značajna u kasnijim fazama stvaranja plaka.U okviru ovog preglednog člana, izloženi su najnoviji podaci iz litearture o uticaju oxLDL-a u patogenezi arteroskleroze., Atherosclerosis is manifested as a disease of coronary, cerebrovascular and peripheral arteries. Atherosclerotic changes lead to narrowing of the diameter of the arteries leading to ischemia in various organs, which disturbes the normal functioning of both organs and organism as a whole. Atherogenic dyslipidemia has a central role in the pathogenesis of atherosclerosis. Development of atherosclerosis begins with endothelial damage caused by variety of factors, which may cause an increase in expression of adhesion molecules. Dysfunctional endothelium is the place where infiltration and accumulation of low density lipoprotein (LDL) in the vascular wall occurs. LDL undergoes oxidative modification and the final product produced is oxidized LDL (oxLDL). Numerous experimental studies sug- gest that small dense LDL particles are particularly atherogenic compared with larger and lighter LDL particles. LDL is subject to varying degrees of oxidation. Minimally oxidized LDL (LDL(- )) exhibits its atherogenic potential by stimulating vascular endothelial cells to secrete a large number of proinflammatory molecules, such as adhesion molecules, chemotactic proteins, and growth factors. Unlike the LDL(-), fully oxidized LDL cannot bind the LDL receptors, but is recognized by scavenger receptors, which leads to the formation of macrophage foam cells and eventually atheroma. The presence of oxLDL in the circulation in humans is a major risk factor for cardiovascular disease and atherosclerosis. Future studies are warranted to elucidate the role of oxLDL in vivo, and whether and to what extent oxidation of LDL, which plays a key role in the development of foam cells, is critical for later stages in creating the plaque. In this review article, we present current knowledge of the impact of oxLDL in the pathogenesis of arteriosclerosis.",
journal = "Medicinska istraživanja",
title = "Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze, Aterosclerosis and effect of oxidation low density lipoprotein in patogenesis of aterosclerosis",
volume = "45",
number = "4",
pages = "66-71",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10325"
}

Obradović, M. M., Nikolić, D., Dobutović, B., Sudar, E., Soskić, S. S., Tanasković, S., Boljević, M., Mušicki, B., Radak, Đ. J.,& Isenović, E. R.. (2011). Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze. in Medicinska istraživanja, 45(4), 66-71.
https://hdl.handle.net/21.15107/rcub_vinar_10325

Obradović MM, Nikolić D, Dobutović B, Sudar E, Soskić SS, Tanasković S, Boljević M, Mušicki B, Radak ĐJ, Isenović ER. Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze. in Medicinska istraživanja. 2011;45(4):66-71.
https://hdl.handle.net/21.15107/rcub_vinar_10325 .

Obradović, Milan M., Nikolić, Dragana, Dobutović, Branislava, Sudar, Emina, Soskić, Sanja S., Tanasković, Slobodan, Boljević, Miljana, Mušicki, Biljana, Radak, Đorđe J., Isenović, Esma R., "Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze" in Medicinska istraživanja, 45, no. 4 (2011):66-71,
https://hdl.handle.net/21.15107/rcub_vinar_10325 .

TY  - JOUR
AU  - Sudar, Emina
AU  - Stokić, Edita
AU  - Nikolić, Dragana
AU  - Dobutović, Branislava
AU  - Soskić, Sanja S.
AU  - Obradović, Milan M.
AU  - Tanasković, Slobodan
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10326
AB  - Sekretagozi hormona rasta (GHS) su sintetička jedinjenja koja su potentni stimulatori oslobađanja hormona rasta (GH) i deluju preko receptora spregnutog sa guanin nukleotid-vezujućim (G) proteinom, koji se naziva GHS-receptor (GHS-R). Metodom reverzne farmakologije identifikovan je i okarakterisan endogeni ligand za GHS-R tipa 1a (GHS-R1a), koji je nazvan grelin. Grelin je peptidni hormon građen od 28 aminokiselina, u kome je aminokiselina Serin-3 (Ser3) noktanoilovana, odnosno ima modifikaciju u vidu lanca masnih kiselina koja je esencijalna za njegovu aktivnost. Grelin se najviše sintetiše u želucu, a GHS-R su eksprimirani većinom u hipotalamusu i hipofizi. Ishrana je najvažniji faktor koji utiče na regulaciju sekrecije grelina. Koncentracija grelina u cirkulaciji povećana je za vreme gladovanja, a opada nakon uzimanja hrane. Grelin stimuliše oslobađanje GH u mnogo većim količinama nego maksimalne doze GH-oslobađajućeg hormona (GHRH) što ukazuje na drugačiji mehanizam delovanja grelina na nivou hipofize. iRNK za grelin i za GHS-R1a identifikovane su i u srcu i u aorti. Proučavanja efekata grelina, pokazala su njegove povoljne efekte na kardiovaskularni sistem (CVS). S obzirom da grelin stimuliše oslobađanje GH, za koji je ranije pokazano da ima kardioprotektivne efekte, grelin može da ispoljava povoljne efekte na CVS posredovane preko GH, ali i efekte koji su nezavisni od efekata GH. Povoljni efekti grelina na CVS pružaju mogućnost da se grelin koristi u terapiji oboljenja CVS kao što su poremećaji u radu srca, hipertenzija i bolesti ishemije srca.
AB  - Small synthetic molecules called growth hormone (GH) secretagogues (GHS) stimulate the release of GH from the pituitary. They act through the GHS-receptor (GHS-R), a G protein coupled receptor. Recently, by using a method of reverse pharmacology the endogenous ligand for the GHS-R type 1a (GHS-R1a) has been discovered. Ghrelin is a 28 amino acid peptide hormone in which the third amino acid serine (Ser3) is modified by a fatty acid and this modification is essential for ghrelin's activity. Ghrelin is produced mainly in the stomach and GHS-R is mainly expressed in hypothalamus and in the pituitary. The discovery of ghrelin indicates that the release of GH from the pituitary might be regulated not only by hypothalamic GH-releasing hormone (GHRH), but also by ghrelin derived from the stomach. In addition, ghrelin stimulates appetite by acting on the hypothalamic arcuate nucleus, a region known to control food intake. The tissue distribution of ghrelin is widespread, and it is also present in cardiomyocytes. In addition, expression of mRNA encoding both ghrelin and GHSR-1a has been observed in the heart and aortas. Recent evidence indicates that ghrelin feature a variety of cardiovascular activities, including increase of myocardial contractility, vasodilatation, and protection from myocardial infarction. It has been shown that ghrelin may improve cardiac function partly through GH dependent mechanisms but also, some evidence suggests that ghrelin's cardioprotective activity is independent from GH secretion. Thus, ghrelin may be a new therapeutic agent for the treatment of some cardiovascular disturbances and diseases. Further studies are necessary to investigate the potential mechanisms for the effects of ghrelin on cardiovascular system.
T2  - Medicinska istraživanja
T1  - Opšte osobine i efekti grelina na kardiovaskularni sistem
T1  - Ghrelin structure and cardiovascular effects
VL  - 45
IS  - 4
SP  - 15
EP  - 29
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10326
ER  - 

@article{
author = "Sudar, Emina and Stokić, Edita and Nikolić, Dragana and Dobutović, Branislava and Soskić, Sanja S. and Obradović, Milan M. and Tanasković, Slobodan and Radak, Đorđe J. and Isenović, Esma R.",
year = "2011",
abstract = "Sekretagozi hormona rasta (GHS) su sintetička jedinjenja koja su potentni stimulatori oslobađanja hormona rasta (GH) i deluju preko receptora spregnutog sa guanin nukleotid-vezujućim (G) proteinom, koji se naziva GHS-receptor (GHS-R). Metodom reverzne farmakologije identifikovan je i okarakterisan endogeni ligand za GHS-R tipa 1a (GHS-R1a), koji je nazvan grelin. Grelin je peptidni hormon građen od 28 aminokiselina, u kome je aminokiselina Serin-3 (Ser3) noktanoilovana, odnosno ima modifikaciju u vidu lanca masnih kiselina koja je esencijalna za njegovu aktivnost. Grelin se najviše sintetiše u želucu, a GHS-R su eksprimirani većinom u hipotalamusu i hipofizi. Ishrana je najvažniji faktor koji utiče na regulaciju sekrecije grelina. Koncentracija grelina u cirkulaciji povećana je za vreme gladovanja, a opada nakon uzimanja hrane. Grelin stimuliše oslobađanje GH u mnogo većim količinama nego maksimalne doze GH-oslobađajućeg hormona (GHRH) što ukazuje na drugačiji mehanizam delovanja grelina na nivou hipofize. iRNK za grelin i za GHS-R1a identifikovane su i u srcu i u aorti. Proučavanja efekata grelina, pokazala su njegove povoljne efekte na kardiovaskularni sistem (CVS). S obzirom da grelin stimuliše oslobađanje GH, za koji je ranije pokazano da ima kardioprotektivne efekte, grelin može da ispoljava povoljne efekte na CVS posredovane preko GH, ali i efekte koji su nezavisni od efekata GH. Povoljni efekti grelina na CVS pružaju mogućnost da se grelin koristi u terapiji oboljenja CVS kao što su poremećaji u radu srca, hipertenzija i bolesti ishemije srca., Small synthetic molecules called growth hormone (GH) secretagogues (GHS) stimulate the release of GH from the pituitary. They act through the GHS-receptor (GHS-R), a G protein coupled receptor. Recently, by using a method of reverse pharmacology the endogenous ligand for the GHS-R type 1a (GHS-R1a) has been discovered. Ghrelin is a 28 amino acid peptide hormone in which the third amino acid serine (Ser3) is modified by a fatty acid and this modification is essential for ghrelin's activity. Ghrelin is produced mainly in the stomach and GHS-R is mainly expressed in hypothalamus and in the pituitary. The discovery of ghrelin indicates that the release of GH from the pituitary might be regulated not only by hypothalamic GH-releasing hormone (GHRH), but also by ghrelin derived from the stomach. In addition, ghrelin stimulates appetite by acting on the hypothalamic arcuate nucleus, a region known to control food intake. The tissue distribution of ghrelin is widespread, and it is also present in cardiomyocytes. In addition, expression of mRNA encoding both ghrelin and GHSR-1a has been observed in the heart and aortas. Recent evidence indicates that ghrelin feature a variety of cardiovascular activities, including increase of myocardial contractility, vasodilatation, and protection from myocardial infarction. It has been shown that ghrelin may improve cardiac function partly through GH dependent mechanisms but also, some evidence suggests that ghrelin's cardioprotective activity is independent from GH secretion. Thus, ghrelin may be a new therapeutic agent for the treatment of some cardiovascular disturbances and diseases. Further studies are necessary to investigate the potential mechanisms for the effects of ghrelin on cardiovascular system.",
journal = "Medicinska istraživanja",
title = "Opšte osobine i efekti grelina na kardiovaskularni sistem, Ghrelin structure and cardiovascular effects",
volume = "45",
number = "4",
pages = "15-29",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10326"
}

Sudar, E., Stokić, E., Nikolić, D., Dobutović, B., Soskić, S. S., Obradović, M. M., Tanasković, S., Radak, Đ. J.,& Isenović, E. R.. (2011). Opšte osobine i efekti grelina na kardiovaskularni sistem. in Medicinska istraživanja, 45(4), 15-29.
https://hdl.handle.net/21.15107/rcub_vinar_10326

Sudar E, Stokić E, Nikolić D, Dobutović B, Soskić SS, Obradović MM, Tanasković S, Radak ĐJ, Isenović ER. Opšte osobine i efekti grelina na kardiovaskularni sistem. in Medicinska istraživanja. 2011;45(4):15-29.
https://hdl.handle.net/21.15107/rcub_vinar_10326 .

Sudar, Emina, Stokić, Edita, Nikolić, Dragana, Dobutović, Branislava, Soskić, Sanja S., Obradović, Milan M., Tanasković, Slobodan, Radak, Đorđe J., Isenović, Esma R., "Opšte osobine i efekti grelina na kardiovaskularni sistem" in Medicinska istraživanja, 45, no. 4 (2011):15-29,
https://hdl.handle.net/21.15107/rcub_vinar_10326 .

TY  - JOUR
AU  - Nikolić, Dragana
AU  - Gluvić, Zoran
AU  - Akšam, Slavica
AU  - Obradović, Milan M.
AU  - Dobutović, Branislava
AU  - Soskić, Sanja S.
AU  - Sudar, Emina
AU  - Trpković, Andreja
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10327
AB  - Oksidativni stres (OxS) je skup poremećaja dinamičke ravnoteže prooksidanasa i antioksidanasa koji nastaje usled povećane produkcije slobodnih radikala (SR) ili usled smanjene aktivnosti antioksidativnog zaštitnog sistema (AOS). Bolest koja se, takođe, povezuje sa OxS je i diabetes mellitus (DM). DM karakteriše povećani nivo glukoze u cirkulaciji, kao i drugi biohemijski poremećaji koji nastaju kao posledica neadekvatne produkcije ili neadekvatnog dejstva insulina. Dijabetes tipa 1 (DMT1) je prototip autoimune bolesti sa intenzivnim OxS. Antioksidativni enzim katalaza (CAT) smanjuje produkciju vodonik-peroksida koji može biti veoma toksičan za ćelije pankreasa. Povećanje aktivnosti CAT u svim fazama DMT1 indirektno potvrđuje značaj OxS u nastanku ove bolesti. Visoko reaktivni SR, nastali uglavnom zbog hiperglikemije, izazivaju OxS što dodatno ubrzava razvoj i napredovanje DM kao i njegovih komplikacija koje su uzrokovane redukovanom aktivnošću AOS. Uprkos brojnim dokazima o štetnim posledicama OxS u DM, veliki broj kliničkih ispitivanja sa klasičnim antioksidansima, nažalost, nije pokazao efikasnost njihove primene u lečenju DM. Novi terapijski pristup, koji uključuje primenu kako standardnih tako i novih antioksidanasa, se predlaže u algoritmima lečenja DM. Važno je ukazati na značaj doze primenjenih antioksidanasa, obzirom da je dokazano da pojedinačne visoke doze mogu delovati prooksidaciono. Takođe, važna je i dozna uravnoteženost primenjenih antioksidanasa i antidijabetika, u cilju efikasnijeg lečenja obolelih od DM. U okviru ovog rada fokusirali smo se na ulogu antioksidansa u lečenju DM.
AB  - Oxidative stress (OxS) represents an imbalance in dynamic equilibrium between prooxidants and antioxidants caused by increased free radical (FR) production or decreased activity of antioxidative system (AOS). OxS is involvedin many diseases such is diabetes mellitus (DM). DM presents with elevated blood glucose level and other biochemical disorders related to the inappropriate insulin secretion or improper insulin action. DM type 1 (DMT1) is an autoimmune disease with excessive OxS. The activity of antioxidative enzyme catalase (CAT) diminishes the production of hydrogen peroxide which is highly toxic for pancreatic cells. The increased activity of catalase (CAT) found in DMT1 patients signifies the importance of OxS in the pathogenesis of this disease. The generation of highly reactive FR, induced by hyperglycaemia, triggers the development of oxidative stress. Furthermore, OxS accelerates the development of DM and its complications which are related to the decreased activity of AOS. However, the standard antioxidant drugs failed in clinical trials for DM. New antioxidant agents combined with standard drugs are now proposed in therapy for DM. It is important to acknowledge that high doses of antioxidant agents could paradoxically have prooxidant effect. In addition, it is important to establish the dosage balance between antioxidant and antidiabetic drugs. In this article, we discuss the antioxidative agents and their significance in treatment of DM.
T2  - Medicinska istraživanja
T1  - Uloga antioksidanasa u lečenju diabetes mellitus-a
T1  - The role of antioxidative treatment in diabetes mellitus
VL  - 45
IS  - 2
SP  - 4
EP  - 12
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10327
ER  - 

@article{
author = "Nikolić, Dragana and Gluvić, Zoran and Akšam, Slavica and Obradović, Milan M. and Dobutović, Branislava and Soskić, Sanja S. and Sudar, Emina and Trpković, Andreja and Isenović, Esma R.",
year = "2011",
abstract = "Oksidativni stres (OxS) je skup poremećaja dinamičke ravnoteže prooksidanasa i antioksidanasa koji nastaje usled povećane produkcije slobodnih radikala (SR) ili usled smanjene aktivnosti antioksidativnog zaštitnog sistema (AOS). Bolest koja se, takođe, povezuje sa OxS je i diabetes mellitus (DM). DM karakteriše povećani nivo glukoze u cirkulaciji, kao i drugi biohemijski poremećaji koji nastaju kao posledica neadekvatne produkcije ili neadekvatnog dejstva insulina. Dijabetes tipa 1 (DMT1) je prototip autoimune bolesti sa intenzivnim OxS. Antioksidativni enzim katalaza (CAT) smanjuje produkciju vodonik-peroksida koji može biti veoma toksičan za ćelije pankreasa. Povećanje aktivnosti CAT u svim fazama DMT1 indirektno potvrđuje značaj OxS u nastanku ove bolesti. Visoko reaktivni SR, nastali uglavnom zbog hiperglikemije, izazivaju OxS što dodatno ubrzava razvoj i napredovanje DM kao i njegovih komplikacija koje su uzrokovane redukovanom aktivnošću AOS. Uprkos brojnim dokazima o štetnim posledicama OxS u DM, veliki broj kliničkih ispitivanja sa klasičnim antioksidansima, nažalost, nije pokazao efikasnost njihove primene u lečenju DM. Novi terapijski pristup, koji uključuje primenu kako standardnih tako i novih antioksidanasa, se predlaže u algoritmima lečenja DM. Važno je ukazati na značaj doze primenjenih antioksidanasa, obzirom da je dokazano da pojedinačne visoke doze mogu delovati prooksidaciono. Takođe, važna je i dozna uravnoteženost primenjenih antioksidanasa i antidijabetika, u cilju efikasnijeg lečenja obolelih od DM. U okviru ovog rada fokusirali smo se na ulogu antioksidansa u lečenju DM., Oxidative stress (OxS) represents an imbalance in dynamic equilibrium between prooxidants and antioxidants caused by increased free radical (FR) production or decreased activity of antioxidative system (AOS). OxS is involvedin many diseases such is diabetes mellitus (DM). DM presents with elevated blood glucose level and other biochemical disorders related to the inappropriate insulin secretion or improper insulin action. DM type 1 (DMT1) is an autoimmune disease with excessive OxS. The activity of antioxidative enzyme catalase (CAT) diminishes the production of hydrogen peroxide which is highly toxic for pancreatic cells. The increased activity of catalase (CAT) found in DMT1 patients signifies the importance of OxS in the pathogenesis of this disease. The generation of highly reactive FR, induced by hyperglycaemia, triggers the development of oxidative stress. Furthermore, OxS accelerates the development of DM and its complications which are related to the decreased activity of AOS. However, the standard antioxidant drugs failed in clinical trials for DM. New antioxidant agents combined with standard drugs are now proposed in therapy for DM. It is important to acknowledge that high doses of antioxidant agents could paradoxically have prooxidant effect. In addition, it is important to establish the dosage balance between antioxidant and antidiabetic drugs. In this article, we discuss the antioxidative agents and their significance in treatment of DM.",
journal = "Medicinska istraživanja",
title = "Uloga antioksidanasa u lečenju diabetes mellitus-a, The role of antioxidative treatment in diabetes mellitus",
volume = "45",
number = "2",
pages = "4-12",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10327"
}

Nikolić, D., Gluvić, Z., Akšam, S., Obradović, M. M., Dobutović, B., Soskić, S. S., Sudar, E., Trpković, A.,& Isenović, E. R.. (2011). Uloga antioksidanasa u lečenju diabetes mellitus-a. in Medicinska istraživanja, 45(2), 4-12.
https://hdl.handle.net/21.15107/rcub_vinar_10327

Nikolić D, Gluvić Z, Akšam S, Obradović MM, Dobutović B, Soskić SS, Sudar E, Trpković A, Isenović ER. Uloga antioksidanasa u lečenju diabetes mellitus-a. in Medicinska istraživanja. 2011;45(2):4-12.
https://hdl.handle.net/21.15107/rcub_vinar_10327 .

Nikolić, Dragana, Gluvić, Zoran, Akšam, Slavica, Obradović, Milan M., Dobutović, Branislava, Soskić, Sanja S., Sudar, Emina, Trpković, Andreja, Isenović, Esma R., "Uloga antioksidanasa u lečenju diabetes mellitus-a" in Medicinska istraživanja, 45, no. 2 (2011):4-12,
https://hdl.handle.net/21.15107/rcub_vinar_10327 .

TY  - JOUR
AU  - Dobutović, Branislava
AU  - Trpković, Andreja
AU  - Putniković, Biljana
AU  - Gluvić, Zoran
AU  - Isenović, Esma R.
PY  - 2008
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10330
AB  - Previous studies have reported increased myocardial inducible nitric oxide synthase (iNOs) expression and activity in chronic heart failure (ChF). Nitric oxide (NO) is a free radical which reacts with various molecules to cause multiple biological effects. Carvedilol is a α1-, β1-, and β2-adrenergic antagonist, used in therapy of hypertension and ChF. recently, it has been shown that carvedilol has an effect as NO quenching agent. Carvedilol presents several other mechanisms of action that converge to improve the symptomatology of hypertension and CHF. In addition to the adrenergic antagonism, carvedilol is also an antioxidant and endothelin suppressor. The molecular mechanism for the NO quenching potency of carvedilol remains to be determined. In cardiac cells the major pathway responsible for the regulation of iNOS activity/expression involves the activation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt). Thus, in our current ongoing and future studies, we will test the hypothesis that in disease states such as CHF where the PI3K/Akt pathway is interrupted, the regulation of iNOS activity/expression will be abolished. as a corollary of this primary hypothesis, we postulate that in CHF carvedilol stimulates cardiovascular iNOS via a mechanism involving activation of PI3K/akt cascade and further amplifies iNOS activity/expression. Moreover, since the PI3K/akt pathway have been acknowledged as a critically important mediator of cardiac iNOS regulation, PI3K/akt are identified as one of key targets for novel therapeutic interventions to minimize irreversible tissue damage associated with CHF and hypertension. A safer technology to regulate in vivo synthesis of PI3K/akt by generic manipulation would be a welcome work.
AB  - Azot oksid (NO) je slobodni radikal čije reakcije dovode do različitih bioloških dejstava. Karvedilol je antagonist α1-, β1-,i β2 adrenergičkih receptora koji se koristi u terapiji hipertenzije i nedavno je pokazano da hemijski reaguje sa NO. Pored adrenergičke blokade karvedilol doprinosi poboljšanju hipertenzije i HSI drugim mehanizmima. Takođe, pokazano je da karvedilol ima ulogu antioksidansa i ulogu u supresiji endotelina. Precizan mehanizam interakcije karvedilola i NO do sada nije u potpunosti razjašnjen. aktivnost/ekspresija inducibilne azot oksid sintetaze (iNOS) u kardiomiocitima dominantno je regulisana aktivacijom fosfatidilinozitol 3-kinaze (PI3K) i protein kinaze B (akt). U našim tekućim i planiranim istraživanjima, polazimo od hipoteze da je u HSI poremećen PI3K/akt signalni put, a time konsekventno i smanjena aktivnost/ekspresija iNOS-a. Takođe, naša hipoteza se bazira na pretpostavci da karvedilol u HSI stimuliše iNOS u kardiovaskularnom sistemu preko aktivacije PI3K/Akt kaskade. U zaključku, regulacija PI3K/Akt signalnog puta ima veoma bitnu ulogu u regulaciji iNOS-a u stanjima HSI. S obzirom da PI3K/Akt signalni put ima biološku ulogu kao kritično-važni signalni put u delovanju adrenergičkih lekova, kao što je karvedilol, to ga čini ključnim za terapeutske intervencije u cilju minimalizacije ireverzibilnih tkivnih i ćelijskih oštećenja koja su asocirana sa HSI i hipertenzijom.
T2  - Materia medica
T1  - Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF)
T1  - Efekti karvedilola na aktivnost/ekspresiju inducibilne azot oksid sintetaze (iNOS) kod bolesnika sa hroničnom srčanom insuficijencijom (HSI)
VL  - 24
IS  - 1
SP  - 21
EP  - 25
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10330
ER  - 

@article{
author = "Dobutović, Branislava and Trpković, Andreja and Putniković, Biljana and Gluvić, Zoran and Isenović, Esma R.",
year = "2008",
abstract = "Previous studies have reported increased myocardial inducible nitric oxide synthase (iNOs) expression and activity in chronic heart failure (ChF). Nitric oxide (NO) is a free radical which reacts with various molecules to cause multiple biological effects. Carvedilol is a α1-, β1-, and β2-adrenergic antagonist, used in therapy of hypertension and ChF. recently, it has been shown that carvedilol has an effect as NO quenching agent. Carvedilol presents several other mechanisms of action that converge to improve the symptomatology of hypertension and CHF. In addition to the adrenergic antagonism, carvedilol is also an antioxidant and endothelin suppressor. The molecular mechanism for the NO quenching potency of carvedilol remains to be determined. In cardiac cells the major pathway responsible for the regulation of iNOS activity/expression involves the activation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt). Thus, in our current ongoing and future studies, we will test the hypothesis that in disease states such as CHF where the PI3K/Akt pathway is interrupted, the regulation of iNOS activity/expression will be abolished. as a corollary of this primary hypothesis, we postulate that in CHF carvedilol stimulates cardiovascular iNOS via a mechanism involving activation of PI3K/akt cascade and further amplifies iNOS activity/expression. Moreover, since the PI3K/akt pathway have been acknowledged as a critically important mediator of cardiac iNOS regulation, PI3K/akt are identified as one of key targets for novel therapeutic interventions to minimize irreversible tissue damage associated with CHF and hypertension. A safer technology to regulate in vivo synthesis of PI3K/akt by generic manipulation would be a welcome work., Azot oksid (NO) je slobodni radikal čije reakcije dovode do različitih bioloških dejstava. Karvedilol je antagonist α1-, β1-,i β2 adrenergičkih receptora koji se koristi u terapiji hipertenzije i nedavno je pokazano da hemijski reaguje sa NO. Pored adrenergičke blokade karvedilol doprinosi poboljšanju hipertenzije i HSI drugim mehanizmima. Takođe, pokazano je da karvedilol ima ulogu antioksidansa i ulogu u supresiji endotelina. Precizan mehanizam interakcije karvedilola i NO do sada nije u potpunosti razjašnjen. aktivnost/ekspresija inducibilne azot oksid sintetaze (iNOS) u kardiomiocitima dominantno je regulisana aktivacijom fosfatidilinozitol 3-kinaze (PI3K) i protein kinaze B (akt). U našim tekućim i planiranim istraživanjima, polazimo od hipoteze da je u HSI poremećen PI3K/akt signalni put, a time konsekventno i smanjena aktivnost/ekspresija iNOS-a. Takođe, naša hipoteza se bazira na pretpostavci da karvedilol u HSI stimuliše iNOS u kardiovaskularnom sistemu preko aktivacije PI3K/Akt kaskade. U zaključku, regulacija PI3K/Akt signalnog puta ima veoma bitnu ulogu u regulaciji iNOS-a u stanjima HSI. S obzirom da PI3K/Akt signalni put ima biološku ulogu kao kritično-važni signalni put u delovanju adrenergičkih lekova, kao što je karvedilol, to ga čini ključnim za terapeutske intervencije u cilju minimalizacije ireverzibilnih tkivnih i ćelijskih oštećenja koja su asocirana sa HSI i hipertenzijom.",
journal = "Materia medica",
title = "Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF), Efekti karvedilola na aktivnost/ekspresiju inducibilne azot oksid sintetaze (iNOS) kod bolesnika sa hroničnom srčanom insuficijencijom (HSI)",
volume = "24",
number = "1",
pages = "21-25",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10330"
}

Dobutović, B., Trpković, A., Putniković, B., Gluvić, Z.,& Isenović, E. R.. (2008). Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF). in Materia medica, 24(1), 21-25.
https://hdl.handle.net/21.15107/rcub_vinar_10330

Dobutović B, Trpković A, Putniković B, Gluvić Z, Isenović ER. Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF). in Materia medica. 2008;24(1):21-25.
https://hdl.handle.net/21.15107/rcub_vinar_10330 .

Dobutović, Branislava, Trpković, Andreja, Putniković, Biljana, Gluvić, Zoran, Isenović, Esma R., "Effects of carvedilol on nitric oxide (NO) activity/expression in patient with chronic heart failure (CHF)" in Materia medica, 24, no. 1 (2008):21-25,
https://hdl.handle.net/21.15107/rcub_vinar_10330 .