雄性C57BL/6J小鼠不同部位脂肪组织功能的差异

目的:研究雄性C57BL/6J小鼠各部位脂肪组织的棕色化功能差异?方法:分离雄性C57BL/6J小鼠各部位脂肪组织,荧光定量PCR检测脂肪组织棕色化?成脂功能的标志基因?脂肪细胞因子?炎症因子表达情况?Western blot检测棕色化功能蛋白解偶联蛋白1(uncoupling protein-1,Ucp1)表达?结果:以肩胛间和肩胛下棕色脂肪为比较标准,其中甲状腺上?下部位脂肪的棕色化功能标志基因表达量最高,接近肩胛间和肩胛下;在肩胛间白色脂肪?腋下脂肪和肾周脂肪,上述棕色化标志基因表达量低于甲状腺周围脂肪;腹股沟皮下?附睾旁及肠系膜脂肪的上述棕色化标志基因表达最低?成脂功能的标志基因在皮下脂肪表达量明显高于附睾旁?肠系膜周围脂肪?脂肪细胞因子在白色脂肪特性的脂肪组织中表达量明显高于有棕色脂肪特性脂肪;附睾旁脂肪?肠系膜脂肪中炎症因子表达量显著升高,皮下脂肪炎症因子表达量最少?结论:甲状腺上?下部位脂肪的棕色化程度接近经典棕色脂肪?肩胛间白色脂肪?腋下脂肪和肾周脂肪较甲状腺周围脂肪的棕色化程度弱,成脂功能?脂肪细胞因子?炎症因子与肩胛间?肩胛下棕色脂肪基本一致且均较强?腹股沟皮下?附睾旁及肠系膜脂肪具有白色脂肪特性?皮下脂肪大量分泌脂肪细胞因子,炎症因子表达量小,成脂功能强?附睾旁脂肪?肠系膜周围脂肪细胞因子表达量较少,但炎症因子分泌相对较高且脂解作用较强?     

Fruit vinegars attenuate cardiac injury via anti-inflammatory and anti-adiposity actions in high-fat diet-induced obese rats

Context: Fruit vinegars (FVs) are used in Mediterranean folk medicine for their hypolipidemic and weight-reducing properties.

Objective: To investigate the preventive effects of three types of FV, commonly available in Algeria, namely prickly pear [Opuntia ficus-indica (L.) Mill (Cectaceae)], pomegranate [Punica granatum L. (Punicaceae)], and apple [Malus domestica Borkh. (Rosaceae)], against obesity-induced cardiomyopathy and its underlying mechanisms.

Materials and methods: Seventy-two male Wistar rats were equally divided into 12 groups. The first group served as normal control (distilled water, 7?mL/kg bw), and the remaining groups were respectively treated with distilled water (7?mL/kg bw), acetic acid (0.5% w/v, 7?mL/kg bw) and vinegars of pomegranate, apple or prickly pear (at doses of 3.5, 7 and 14?mL/kg bw, acetic acid content as mentioned above) along with a high-fat diet (HFD). The effects of the oral administration of FV for 18 weeks on the body and visceral adipose tissue (VAT) weights, plasma inflammatory and cardiac enzymes biomarkers, and in heart tissue were evaluated.

Results: Vinegars treatments significantly (p?Discussion and conclusion: These findings suggest that pomegranate, apple and prickly pear vinegars may prevent HFD-induced obesity and obesity-related cardiac complications, and that this prevention may result from the potent anti-inflammatory and anti-adiposity properties of these vinegars.     

脂肪因子和代谢综合征

脂肪组织被认为不仅是能量储存器官,而且是功能活跃的内分泌器官。脂肪因子在代谢综合征的发生、发展过程中起重要作用,尤其是肥胖时内脏脂肪组织分泌的促炎症脂肪因子可直接导致胰岛素抵抗和血管损伤,充分理解脂肪组织的内分泌功能将有助于对代谢综合征作出更合理的治疗。     

脂肪组织和脂肪细胞因子的研究进展

脂肪组织是一个活跃的内分泌和旁分泌器官，分泌许多细胞因子和生物活性因子。脂肪组织的分泌功能存在节律性，全身各脂肪库脂肪因子的表达和分泌具有特异性，提示其复杂的生物学功能。脂肪组织是促炎症反应介质的丰富来源，这些介质参与炎症、凝血和纤溶反应，可直接引起血管损伤、胰岛素抵抗和动脉粥样硬化；脂肪细胞因子是肥胖和代谢综合征的分子联系。     

Adiponectin and cardiovascular health: an update

The global epidemic of obesity is accompanied by an increased prevalence of cardiovascular disease (CVD), in particular stroke and heart attack. Dysfunctional adipose tissue links obesity to CVD by secreting a multitude of bioactive lipids and pro-inflammatory factors (adipokines) with detrimental effects on the cardiovascular system. Adiponectin is one of the few adipokines that possesses multiple salutary effects on insulin sensitivity and cardiovascular health. Clinical investigations have identified adiponectin deficiency (hypoadiponectinaemia) as an independent risk factor for CVD. In animals, elevation of plasma adiponectin by either pharmacological or genetic approaches alleviates obesity-induced endothelial dysfunction and hypertension, and also prevents atherosclerosis, myocardial infarction and diabetic cardiomyopathy. Furthermore, many therapeutic benefits of the peroxisome-proliferator activated receptor gamma agonists, the thiazolidinediones, are mediated by induction of adiponectin. Adiponectin protects cardiovascular health through its vasodilator, anti-apoptotic, anti-inflammatory and anti-oxidative activities in both cardiac and vascular cells. This review summarizes recent findings in the understanding of the physiological role and clinical relevance of adiponectin in cardiovascular health, and in the identification of the receptor and postreceptor signalling events that mediate the cardiovascular actions of adiponectin. It also discusses adiponectin-targeted drug discovery strategies for treating obesity, diabetes and CVD. LINKED ARTICLES: This article is part of a themed section on Fat and Vascular Responsiveness. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2012.165.issue-3.     

马尾松花粉水提物预防小鼠肥胖的初步探究

目的观察马尾松花粉水提物(PWE)对肥胖模型小鼠的体重、体脂肪和血脂的影响。方法选取60只昆明白雄性小鼠,体重(19±1)g,随机分为6组:空白对照组,高脂肥胖组,奥利司他组(0.05g/kg bw.d),PWE低、中、高(0.0625、0.125、0.25g/kg bw.d)剂量组。每三天测定一次体重,6w后检测血脂水平、脂肪因子和肉碱棕榈转移酶Ⅰ(CPT-Ⅰ)含量及CPT-ⅠmRNA的表达水平等。结果 PWE三个剂量均能降低小鼠体重和体脂总重,也能降低小鼠血清中TC、TG的含量,升高HDLC的含量,显著地升高肝脏组织和脂肪组织中CPT-Ⅰ的含量,PWE中剂量组尤为明显(P<0.01),显著上调CPT-ⅠmRNA的表达。结论 PWE早期应用能够有效的预防高脂饲料诱导的小鼠肥胖。[营养学报,2013,35(2):195-198]     

The role of adiponectin in the pathogenesis and treatment of non‐alcoholic fatty liver disease

Non‐alcoholic fatty liver disease (NAFLD) is recognized as the most common type of chronic liver disease in Western countries and the leading cause of cryptogenic cirrhosis. Insulin resistance (IR) is a key factor in the pathogenesis of NAFLD, the latter being considered as the hepatic component of IR or metabolic syndrome (MetS). Although the pathogenesis of NAFLD is not fully elucidated, a complex interaction between adipokines and cytokines produced by adipocytes and/or inflammatory cells infiltrating adipose tissue appears to play a crucial role in MetS and NAFLD. Adiponectin is the most abundant and adipose‐specific adipokine. In the liver, adiponectin acts through the activation of 5‐AMP‐activated protein kinase and peroxisome proliferator‐activated receptor‐α pathways and inhibition of toll‐like receptor‐4 mediated signalling. There is an evidence that adiponectin decreases hepatic and systematic IR and attenuates liver inflammation and fibrosis. Adiponectin generally predicts steatosis grade and severity of NAFLD, but it remains to be addressed to what extent this is a direct effect or related to the presence of more severe IR. Although there is no proven pharmacotherapy for the treatment of NAFLD, recent therapeutic strategies have focused on the indirect upregulation of adiponectin through the administration of various therapeutic agents and/or lifestyle modifications. Weight loss, through diet, lifestyle changes and/or medications including orlistat, sibutramine, rimonabant or bariatric surgery, increase adiponectin and may improve liver histology. Insulin sensitizers, including pioglitazone and rosiglitazone, and lipid‐lowering agents, including statins and fibrates, also upregulate adiponectin and ameliorate liver histology. The wider use of new treatment approaches appears to signal the dawn of a new era in the management of NAFLD. In this adiponectin‐focused review, the pathogenetic role and the potential therapeutic benefits of adiponectin in NAFLD are systematically analysed.     

Synergistic effects of ascorbic acid and thiazolidinedione on secretion of high molecular weight adiponectin from human adipocytes

Aim: To test the hypothesis that ascorbic acid (AA) and thiazolidinedione (TZD) would have additive effects on HMW adiponectin secretion by virtue of different modes of action. Methods: We determined the effects of supplementation of AA and/or TZD on expression and secretion of total and HMW adiponectin from human Simpson–Golabi–Behmel syndrome (SGBS) adipocytes in the absence or presence of the proinflammatory cytokine TNFα. Results: AA supplementation significantly increased secretion of HMW adiponectin (1.7‐fold) without altering adiponectin expression or total adiponectin secretion. TZD significantly increased expression (3‐fold) and secretion of total (1.4‐fold) but not HMW adiponectin. Combined supplementation resulted in a significant increase in expression (3‐fold) and secretion of total (1.8‐fold) and HMW (5‐fold) adiponectin. Similar results were seen in cells co‐treated with TNFα. Conclusions: These data show that AA and TZD have synergistic rather than simple additive effects on secretion of HMW adiponectin from human adipocytes and raise the possibility that differences in AA levels may contribute to the variability in adiponectin multimer profiles and efficacy of TZD in humans. Our results also provide a rationale for longitudinal clinical trials investigating the effects of AA supplementation with or without TZD on adiponectin and metabolic profiles.