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Article ; Online: Adrenomedullin: a protective factor for blood vessels.

Kato, Johji / Tsuruda, Toshihiro / Kita, Toshihiro / Kitamura, Kazuo / Eto, Tanenao

Arteriosclerosis, thrombosis, and vascular biology

2005 Volume 25, Issue 12, Page(s) 2480–2487

Abstract: ... a relatively short period, AM dilates blood vessels via an endothelium-dependent or independent mechanism ... Adrenomedullin (AM) is a vasodilator peptide having a wide range of biological actions ... protective or inhibitory against vascular damage and progression of arteriosclerosis. Either prolonged ...

Abstract	Adrenomedullin (AM) is a vasodilator peptide having a wide range of biological actions such as reduction of oxidative stress and inhibition of endothelial cell apoptosis. The AM gene is expressed in vascular walls, and AM was found to be secreted from cultured vascular endothelial cells, smooth muscle cells, and adventitial fibroblasts. Plasma AM levels in patients with arteriosclerotic vascular diseases are elevated in possible association with the severity of the disease. When administered over a relatively short period, AM dilates blood vessels via an endothelium-dependent or independent mechanism. Experiments in vitro have shown that AM exerts multiple actions on cultured vascular cells, which are mostly protective or inhibitory against vascular damage and progression of arteriosclerosis. Either prolonged infusion or overexpression of AM suppressed intimal thickening, fatty streak formation, and perivascular hyperplasia in rodent models for vascular remodeling or atherosclerosis. Intimal thickening induced by periarterial cuff was more severe in AM gene-knockout mice than their littermates, suggesting a protective role for endogenous AM. Moreover, AM has recently been suggested to possess angiogenetic properties. Collectively, a body of evidence suggests that AM participates in the mechanism against progression of vascular damage and remodeling, thereby alleviating the ischemia of tissues and organs.
MeSH term(s)	Adrenomedullin ; Amino Acid Sequence ; Animals ; Arteriosclerosis/physiopathology ; Blood Vessels/physiology ; Humans ; Molecular Sequence Data ; Peptides/genetics ; Peptides/physiology ; Vasodilation/physiology
Chemical Substances	Peptides ; Adrenomedullin (148498-78-6)
Language	English
Publishing date	2005-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/01.ATV.0000184759.91369.f8
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Zs.A 1705: Show issues

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Article ; Online: Combination of adrenomedullin with its binding protein accelerates cutaneous wound healing.

Idrovo, Juan-Pablo / Yang, Weng-Lang / Jacob, Asha / Ajakaiye, Michael A / Cheyuo, Cletus / Wang, Zhimin / Prince, Jose M / Nicastro, Jeffrey / Coppa, Gene F / Wang, Ping

PloS one

2015 Volume 10, Issue 3, Page(s) e0120225

Abstract: ... the alpha smooth muscle actin expression (mature blood vessels) and Masson-Trichrome staining (collagen ... medical need exists for efficient therapy for cutaneous wound. Combined treatment of adrenomedullin (AM ... and its binding protein-1 (AMBP-1) is protective in various disease conditions. To examine the effect ...

Abstract	Cutaneous wound continues to cause significant morbidity and mortality in the setting of diseases such as diabetes and cardiovascular diseases. Despite advances in wound care management, there is still an unmet medical need exists for efficient therapy for cutaneous wound. Combined treatment of adrenomedullin (AM) and its binding protein-1 (AMBP-1) is protective in various disease conditions. To examine the effect of the combination treatment of AM and AMBP-1 on cutaneous wound healing, full-thickness 2.0-cm diameter circular excision wounds were surgically created on the dorsum of rats, saline (vehicle) or AM/AMBP-1 (96/320 μg kg BW) was topically applied to the wound daily and wound size measured. At days 3, 7, and 14, skin samples were collected from the wound sites. AM/AMBP-1 treated group had significantly smaller wound surface area than the vehicle group over the 14-day time course. At day 3, AM/AMBP-1 promoted neutrophil infiltration (MPO), increased cytokine levels (IL-6 and TNF-α), angiogenesis (CD31, VEGF and TGFβ-1) and cell proliferation (Ki67). By day 7 and 14, AM/AMBP-1 treatment decreased MPO, followed by a rapid resolution of inflammation characterized by a decrease in cytokines. At the matured stage, AM/AMBP-1 treatment increased the alpha smooth muscle actin expression (mature blood vessels) and Masson-Trichrome staining (collagen deposition) along the granulation area, and increased MMP-9 and decreased MMP-2 mRNA expressions. TGFβ-1 mRNA levels in AM/AMBP-1 group were 5.3 times lower than those in the vehicle group. AM/AMBP-1 accelerated wound healing by promoting angiogenesis, collagen deposition and remodeling. Treatment also shortened the days to reach plateau for wound closure. Thus, AM/AMBP-1 may be further developed as a therapeutic for cutaneous wound healing.
MeSH term(s)	Adrenomedullin/pharmacology ; Animals ; Complement Factor H/pharmacology ; Male ; Neovascularization, Physiologic/drug effects ; Neutrophil Infiltration/drug effects ; Neutrophils/metabolism ; Neutrophils/pathology ; Rats ; Rats, Sprague-Dawley ; Skin/metabolism ; Skin/pathology ; Wound Healing/drug effects
Chemical Substances	adrenomedullin-binding protein 1, rat ; Adrenomedullin (148498-78-6) ; Complement Factor H (80295-65-4)
Language	English
Publishing date	2015-03-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0120225
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Article ; Online: Adrenomedullin alleviates pulmonary artery collagen accumulation in rats with pulmonary hypertension induced by high blood flow.

Pang, Lulu / Qi, Jianguang / Gao, Yang / Jin, Hongfang / Du, Junbao

Peptides

2014 Volume 54, Page(s) 101–107

Abstract: ... accumulation induced by high pulmonary blood flow, by investigating the effect of ADM [1.5 μg/(kg h ... pulmonary artery collagen accumulation and synthesis in rats with high pulmonary blood flow induced by aortocaval ... the muscularization of small pulmonary vessels and relative medial thickness (RMT) of pulmonary arteries in rats ...

Abstract	Collagen accumulation is one of the important pathologic changes in the development of pulmonary hypertension. Previous research showed that adrenomedullin (ADM) mitigates the development of pulmonary hypertension. The present study explored the role of ADM in the development of pulmonary artery collagen accumulation induced by high pulmonary blood flow, by investigating the effect of ADM [1.5 μg/(kg h)] subcutaneously administered by mini-osmotic pump on pulmonary hemodynamics, pulmonary vascular structure and pulmonary artery collagen accumulation and synthesis in rats with high pulmonary blood flow induced by aortocaval shunting. The results showed that ADM significantly decreased mean pulmonary artery pressure (mPAP) and the ratio of right ventricular mass to left ventricular plus septal mass [RV/(LV+SP)], attenuated the muscularization of small pulmonary vessels and relative medial thickness (RMT) of pulmonary arteries in rats with high pulmonary blood flow. Meanwhile, ADM ameliorated pulmonary artery collagen deposition represented by a decrease in lung tissue hydroxyproline, collagens I and III content and pulmonary artery collagens I and III expression, reduced collagen synthesis represented by a decrease in lung tissue procollagens I and III mRNA expression. The results suggest that ADM plays a protective role in the development of pulmonary hypertension induced by high blood flow, by inhibiting pulmonary procollagen synthesis and alleviating pulmonary artery collagen accumulation.
MeSH term(s)	Adrenomedullin/pharmacology ; Animals ; Collagen/biosynthesis ; Collagen/metabolism ; Hypertension, Pulmonary/drug therapy ; Hypertension, Pulmonary/physiopathology ; Lung/drug effects ; Lung/metabolism ; Male ; Pulmonary Artery/drug effects ; Pulmonary Artery/metabolism ; Pulmonary Artery/ultrastructure ; Rats, Sprague-Dawley ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Transforming Growth Factor beta1 ; Adrenomedullin (148498-78-6) ; Collagen (9007-34-5)
Language	English
Publishing date	2014-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	769028-9
ISSN	1873-5169 ; 0196-9781
ISSN (online)	1873-5169
ISSN	0196-9781
DOI	10.1016/j.peptides.2014.01.013
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Zs.A 1649: Show issues

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Article ; Online: Effects of adrenomedullin and vascular endothelial growth factor on ischemia/reperfusion injury in skeletal muscle in rats.

Kirisci, Mehmet / Oktar, Gursel Levent / Ozogul, Candan / Oyar, Eser Oz / Akyol, Seda Nur / Demirtas, Canan Yilmaz / Arslan, Mustafa

The Journal of surgical research

2013 Volume 185, Issue 1, Page(s) 56–63

Abstract: ... and hypoxia inducible factor 1 alpha (HIF 1α) were found to be significantly higher in Group I/R ... a larger central muscular necrosis than the peripheral necrosis, red blood cells in the lumens of capillary ... vessels, and a stronger atrophy and elliptical or round shape in muscle fibers in Group I/R ...

Abstract	Background: In this study we investigated the effects of adrenomedullin (AM) and vascular endothelial growth factor (VEGF) on skeletal muscle ischemia/reperfusion (I/R) injury in a rat model. Materials and methods: Thirty-six Wistar rats were randomized into six groups (n = 6). Laparotomy was performed in all groups under general anesthesia. Nothing else was done in Group S (Sham). The Group I/R underwent I/R performed by clamping and declamping of the infrarenal abdominal aorta for 120 min, respectively. Group VEGF and Group AM received intravenous infusion of VEGF (0.8 μg/kg) or AM (12 μg/kg) respectively, without I/R. Group I/R + VEGF and Group I/R + AM received intravenous infusion of VEGF (0.8 μg/kg) or AM (12 μg/kg) immediately after 2 h period of ischemia, respectively. At the end of reperfusion period, skeletal muscle samples of lower extremity were taken from all groups for biochemical and histopathologic examinations. Results: Tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), nitric oxide (NO), and hypoxia inducible factor 1 alpha (HIF 1α) were found to be significantly higher in Group I/R than the levels in Group S (P < 0.05). Tissue levels of MDA, SOD, NO, and HIF 1α were significantly lower in Group I/R + AM compared with the levels in Group I/R (P < 0.05). In Group I/R + VEGF, tissue levels of MDA and NO were significantly lower than the levels in Group I/R (P < 0.05). No statistically significant difference was found in the tissue levels of catalase among the groups. Histologic examination revealed a larger central muscular necrosis than the peripheral necrosis, red blood cells in the lumens of capillary vessels, and a stronger atrophy and elliptical or round shape in muscle fibers in Group I/R. Terminal deoxynucleotidyl transferase mediated dUPT nick end labeling (TUNEL)-positive cell count was significantly lower in groups I/R + AM and I/R + VEGF than Group I/R (P < 0.0001, P < 0.0001, respectively). Conclusions: These results indicate that AM and VEGF have protective effects on I/R injury in skeletal muscle in a rat model.
MeSH term(s)	Adrenomedullin/pharmacology ; Animals ; Catalase/metabolism ; Cytoprotection/drug effects ; Disease Models, Animal ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Malondialdehyde/metabolism ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Nitric Oxide/metabolism ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Random Allocation ; Rats ; Rats, Wistar ; Reperfusion Injury/drug therapy ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; Superoxide Dismutase/metabolism ; Vascular Endothelial Growth Factor A/pharmacology
Chemical Substances	Hif1a protein, rat ; Hypoxia-Inducible Factor 1, alpha Subunit ; Vascular Endothelial Growth Factor A ; Adrenomedullin (148498-78-6) ; Nitric Oxide (31C4KY9ESH) ; Malondialdehyde (4Y8F71G49Q) ; Catalase (EC 1.11.1.6) ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2013-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	80170-7
ISSN	1095-8673 ; 0022-4804
ISSN (online)	1095-8673
ISSN	0022-4804
DOI	10.1016/j.jss.2013.05.053
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Zs.A 178: Show issues

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Article ; Online: Adrenomedullin protects against fructose-induced insulin resistance and myocardial hypertrophy in rats.

Zhang, Jing / Zhang, Bao-Hong / Yu, Yan-Rong / Tang, Chao-Shu / Qi, Yong-Fen

Peptides

2011 Volume 32, Issue 7, Page(s) 1415–1421

Abstract: ... protective factor in IR. ... in the myocardium and vessels and the effect of ADM supplementation on rats with IR induced by fructose feeding ... with controls, rats with IR showed increased levels of fasting blood sugar and serum insulin, by 95% and 67 ...

Abstract	Adrenomedullin (ADM) has been recognized as a multipotent multifunctional peptide. To explore the pathophysiological roles of ADM in insulin resistance (IR), we studied the changes in ADM mRNA level in the myocardium and vessels and the effect of ADM supplementation on rats with IR induced by fructose feeding. Rats were fed 4% fructose in drinking water for 8 weeks, and ADM was administered subcutaneously in pure water through an Alzet Mini-osmotic Pump at 300 ng/kg/h for the last 4 weeks. Compared with controls, rats with IR showed increased levels of fasting blood sugar and serum insulin, by 95% and 67%, respectively (all P<0.01), and glycogen synthesis and glucose transport activity of the soleus decreased by 54% and 55% (all P<0.01). mRNA level and content of brain natriuretic peptide (BNP) in myocardial were all increased significantly. Fructose-fed rats showed increased immunoreactive-ADM content in plasma by 110% and in myocardia by 55% and increased mRNA level in myocardia and vessels (all P<0.01). ADM administration ameliorated the induced IR and myocardial hypertrophy. The glycogen synthesis and glucose transport activity of the soleus muscle increased by 41% (P<0.01) and 32% (P<0.05). ADM therapy attenuated myocardial and soleus lipid peroxidation injury and enhanced the antioxidant ability. Our results showed upregulation of endogenous ADM during fructose-induced IR and the protective effect of ADM on fructose-induced IR and concomitant cardiovascular hypertrophy probably by its antioxidant effect, which suggests that ADM could be an endogenous protective factor in IR.
MeSH term(s)	Adrenomedullin/blood ; Adrenomedullin/pharmacology ; Animals ; Blood Glucose/analysis ; Cardiomegaly/blood ; Cardiomegaly/chemically induced ; Cardiomegaly/pathology ; Cardiotonic Agents/blood ; Cardiotonic Agents/pharmacology ; Fructose/adverse effects ; Fructose/pharmacology ; Glycogen/biosynthesis ; Infusion Pumps ; Infusions, Subcutaneous ; Insulin/blood ; Insulin Resistance ; Lipid Peroxidation/drug effects ; Male ; Malondialdehyde/analysis ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/metabolism ; Myocardium/metabolism ; Myocardium/pathology ; Natriuretic Peptide, Brain/analysis ; Natriuretic Peptide, Brain/biosynthesis ; RNA, Messenger/analysis ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction
Chemical Substances	Blood Glucose ; Cardiotonic Agents ; Insulin ; RNA, Messenger ; Natriuretic Peptide, Brain (114471-18-0) ; Adrenomedullin (148498-78-6) ; Fructose (30237-26-4) ; Malondialdehyde (4Y8F71G49Q) ; Glycogen (9005-79-2)
Language	English
Publishing date	2011-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	769028-9
ISSN	1873-5169 ; 0196-9781
ISSN (online)	1873-5169
ISSN	0196-9781
DOI	10.1016/j.peptides.2011.05.024
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Article ; Online: Adrenomedullin, an endogenous peptide, counteracts cardiovascular damage.

Shimosawa, Tatsuo / Shibagaki, Yugo / Ishibashi, Kotaro / Kitamura, Kazuo / Kangawa, Kenji / Kato, Shigeaki / Ando, Katsuyuki / Fujita, Toshiro

Circulation

2002 Volume 105, Issue 1, Page(s) 106–111

Abstract: ... another hypotensive peptide. Although both AM and PAMP have the potential not only to decrease blood pressure but also ... Background: Adrenomedullin (AM), a potent vasodilator peptide, is produced by posttranslational ... splicing of pro-adrenomedullin together with proadrenomedullin N-terminal 20 peptide (PAMP ...

Abstract	Background: Adrenomedullin (AM), a potent vasodilator peptide, is produced by posttranslational splicing of pro-adrenomedullin together with proadrenomedullin N-terminal 20 peptide (PAMP), another hypotensive peptide. Although both AM and PAMP have the potential not only to decrease blood pressure but also to protect organs from damage, there is no direct evidence for their individual physiological roles in vivo. Methods and results: Using knockout mice with the disruption of AM peptide alone, we investigated the organ-protective effect of AM. Although the AM(-/-) mutation in mice was embryonic lethal without any apparent phenotypic changes, AM(+/-) mice were viable and fertile; plasma and organ AM concentrations were almost half of those in AM(+/+) mice. With the administration of angiotensin II (Ang II) on a high-salt diet for 12 days, marked perivascular fibrosis and intimal hyperplasia were found in coronary arteries of Ang II/salt-treated AM(+/-) mice, without the AM upregulation that was observed in Ang II/salt-treated AM(+/+) mice. In AM(+/-) mice, Ang II/salt loading increased both urinary excretion of 8-hydroxydeoxyguanosine and isoprostane, markers of oxidative stress. Consistently, immunostaining of both p67phox and gp91phox, subunits of NAD(P)H oxidase and 3-nitrotyrosine, the metabolites of reactive oxygen species (ROS), and the generation of ROS measured by electron spin resonance spectroscopy apparently increased in the Ang II/salt-treated heart. These data suggested that the overproduction of oxidative stress might be involved in the cardiovascular changes induced by Ang II/salt loading. Conclusions: The evidence presented supports the hypothesis that endogenous AM possesses a protective action against cardiovascular damage, possibly through the inhibition of oxidative stress production.
MeSH term(s)	Adrenal Glands/metabolism ; Adrenomedullin ; Angiotensin II/administration & dosage ; Animals ; Blood Pressure/physiology ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/physiopathology ; Coronary Vessels/drug effects ; Coronary Vessels/pathology ; Coronary Vessels/physiopathology ; Female ; Genotype ; Lung/metabolism ; Male ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NADH, NADPH Oxidoreductases/metabolism ; NADPH Oxidase 2 ; NADPH Oxidases ; Peptide Fragments/blood ; Peptide Fragments/metabolism ; Peptides/blood ; Peptides/genetics ; Peptides/metabolism ; Phosphoproteins/metabolism ; Proteins/metabolism ; Reactive Oxygen Species/urine ; Sodium, Dietary/administration & dosage ; Time Factors ; Tyrosine/analogs & derivatives ; Tyrosine/metabolism
Chemical Substances	Membrane Glycoproteins ; Peptide Fragments ; Peptides ; Phosphoproteins ; Proteins ; Reactive Oxygen Species ; Sodium, Dietary ; neutrophil cytosol factor 67K ; Angiotensin II (11128-99-7) ; Adrenomedullin (148498-78-6) ; 3-nitrotyrosine (3604-79-3) ; Tyrosine (42HK56048U) ; NADH, NADPH Oxidoreductases (EC 1.6.-) ; CYBB protein, human (EC 1.6.3.-) ; NADPH Oxidase 2 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-)
Language	English
Publishing date	2002-01-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/hc0102.101399
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Article: Adrenomedullin expression is up-regulated by ischemia-reperfusion in the cerebral cortex of the adult rat.

Serrano, J / Alonso, D / Encinas, J M / Lopez, J C / Fernandez, A P / Castro-Blanco, S / Fernández-Vizarra, P / Richart, A / Bentura, M L / Santacana, M / Uttenthal, L O / Cuttitta, F / Rodrigo, J / Martinez, A

Neuroscience

2002 Volume 109, Issue 4, Page(s) 717–731

Abstract: ... a potential cell-specific protective role for adrenomedullin. The number and intensity of immunoreactive ... Changes in the pattern of adrenomedullin expression in the rat cerebral cortex after ischemia ... against human adrenomedullin (22-52). Animals were subjected to 30 min of oxygen and glucose deprivation ...

Abstract	Changes in the pattern of adrenomedullin expression in the rat cerebral cortex after ischemia-reperfusion were studied by light and electron microscopic immunohistochemistry using a specific antibody against human adrenomedullin (22-52). Animals were subjected to 30 min of oxygen and glucose deprivation in a perfusion model simulating global cerebral ischemia, and the cerebral cortex was studied after 0, 2, 4, 6, 8, 10 or 12 h of reperfusion. Adrenomedullin immunoreactivity was elevated in certain neuronal structures after 6-12 h of reperfusion as compared with controls. Under these conditions, numerous large pyramidal neurons and some small neurons were intensely stained in all cortical layers. The number of immunoreactive pre- and post-synaptic structures increased with the reperfusion time. Neurons immunoreactive for adrenomedullin presented a normal morphology whereas non-immunoreactive neurons were clearly damaged, suggesting a potential cell-specific protective role for adrenomedullin. The number and intensity of immunoreactive endothelial cells were also progressively elevated as the reperfusion time increased. In addition, the perivascular processes of glial cells and/or pericytes followed a similar pattern, suggesting that adrenomedullin may act as a vasodilator in the cerebrocortical circulation. In summary, adrenomedullin expression is elevated after the ischemic insult and seems to be part of CNS response mechanism to hypoxic injury.
MeSH term(s)	Adrenomedullin ; Animals ; Blood Vessels/metabolism ; Blood Vessels/pathology ; Blood Vessels/ultrastructure ; Cell Death/physiology ; Cell Survival/physiology ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Cerebral Cortex/ultrastructure ; Hypoxia-Ischemia, Brain/metabolism ; Hypoxia-Ischemia, Brain/pathology ; Hypoxia-Ischemia, Brain/physiopathology ; Immunohistochemistry ; Interneurons/metabolism ; Interneurons/pathology ; Interneurons/ultrastructure ; Male ; Microscopy, Electron ; Nerve Degeneration/metabolism ; Nerve Degeneration/pathology ; Nerve Degeneration/physiopathology ; Neurons/metabolism ; Neurons/pathology ; Neurons/ultrastructure ; Peptides/metabolism ; Pyramidal Cells/metabolism ; Pyramidal Cells/pathology ; Pyramidal Cells/ultrastructure ; Rats ; Rats, Wistar ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; Reperfusion Injury/physiopathology ; Time Factors ; Up-Regulation/physiology
Chemical Substances	Peptides ; Adrenomedullin (148498-78-6)
Language	English
Publishing date	2002
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	196739-3
ISSN	1873-7544 ; 0306-4522
ISSN (online)	1873-7544
ISSN	0306-4522
DOI	10.1016/s0306-4522(01)00532-2
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Article: Adrenomedullin protects against fructose-induced insulin resistance and myocardial hypertrophy in rats

Zhang, Jing / Zhang, Bao-Hong / Yu, Yan-Rong / Tang, Chao-Shu / Qi, Yong-Fen

Peptides

Volume v. 32,, Issue no. 7

Abstract	Adrenomedullin (ADM) has been recognized as a multipotent multifunctional peptide. To explore the pathophysiological roles of ADM in insulin resistance (IR), we studied the changes in ADM mRNA level in the myocardium and vessels and the effect of ADM supplementation on rats with IR induced by fructose feeding. Rats were fed 4% fructose in drinking water for 8 weeks, and ADM was administered subcutaneously in pure water through an Alzet Mini-osmotic Pump at 300ng/kg/h for the last 4 weeks. Compared with controls, rats with IR showed increased levels of fasting blood sugar and serum insulin, by 95% and 67%, respectively (all P<0.01), and glycogen synthesis and glucose transport activity of the soleus decreased by 54% and 55% (all P<0.01). mRNA level and content of brain natriuretic peptide (BNP) in myocardial were all increased significantly. Fructose-fed rats showed increased immunoreactive-ADM content in plasma by 110% and in myocardia by 55% and increased mRNA level in myocardia and vessels (all P<0.01). ADM administration ameliorated the induced IR and myocardial hypertrophy. The glycogen synthesis and glucose transport activity of the soleus muscle increased by 41% (P<0.01) and 32% (P<0.05). ADM therapy attenuated myocardial and soleus lipid peroxidation injury and enhanced the antioxidant ability. Our results showed upregulation of endogenous ADM during fructose-induced IR and the protective effect of ADM on fructose-induced IR and concomitant cardiovascular hypertrophy probably by its antioxidant effect, which suggests that ADM could be an endogenous protective factor in IR.
Keywords	myocardium ; blood serum ; hypertrophy ; therapeutics ; messenger RNA ; blood glucose ; insulin ; glycogen ; fasting ; protective effect ; insulin resistance ; lipid peroxidation ; drinking water ; antioxidant activity ; natriuretic peptides ; muscles ; glucose ; fructose ; gene expression ; synthesis ; brain ; rats
Language	English
Document type	Article
ISSN	0196-9781
Database	AGRIS - International Information System for the Agricultural Sciences and Technology

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