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Adipose tissue plays an important role in storing excess nutrients and preventing ectopic lipid accumulation in other organs. Obesity leads to excess lipid storage in adipocytes, resulting in the generation of stress signals and the derangement of metabolic functions. SIRT1 is an important regulatory sensor of nutrient availability in many metabolic tissues. Here we report that SIRT1 functions in adipose tissue to protect from inflammation and obesity under normal feeding conditions, and to forestall the progression to metabolic dysfunction under dietary stress and aging. Genetic ablation of SIRT1 in adipose tissue leads to gene expression changes that highly overlap with changes induced by high-fat diet in wild-type mice, suggesting that dietary stress signals inhibit the activity of SIRT1. Indeed, we show that high-fat diet induces the cleavage of SIRT1 protein in adipose tissue by the inflammation-activated caspase-1, providing a link between dietary stress and predisposition to metabolic dysfunction. 相似文献
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《Endocrine practice》2010,16(4):692-698
ObjectiveTo describe the contribution of adipocytes and adipose tissue to increased cardiometabolic risk as well as the mechanisms by which adipose tissue and obesity contribute to dysglycemia, dyslipidemia, hypertension, and a prothrombotic, inflammatory state favoring atherogenesis.MethodsA review was undertaken of the relevant available reports, compiled by means of a search(PubMed) of the English-language literature published between 1994 and 2010.ResultsCoronary risk factors cause susceptibility to development of atherosclerosis. Traditional coronary risk factors are obesity, smoking, hypertension, diabetes, elevated serum cholesterol levels, male sex, advancing age, and a family history of early coronary events. The currently preferred term of cardiometabolic risk encompasses both the traditional coronary risk factors and the additional contributing factors of insulin resistance, atherogenic dyslipidemia, physical inactivity, unhealthful eating, inflammation, and hypercoagulation. The accumulation of adipose tissue (adiposity) and dysfunctional adipose tissue (adiposopathy) contribute to most, if not all, of the cardiometabolic risk factors. Adipose tissue promotes atherosclerosis through several different pathologic mechanisms, which are reviewed in this report. The treatment of obesity should focus on reducing fat mass and minimizing adipocyte dysfunction.ConclusionAdipose tissue contributes to the development of insulin resistance, hyperglycemia, atherogenic dyslipidemia, and arterial hypertension and favors a prothrombotic and proinflammatory state. Adipose tissue dysfunction increases cardiometabolic risk through a variety of mechanisms. (Endocr Pract. 2010;16:692-698) 相似文献
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Yu‐Jing Gao Alison C. Holloway Zhao‐Hua Zeng Gareth E. Lim James J. Petrik Warren G. Foster Robert M.K.W. Lee 《Obesity (Silver Spring, Md.)》2005,13(4):687-692
Objective: Recent epidemiological studies have shown that there is an increased risk of obesity and hypertension in children born to women who smoked during pregnancy. The aim of this study was to examine the effect of fetal and neonatal exposure to nicotine, the major addictive component of cigarette smoke, on postnatal adiposity and blood vessel function. Research Methods and Procedures: Female Wistar rats were given nicotine or saline (vehicle) during pregnancy and lactation. Postnatal growth was determined in the male offspring from weaning until 26 weeks of age. At 26 weeks of age, fat pad weight and the function of the perivascular adipose tissue (PVAT) in the thoracic aorta and mesenteric arteries were examined. Results: Exposure to nicotine resulted in increased postnatal body weight and fat pad weight and an increased amount of PVAT in the offspring. Contraction of the aorta induced by phenylephrine was significantly attenuated in the presence of PVAT, whereas this effect was not observed in the aortic rings from the offspring of nicotine‐exposed dams. Phenylephrine‐induced contraction without PVAT was not different between saline‐ and nicotine‐exposed rats. Transfer of solution incubated with PVAT‐intact aorta to PVAT‐free aorta induced a marked relaxation response in the rats from saline‐exposed dams, but this relaxation response was significantly impaired in the rats from nicotine‐exposed dams. Discussion: Our results showed that prenatal nicotine exposure increased adiposity and caused an alteration in the modulatory function of PVAT on vascular relaxation response, thus providing insight into the mechanisms underlying the increased prevalence of obesity and hypertension in children exposed to cigarette smoke in utero. 相似文献
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血管内皮细胞功能紊乱与心血管疾病关系的研究进展 总被引:2,自引:1,他引:1
本文综述了血管内皮细胞合成与释放的一氧化氮、内皮素、血管紧张素Ⅱ等多种生物活性物质及VEC功能紊乱与心血管疾病的关系,为进一步深入研究提供了思路。 相似文献
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目的:通过构建肥胖合并动脉粥样硬化大鼠模型,评估模型血管旁脂肪组织中趋化因子chemerin基因及蛋白的表达变化.方法:建立肥胖合并动脉粥样硬化大鼠模型;于模型构建不同时期(8周、12周、16周及24周)取胸主动脉旁脂肪组织,应用real-time-PCR检测chemerin的mRNA表达变化;应用免疫组织化学染色的方... 相似文献
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Obesity causes white adipose tissue (WAT) inflammation and insulin resistance in some, but not all individuals. Here, we used a mouse model of early postnatal overfeeding to determine the role of neonatal nutrition in lifelong WAT inflammation and metabolic dysfunction. C57BL/6J mice were reared in small litters of 3 (SL) or normal litters of 7 pups (NL) and fed either regular chow or a 60% high fat diet (HFD) from 5 to 17 weeks. At weaning, SL mice did not develop WAT inflammation despite increased fat mass, although there was an up-regulation of WAT Arg1 and Tlr4 expression. On HFD, adult SL mice had greater inguinal fat mass compared to NL mice, however both groups showed similar increases in visceral fat depots and adipocyte hypertrophy. Despite the similar levels of visceral adiposity, SL-HFD mice displayed greater impairments in glucose homeostasis and more pronounced hepatic steatosis compared to NL-HFD mice. In addition, WAT from SL mice fed a HFD displayed greater crown-like structure formation, increased M1 macrophages, and higher cytokine gene expression. Together, these data suggest that early postnatal overnutrition may be a critical determinant of fatty liver and insulin resistance in obese adults by programming the inflammatory capacity of adipose tissue. 相似文献
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Ulrika S. Pettersson Tomas B. Waldén Per-Ola Carlsson Leif Jansson Mia Phillipson 《PloS one》2012,7(9)
Sex differences in obesity-induced complications such as type 2 diabetes have been reported. The aim of the study was to pinpoint the mechanisms resulting in different outcome of female and male mice on a high-fat diet (HFD). Mice fed control or HFD were monitored for weight, blood glucose, and insulin for 14 weeks. Circulating chemokines, islet endocrine function and blood flow, as well as adipose tissue populations of macrophages and regulatory T-lymphocytes (Treg) were thereafter assessed. Despite similar weight (43.8±1.0 and 40.2±1.5 g, respectively), male but not female mice developed hyperinsulinemia on HFD as previously described (2.5±0.7 and 0.5±0.1 pmol/l, respectively) consistent with glucose intolerance. Male mice also exhibited hypertrophic islets with intact function in terms of insulin release and blood perfusion. Low-grade, systemic inflammation was absent in obese female but present in obese male mice (IL-6 and mKC, males: 77.4±17 and 1795±563; females: 14.6±4.9 and 240±22 pg/ml), and the population of inflammatory macrophages was increased in intra-abdominal adipose tissues of high-fat-fed male but not female mice. In contrast, the anti-inflammatory Treg cell population increased in the adipose tissue of female mice in response to weight gain, while the number decreased in high-fat-fed male mice. In conclusion, female mice are protected against HFD-induced metabolic changes while maintaining an anti-inflammatory environment in the intra-abdominal adipose tissue with expanded Treg cell population, whereas HFD-fed male mice develop adipose tissue inflammation, glucose intolerance, hyperinsulinemia, and islet hypertrophy. 相似文献
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目的探讨肥胖者网膜脂肪和皮下脂肪两处肿瘤坏死因子-α(TNF-α)蛋白的表达与脂肪细胞大小的相关性。方法选取正常体重者16名,中心型肥胖者32名拟行外科手术患者,术中取出网膜脂肪和皮下脂肪标本,测定脂肪细胞大小,采用western blot方法测定TNF-α蛋白表达。结果肥胖者网膜脂肪和皮下脂肪两处TNF-α蛋白的水平均比正常体重对照组表达高(P<0.01),肥胖者网膜脂肪组织TNF-α蛋白表达高于皮下脂肪(P<0.05),同时研究发现肥胖者皮下脂肪细胞和网膜脂肪细胞大小均明显大于正常体重组(P<0.05),且肥胖者网膜脂肪和皮下脂肪两处脂肪组织TNF-α蛋白表达与脂肪细胞大小呈正相关(网膜:r=0.808,P<0.01;皮下:r=0.452,P<0.05)。结论肥胖者网膜脂肪和皮下脂肪细胞增大,在肥胖相关胰岛素抵抗的发生中起到了重要的作用。 相似文献
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Adipose Tissue Dysfunction Occurs Independently of Obesity in Adipocyte‐Specific Oncostatin Receptor Knockout Mice
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Jacqueline M. Stephens Jennifer L. Bailey Hardy Hang Victoria Rittell Marilyn A. Dietrich Randall L. Mynatt Carrie M. Elks 《Obesity (Silver Spring, Md.)》2018,26(9):1439-1447
Objective
This study examined the phenotypic effects of adipocyte‐specific oncostatin M receptor (OSMR) loss in chow‐fed mice.Methods
Chow‐fed adipocyte‐specific OSMR knockout (FKO) mice and littermate OSMRfl/fl controls were studied. Tissue weights, insulin sensitivity, adipokine production, and stromal cell immunophenotypes were assessed in epididymal fat (eWAT); serum adipokine production was also assessed. In vitro, adipocytes were treated with oncostatin M, and adipokine gene expression was assessed.Results
Body weights, fasting blood glucose levels, and eWAT weights did not differ between genotypes. However, the eWAT of OSMRFKO mice was modestly less responsive to insulin stimulation than that of OSMRfl/fl mice. Notably, significant increases in adipokines, including C‐reactive protein, lipocalin 2, intercellular adhesion molecule‐1, and insulinlike growth factor binding protein 6, were observed in the eWAT of OSMRFKO mice. In addition, significant increases in fetuin A and intercellular adhesion molecule‐1 were detected in OSMRFKO serum. Flow cytometry revealed a significant increase in leukocyte number and modest, but not statistically significant, increases in B cells and T cells in the eWAT of OSMRFKO mice.Conclusions
The chow‐fed OSMRFKO mice exhibited adipose tissue dysfunction and increased proinflammatory adipokine production. These results suggest that intact adipocyte oncostatin M–OSMR signaling is necessary for adipose tissue immune cell homeostasis.16.
Sulin Cheng Petri Wiklund Reija Autio Ronald Borra Xiaowei Ojanen Leiting Xu Timo T?rm?kangas Markku Alen 《PloS one》2015,10(10)
Background
Fatty liver is a major cause of obesity-related morbidity and mortality. The aim of this study was to identify early metabolic alterations associated with liver fat accumulation in 50- to 55-year-old men (n = 49) and women (n = 52) with and without NAFLD.Methods
Hepatic fat content was measured using proton magnetic resonance spectroscopy (1H MRS). Serum samples were analyzed using a nuclear magnetic resonance (NMR) metabolomics platform. Global gene expression profiles of adipose tissues and skeletal muscle were analyzed using Affymetrix microarrays and quantitative PCR. Muscle protein expression was analyzed by Western blot.Results
Increased branched-chain amino acid (BCAA), aromatic amino acid (AAA) and orosomucoid were associated with liver fat accumulation already in its early stage, independent of sex, obesity or insulin resistance (p<0.05 for all). Significant down-regulation of BCAA catabolism and fatty acid and energy metabolism was observed in the adipose tissue of the NAFLD group (p<0.001for all), whereas no aberrant gene expression in the skeletal muscle was found. Reduced BCAA catabolic activity was inversely associated with serum BCAA and liver fat content (p<0.05 for all).Conclusions
Liver fat accumulation, already in its early stage, is associated with increased serum branched-chain and aromatic amino acids. The observed associations of decreased BCAA catabolism activity, mitochondrial energy metabolism and serum BCAA concentration with liver fat content suggest that adipose tissue dysfunction may have a key role in the systemic nature of NAFLD pathogenesis. 相似文献17.
Genetic Markers of Brown Adipose Tissue Identity and In Vitro Brown Adipose Tissue Activity in Humans
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Emmani B.M. Nascimento Lauren M. Sparks Adeline Divoux Marike W. van Gisbergen Evie P.M. Broeders Johanna A. Jörgensen Gert Schaart Nicole D. Bouvy Wouter D. van Marken Lichtenbelt Patrick Schrauwen 《Obesity (Silver Spring, Md.)》2018,26(1):135-140
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肥胖已经成为威胁人类健康的全球性问题,棕色脂肪(Brown adipose tissue,BAT)及米色脂肪因其能够通过产热作用增加能量消耗这一特性,已成为一种备受关注的潜在肥胖治疗方法。近年来的研究发现M2型巨噬细胞(Alternatively activated macrophages,M2 type)能够促进BAT产热和白色脂肪(White adipose tissue,WAT)的棕色化(即米色脂肪的形成过程),但随后的一些研究却得到了相反的结论。到目前为止,M2型巨噬细胞是否参与促进WAT的棕色化过程仍是一个备受争议的话题。主要对M2型巨噬细胞、II型固有淋巴细胞(Type 2 Innate Lymphoid Cells,ILC2s)和嗜酸性粒细胞(Eosinophils)对BAT产热和WAT的棕色化的促进作用,以及M2型巨噬细胞不参与/抑制WAT棕色化这两个方面的研究状况做一综述。 相似文献
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脂肪作为机体内最大的分泌器官,可以通过释放激素,细胞因子等调节其他的组织器官.近年来研究发现,脂肪组织可以释放外泌体并通过体液循环传递信号至其他组织器官,调节其靶器官的生理功能,且针对不同的靶器官,外泌体会产生不同的作用效果.机体的稳态是各组织间相互作用的结果,外泌体的发现,为脂肪组织与其他组织互作提供了稳定的物质基础,但是,脂肪外泌体的作用依旧存在着许多未知效果.从脂肪组织外泌体的发现,鉴定,以及脂肪外泌体与肝脏,肌肉和其他组织器官的相互作用等方面进行综述,为脂肪外泌体的研究提供理论依据,以便更好地探索生命的奥秘. 相似文献