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      Expression of BMP4 in myocardium and vascular tissue of obese mice

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          Abstract

          Background

          Obesity is regarded as a risk factor for cardiovascular disease. Bone morphogenetic protein 4 (BMP4) is a proinflammatory and profibrotic factor, and the reduced expression of this molecule in obese mice seems to be inconsistent with the known proinflammatory effects of obesity. Therefore, we studied BMP4 expression and inflammation in the myocardial tissue and aortas of obese mice.

          Methods and Results

          Four-week-old ob/ob mice were used as the experimental group, and C57BL/6 mice comprised the control group. Animals were sacrificed after a 12-week full diet, and then the blood, heart, abdominal aorta, and inguinal adipose tissue were collected. The expression of BMP4 mRNA and protein in the heart and aorta was significantly higher in the experimental group than in the control group, but expression was lower in adipose tissue. Inflammation measured by the expression of IL-1β and IL-9 mRNA and protein and Smad1 and phosphorylated Smad1/5/8 protein in the heart and aorta was higher in the experimental group than in the control group. In addition, the expression of BMP4 in the serum was significantly higher in the experimental group than in the control group.

          Conclusion

          BMP4 is significantly overexpressed in the myocardial tissue and aortas of obese mice, and mediates local inflammatory responses.

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          Most cited references13

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          Obesity and Metabolic Syndrome in Korea

          Sang Oh (2011)
          In Korea, a person with a body mass index (BMI) ≥25 kg/m2 is considered obese, and a person with a BMI ≥30 kg/m2 is classified as severely obese. Central obesity is defined as a waist circumference ≥90 cm for Korean men and ≥85 cm for Korean women. Recent epidemiologic data show that the prevalence of severe obesity and metabolic syndrome is steadily increasing. These epidemics increased morbidity and mortality of type 2 diabetes, cardiovascular diseases, and obesity-related cancers such as breast, colorectal, and other cancers in Korea. Decreased physical activity, increased fat and alcohol consumption, heavy smoking, and stress/depressed mood are the primary modifiable life-style risk factors for Koreans. Recently, public health interventions to encourage life-style changes have shown promising results in reducing the prevalence of severe obesity and metabolic syndrome.
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            Oxidative stress and inflammation interactions in human obesity.

            Obesity is often characterized by increased oxidative stress and exacerbated inflammatory outcomes accompanying infiltration of immune cells in adipocytes. The oxidative stress machinery and inflammatory signaling are not only interrelated, but their impairment can lead to an inhibition of insulin responses as well as a higher risk of cardiovascular diseases and associated features. Mitochondria, in addition to energy transformation, play a role in apoptosis, cellular proliferation, as well as in the cellular redox state control. Under certain circumstances, protons are able to re-enter the mitochondrial matrix via different uncoupling proteins, disturbing free radical production by mitochondria. Disorders of the mitochondrial electron transport chain, over-generation of reactive oxygen species, and lipoperoxides or alterations in antioxidant defenses have been reported in situations of obesity and type-2 diabetes. On the other hand, obesity has been linked to a low grade pro-inflammatory state, in which impairments in the oxidative stress and antioxidant mechanism could be involved. The current scientific evidence highlights the need of investigating the interplay between oxidative stress and inflammation with obesity/diabetes onset as well as the interactions of such factors either as a cause or consequence of obesity. The signaling mediated by the activation of inflammatory markers or nuclear factor kappa β and other transcription factors as central regulators of inflammation are key issues to understanding oxidative stress responses in obesity. This review aims at summarizing the main mechanisms and interplay factors between oxidative stress and inflammation in human obesity according to the last 10 years of research in the field.
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              Diet-induced obese mice develop peripheral, but not central, resistance to leptin.

              Leptin administration reduces obesity in leptin-deficient ob/ob mice; its effects in obese humans, who have high circulating leptin levels, remain to be determined. This longitudinal study was designed to determine whether diet-induced obesity in mice produces resistance to peripheral and/or central leptin treatment. Obesity was induced in two strains of mice by exposure to a 45% fat diet. Serum leptin increased in proportion to body weight (P < 0.00001). Whereas C57BL/6 mice initially responded to peripherally administered leptin with a marked decrease in food intake, leptin resistance developed after 16 d on high fat diet; mice on 10% fat diet retained leptin sensitivity. In AKR mice, peripheral leptin significantly decreased food intake in both 10 and 45% fat-fed mice after 16 d of dietary treatment. However, after 56 d, both groups became resistant to peripherally administered leptin. Central administration of leptin to peripherally leptin-resistant AKR mice on 45% fat diet resulted in a robust response to leptin, with a dose-dependent decrease in food intake (P < 0.00001) and body weight (P < 0.0001) after a single intracerebroventricular infusion. These data demonstrate that, in a diet-induced obesity model, mice exhibit resistance to peripherally administered leptin, while retaining sensitivity to centrally administered leptin.
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                Author and article information

                Contributors
                wutingdoctor@163.com
                15370850766@189.cn
                zhongcheng0815@163.com
                guiltatlantis@163.com
                15861587584@163.com
                wxycat1986@gmail.com
                381060966@qq.com
                zonggj@163.com
                Journal
                J Inflamm (Lond)
                J Inflamm (Lond)
                Journal of Inflammation (London, England)
                BioMed Central (London )
                1476-9255
                7 February 2015
                7 February 2015
                2015
                : 12
                : 8
                Affiliations
                [ ]Department of Cardiology, Wuxi Clinical Hospital, Anhui Medical University, Wuxi, Jiangsu Province China
                [ ]Department of Cardiology, 101 Hospital of PLA, Wuxi, Jiangsu Province China
                [ ]Central Laboratory, Zhenjiang No.4 People’s Hospital, Zhenjiang, Jiangsu Province China
                Article
                47
                10.1186/s12950-015-0047-6
                4326186
                25678859
                aff40312-d164-493c-bd38-8928a1f98b87
                © Wu et al.; licensee BioMed Central. 2015

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 24 January 2014
                : 4 January 2015
                Categories
                Research
                Custom metadata
                © The Author(s) 2015

                Immunology
                bmp4,obesity,inflammation,cardiovascular disease
                Immunology
                bmp4, obesity, inflammation, cardiovascular disease

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