Oxytocin Treatment Prevents the Cardiomyopathy Observed in Obese Diabetic Male db/db Mice
Éric PlanteAhmed MénaouarBogdan DanalacheDenis YipTom L. BroderickJean‐Louis ChiassonMarek JankowskiJolanta Gutkowska
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Abstract:
Oxytocin (OT) is involved in the regulation of energy metabolism and in the activation of cardioprotective mechanisms. We evaluated whether chronic treatment with OT could prevent the metabolic and cardiac abnormalities associated with diabetes and obesity using the db/db mice model. Four-week-old male db/db mice and their lean nondiabetic littermates (db/+) serving as controls were treated with OT (125 ng/kg · h) or saline vehicle for a period of 12 weeks. Compared with db/+ mice, the saline-treated db/db mice developed obesity, hyperglycemia, and hyperinsulinemia. These mice also exhibited a deficient cardiac OT/natriuretic system and developed systolic and diastolic dysfunction resulting from cardiomyocyte hypertrophy, fibrosis, and apoptosis. These abnormalities were associated with increased reactive oxygen species (ROS) production, inflammation, and suppressed 5′-adenosine monophosphate kinase signaling pathway. The db/db mice displayed reduced serum levels of adiponectin and adipsin and elevated resistin. OT treatment increased circulating OT levels, significantly reduced serum resistin, body fat accumulation (19%; P < .001), fasting blood glucose levels by (23%; P < .001), and improved glucose tolerance and insulin sensitivity. OT also normalized cardiac OT receptors, atrial natriuretic peptide, and brain natriuretic peptide, expressions and prevented systolic and diastolic dysfunction as well as cardiomyocyte hypertrophy, fibrosis, and apoptosis. Furthermore, OT reduced cardiac oxidative stress and inflammation and normalized the 5′-adenosine monophosphate-activated protein kinase signaling pathway. The complete normalization of cardiac structure and function by OT treatment in db/db mice contrasted with only partial improvement of hyperglycemia and hyperinsulinemia. These results indicate that chronic treatment with OT partially improves glucose and fat metabolism and reverses abnormal cardiac structural remodeling, preventing cardiac dysfunction in db/db mice.Keywords:
Hyperinsulinemia
Atrial natriuretic peptide
Diabetic Cardiomyopathy
Resistin
Resistin is an adipokine which is related to obesity and associated diseases.However,an increasing number of evidences indicate that this cytokine participates in the establishment of inflammation.In this paper,the research reviewed advances of the relationship between resistin and inflammatory cytokines and C reactive protein,the reciprocal effects of resistin on vascular endothelial cells and the clinical and experimental evidences.
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The initial discovery of resistin and resistin-like molecules (RELMs) in rodents suggested a role for these adipocytokines in molecular linkage of obesity, Type 2 Diabetes mellitus and metabolic syndrome. Since then, it became apparent that the story of resistin and RELMs was very much of mice and men. The putative role of this adipokine family evolved from that of a conveyor of insulin resistance in rodents to instigator of inflammatory processes in humans. Structural dissimilarity, variance in distribution profiles and a lack of corroborating evidence for functional similarities separate the biological functions of resistin in humans from that of rodents. Although present in gross visceral fat deposits in humans, resistin is a component of inflammation, being released from infiltrating white blood cells of the sub-clinical chronic low grade inflammatory response accompanying obesity, rather than from the adipocyte itself. This led researchers to further explore the functions of the resistin family of proteins in inflammatory-related conditions such as atherosclerosis, as well as in cancers such as endometrial and gastric cancers. Although elevated levels of resistin have been found in these conditions, whether it is causative or as a result of these conditions still remains to be determined.
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Abstract Resistin is still a little known hormone of the adipose tissue. The potential role of resistin in the development of DM2 has been currently investigated. The aim of our study was to detect the resistin blood level in patients with DM2, depending on the duration of the disease. In so doing, a determination of resistin and insulin blood level was conducted in 305 patients with DM2, and in a control group of 32 persons. Before testing, the patients were placed into four groups, depending on the duration of type 2 diabetes. Our results indicate that the resistin level was significantly lower in the control group of patients, in comparison with the DM2 patients groups. Moreover, a significantly lower resistin level was found in group I (firstly diagnosed DM2), in comparison with the groups of patients with a different duration of DM2. No correlation between resistin level and BMI, and between resistin and insulin blood level was found. However, a tendency towards increase of resistin blood level is noticeably evident in co-relation with increment of DM2 duration. In addition, the resistin level was considerably lower in patients with no DM2, when compared with patients with diagnosed DM2. Yet, there was no significant difference in the resistin blood level depending on the sex of the patients at the same duration of DM2
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Resistin has strong pro-inflammatory and profibrotic properties, which are key pathogenetic processes in systemic sclerosis. We hypothesised that resistin may be associated with organ involvement and inflammatory process in SSc patients. To address this hypothesis, the aim of this study was to define serum resistin levels in SSc patients and control group and determine the correlation between this adipokine and internal organ involvement in SSc patients.The study enrolled 48 Caucasian female patients with SSc and 38 healthy subjects of control group. Serum concentrations of resistin were measured using commercially available ELISA Kits (Quantikine ELISA Kit R & D Systems, Minneapolis, MN, USA).Patients with SSc had higher resistin levels [mean (SD): 10.2, (4.87)] than the control group [7.64, (4.43)] and the difference was statistically significant (p=0.017, p<0.05). We found statistically significant association between serum resistin and ILD, arthralgia and oesophageal involvement (r=0.31, p=0.042; r=0.48, p=0.001; r=0.32, p=0.034; respectively). Moreover, the assessment of the relation between plasma concentrations of resistin and inflammatory parameters in SSc patients indicated a positive correlation between resistin and C-reactive protein levels (r=0.37; p=0.011).The results of our study indicate that resistin levels might correlate with organ involvement and inflammatory process in SSc patients.
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Obesity and its associated complications, such as metabolic syndrome, are an increasing problem in both humans and horses in the developed world. The expression patterns of resistin differ considerably between species. In rodents, resistin is expressed by adipocytes and is related to obesity and ID. In humans, resistin is predominantly produced by inflammatory cells, and resistin concentrations do not reflect the degree of obesity, although they may predict cardiovascular outcomes. The aim of this study was to investigate the usefulness of resistin and its relationship with ID and selected indicators of inflammation in horses. Seventy-two horses, included in one of the four following groups, were studied: healthy controls (C, n = 14), horses with inflammatory conditions (I, n = 21), horses with mild ID (ID1, n = 18), and horses with severe ID (ID2, n = 19). Plasma resistin concentrations were significantly different between groups and the higher values were recorded in the I and ID2 groups (C: 2.38 ± 1.69 ng/mL; I: 6.85 ± 8.38 ng/mL; ID1: 2.41 ± 2.70 ng/mL; ID2: 4.49 ± 3.08 ng/mL). Plasma resistin was not correlated with basal insulin concentrations. A significant (r = 0.336, p = 0.002) correlation was found between resistin and serum amyloid A. Our results show that, as is the case in humans, plasma resistin concentrations in horses are predominantly related to inflammatory conditions and not to ID. Horses with severe ID showed an elevation in resistin that may be secondary to the inflammatory status associated with metabolic syndrome.
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Background: Adipokines play a role in pathogenesis and progression of certain cancers. Resistin is an adipokine with diverse findings in disease development and progression. The present study aimed to determine Resistin serum levels in bladder cancer cases in order to identify novel tumor markers. Methods: This research was based on a case-control study, including 45 patients with bladder cancer and 45 healthy controls. Resistin levels were measured by ELISA in both groups. Height and weight were measured and body mass index (kg/m2) was calculated. Results: Resistin levels were significantly different between bladder cancer and the control group (p<0.0001) but Resistin levels in different stages were not significantly different. Also there was no correlation among sex, age, body mass index and the serum Resistin levels. Conclusions: These results suggest that changes in serum Resistin levels play an important role in the diagnosis and could act as a biomarkers for bladder cancer.
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背景 Resistin ，在啮齿类动物连接到胰岛素抵抗和肥胖的新奇 adipokine ，主要从巨噬细胞被导出并且在人在粉瘤识别了，被显示了在 atherosclerosis.Resistin 层次起一个潜在的作用被报导在冠的动脉疾病( CAD )增加，当有关在在中国人民的 CAD 的不同阶段的 resistin 的数据正在缺乏时。这研究的目的是估计 resistin 的血浆集中是否在病人之间不同与不稳定的，稳定的咽峡炎 pectoris.Methods 血浆 resistin 层次在有不稳定的咽峡炎( UAP )的 46 个病人借助于连接酶的 immunosorbent 试金( ELISA )是坚定的， 37 显著地在 UAP 组与稳定的咽峡炎(树液)和 resistin 的 31 控制 subjects.Results 血浆集中被增加(几何平均数( interquartile 范围) 12.09 ng/ml ( 8.40 ， 18.08 ))与 S 比较在 resistin 层次的差别都没与树液和控制一起在病人之间被发现。我们也发现血浆 resistin 断然与白血球计数相关( r=0.21 ， P=0.027 )，高敏感的C反应的蛋白质( hs-CRP )( r=0.25 ， P=0.008 )，并且 endothelin-1 ( r=0.21 ， P=0.025 )在调整以后好久，性和 BMI.Conclusion Resistin 可以被影响全身的发炎和 endothelial 激活涉及 CAD 的发展。
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Over the past decade,resistin,as a novel adipokine,is regarded to link insulin resistance,obesity and type 2 diabetes.Many studies on rodents showed that resistin caused insulin resistance in mice and was associated with obesity and diabetes.However,the role of resistin in human disease remains controversial.The physiological functions of resistin are unknown at present.On the other hand,current evidence appears to suggest that resistin is a kind of proinflammatory cytokine.This article reviewed the relationships among resistin,insulin resistance,obesity and type 2 diabetes.
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Proinflammatory cytokine
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Resistin may be an independent inflammatory marker of atherosclerosis. Therefore, its circulating level might be important prognostic factor of cardiovascular disease in humans. We aimed in this study to assess plasma resistin concentration in Polish women with acute ischemic stroke, who additionally suffer from chronic diseases: diabetes, hypertension and/or obesity. The changes of resistin levels after 10 days from the onset of stroke and possible associations between resistin and pro-inflammatory cytokine TNFα were also evaluated.Material consisted of 41 women with ischemic stroke (aged 60-85 years) and 64 controls (aged 60-85 years). Circulating resistin and TNFα concentrations were measured using ELISA. Blood was taken twice in the stroke group, in the first and tenth day from the onset of clinical symptoms, and only once in the controls. Clinical and biochemical data (blood pressure, weight, height, glucose, insulin, lipid profile) were collected.Higher concentrations of resistin and TNFα were observed in ischemic stroke patients at the first day comparing to the controls. Second evaluation after 10 days in comparison with the first measurement revealed significantly higher TNFα levels and non-significant lower values of resistin. Resistin positively correlated with TNFα and stroke severity.Changes in resistin and TNFα concentrations were observed in the course of stroke. Further investigations are required to assess the implication of these findings. Higher resistin concentration might be associated with worse neurological deficits.
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