Curcuminoids Target Decreasing Serum Adipocyte-fatty Acid Binding Protein Levels in Their Glucose-lowering Effect in Patients with Type 2 Diabetes

Whether supplementation of curcuminoids decreases serum adipocyte-fatty acid binding protein(A-FABP) level and whether this decrease benefits glucose control is unclear.One-hundred participants(n=50 administered curcuminoids,n=50 administered placebo) from our previous report on the effect of curcuminoids on type 2 diabetes in a 3-month intervention were assessed for levels of serum A-FABP,oxidative stress,and inflammatory biomarkers.Curcuminoids supplementation led to significant decreases in serum A-FABP,C-reactive protein(CRP),tumor necrosis factor-α,and interleukin-6 levels.Curcuminoids supplementation also significantly increased serum superoxide dismutase(SOD) activity.The change in serum A-FABP levels showed positive correlations with changes in levels of glucose,free fatty acids(FFAs),and CRP in subjects supplemented with curcuminoids.Further stepwise regression analysis showed that A-FABP was an independent predictor for levels of FFAs,SOD,and CRP.These results suggest that curcuminoids may exert anti-diabetic effects,at least in part,by reductions in serum A-FABP level.A-FABP reduction is associated with improved metabolic parameters in human type 2 diabetes.     

has-miR-26b沉默载体的构建及验证

目的构建hsa-miR-26b沉默载体,与其靶基因PTEN共转染HEK-293T细胞验证其沉默效果。方法用miRNA海绵体技术设计并合成与hsa-miR-26b成熟序列反向互补的3个重复序列的双链DNA,将短发卡状RNA(shRNA)克隆入LV3-GFP-Puro载体,与靶基因PTEN共转染HEK-293T细胞,于24 h后收集细胞RNA,用real-time PCR检测hsa-miR-26b表达水平,同时用双荧光素报告系统检测其对靶基因的作用。结果成功构建了有效的hsa-miR-26b沉默载体,经测序验证与设计序列一致;real-time PCR验证hsa-miR-26b表达水平降低了75%;双荧光素报告系统验证其对靶基因无抑制作用(P>0.05)。结论成功构建hsa-miR-26b沉默载体,并验证其对靶基因PTEN无抑制作用。     

Pathogenic potential of adipose tissue and metabolic consequences of adipocyte hypertrophy and increased visceral adiposity

When caloric intake exceeds caloric expenditure, the positive caloric balance and storage of energy in adipose tissue often causes adipocyte hypertrophy and visceral adipose tissue accumulation. These pathogenic anatomic abnormalities may incite metabolic and immune responses that promote Type 2 diabetes mellitus, hypertension and dyslipidemia. These are the most common metabolic diseases managed by clinicians and are all major cardiovascular disease risk factors. ‘Disease’ is traditionally characterized as anatomic and physiologic abnormalities of an organ or organ system that contributes to adverse health consequences. Using this definition, pathogenic adipose tissue is no less a disease than diseases of other body organs. This review describes the consequences of pathogenic fat cell hypertrophy and visceral adiposity, emphasizing the mechanistic contributions of genetic and environmental predispositions, adipogenesis, fat storage, free fatty acid metabolism, adipocyte factors and inflammation. Appreciating the full pathogenic potential of adipose tissue requires an integrated perspective, recognizing the importance of ‘cross-talk’ and interactions between adipose tissue and other body systems. Thus, the adverse metabolic consequences that accompany fat cell hypertrophy and visceral adiposity are best viewed as a pathologic partnership between the pathogenic potential adipose tissue and the inherited or acquired limitations and/or impairments of other body organs. A better understanding of the physiological and pathological interplay of pathogenic adipose tissue with other organs and organ systems may assist in developing better strategies in treating metabolic disease and reducing cardiovascular disease risk.     

Effects of Whey Peptide Supplementation on Sarcopenic Obesity in High-Fat Diet-Fed Mice

The incidence of sarcopenic obesity gradually increased in parallel with the aged population. This research examined the effects of whey peptide (WP) supplementation with/without resistant exercise (RE) on sarcopenic obesity. Male 8-month-old C57BL/6J mice were fed a control diet (10 kcal% fat) or a high-fat diet (60 kcal% fat) for 8 weeks. High-fat diet-fed mice were randomly divided into four groups: obesity control group (OB), RE (RE only), WP (WP only), and WPE (RE and WP). WP supplementation (1500 mg/day/kg B.W.) gavage and RE (ladder climbing, five times weekly, 8–10 repetitions, 10–20% B.W. load) were conducted for an additional 8 weeks. Protein and mRNA levels of markers related to energy, protein, and lipid metabolism were analyzed in skeletal muscle and adipose tissue by one-way analysis of variance (ANOVA). WP supplementation regardless of RE significantly suppressed the increasing fat mass (p = 0.016) and decreasing lean mass (p = 0.014) and alleviated abnormal morphological changes in skeletal muscle and adipose tissue (p < 0.001). In adipose tissue, WP supplementation regardless of RE ameliorated dysregulated energy metabolism and contributed to the reduction in adipocyte differentiation (PPAR-γ (p = 0.017), C/EBPα (p = 0.034)). In skeletal muscle, WP supplementation regardless of RE alleviated energy metabolism dysregulation and resulted in down-regulated protein degradation (Atrogin-1 (p = 0.003), MuRF1 (p = 0.006)) and apoptosis (Bax) (p = 0.004). Taken together, the current study elucidated that WP supplementation regardless of RE has potential anti-obesity and anti-sarcopenic effects in sarcopenic obesity.     

Increment of subcutaneous adipose tissue is associated with decrease of elastic fibres in the dermal layer

Obesity is a significant risk factor for various skin disorders, including pressure ulcer and delayed wound healing. We previously showed that increment of subcutaneous adipose tissue contributes to poor skin condition by decreasing dermal elasticity. Here, we examined the mechanism involved. Histologic observation of abdominal skin from middle‐aged females with a wide range of body mass index (BMI), an indicator of subcutaneous fat mass, showed that dermal elastic fibre abundance was significantly decreased with increment of BMI. Concomitantly, adipocytes were significantly enlarged. Adipocyte enlargement was significantly negatively correlated with dermal elastic fibre abundance. We hypothesized that enlarged adipocytes negatively influence dermal elastic fibres, so we investigated elastic fibre‐degrading factors in in vitro‐cultured enlarged adipocytes. MMP9 gene expression and secretion were significantly increased; further, these changes were blocked by extracellular signal‐regulated kinase (ERK) inhibitor. Nuclear translocation (activation) of AP‐1, a downstream ERK signalling molecule, was also observed in enlarged adipocytes. MMP9 abundance was significantly increased in skin of subjects with high BMI and enlarged adipocytes. These results suggest that increment of subcutaneous adipose tissue leads to adipocyte enlargement together with increased degradation of dermal elastic fibres, mediated at least in part by an ERK signalling‐mediated increase of MMP9 in enlarged adipocytes.     

Lipolysis using a new 1540-nm diode laser: A retrospective analysis of 230 consecutive procedures

Abstract

Background: Although traditional liposuction still remains the most required body sculpting procedure, laser lipolysis systems are becoming increasingly popular. The feasibility and efficacy of a new 1540-nm diode laser for suction-assisted laser lipolysis were evaluated. Methods: Two hundred-thirty patients underwent a new 1540-nm diode laser lipolysis. Outcomes were determined by case notes, clinical review of side effects, and a questionnaire through which patient satisfaction was assessed. Macroscopic and histologic effects on subcutaneous fat and collagen deposition were evaluated. Moreover thermal effects were studied through thermography. Results: The treated regions were abdomen in 56 cases, thighs in 54, trochanteric area in 27, flanks in 17, neck in 14, arms in 12, breast in 11, hips in 7, knees in 3; 29 cases were revisions of previous lipoplasties. No adverse effect as scarring, infection, burns, hypopigmentation, bruising, or swelling was observed. The required effects of laser lipolysis such as contour reshaping and skin tightening were achieved in almost all patients with high levels of satisfaction after treatment. Conclusion: Our investigation highlighted the safety and efficacy of the new 1540-nm diode laser assisted liposuction device for removal of small volumes of fat deposits associated with concurrent subdermal tissue contraction, tolerance and quick recovery time.     

The Function of Leptin in Nutrition, Weight, and Physiology

Recent advances indicate that a robust physiologic system acts to maintain relative constancy of weight in mammals. A key component of this system is leptin. Leptin is an adipocyte hormone that functions as the afferent signal in a negative feedback loop regulating body weight. In addition, leptin functions as a key link between nutrition and the function of most, if not all other physiologic systems. When at their set point, individuals produce a given amount of leptin and in turn maintain a state of energy balance. Weight gain results in an increased plasma leptin level, which elicits a biologic response characterized in part by a state of negative energy balance. Weight loss among both lean and obese subjects results in decreased plasma levels of leptin, which lead to a state of positive energy balance and a number of other physiologic responses. In humans, both the intrinsic sensitivity to leptin and its rate of production vary and both appear to contribute to differences in weight. Further studies of leptin, its receptor, and the molecular components of this system are likely to have a major impact on our understanding of obesity and the interplay between nutrition and physiology.     

黄芪多糖对体外培养大鼠脂肪细胞分泌脂联素及IL-6的影响

目的探讨黄芪多糖对体外诱导培养大鼠脂肪细胞分泌脂联素及IL-6的影响。方法将大鼠诱导脂肪细胞与不同浓度的黄芪多糖(0.001、0.1、10μg.μl-1)孵育48h,以ELISA方法检测上清液脂联素及IL-6改变。结果与对照组比较,0.1μmol.L-1黄芪多糖可使脂联素分泌显著增加(P<0.05),而低浓度则则降低脂联素的分泌(P<0.05)。黄芪多糖减少IL-6分泌呈浓度剂量依赖性,0.1μg.μl-1和10μg.μl-1组有统计学意义(P<0.05)。结论体外实验中,0.1μg.μl-1黄芪多糖使大鼠脂肪细胞增加脂联素分泌,而剂量依赖性减少IL-6分泌,这可能使体内黄芪多糖改善胰岛素抵抗的途径之一。     

脂肪因子与代谢综合征的关系探讨

目的探讨以血清瘦素、抵抗素和脂联素为代表的脂肪因子与代谢综合征的关系。方法选择代谢综合征患者50例,正常对照30例,观察一般情况,并测定血清瘦素、抵抗素、脂联素、空腹血糖、空腹血胰岛素和血脂等指标,计算胰岛素敏感指数。结果代谢综合征患者的血清瘦素和抵抗素水平均显著高于正常对照,血清脂联素水平显著低于正常对照。瘦素:代谢综合征14.9±2.1μg/L,正常对照7.5±1.4μg/L,P<0.05;抵抗素:代谢综合征24.1±7.2μg/L,正常对照14.3±5.6μg/L,P<0.05;脂联素:代谢综合征9.7±2.2 m g/L,正常对照12.1±3.6 m g/L,P<0.05。相关分析显示瘦素、抵抗素和脂联素水平与体重指数、胰岛素敏感指数等指标显著相关。结论脂肪因子与代谢综合征密切相关,代谢综合征常伴有高瘦素血症、低脂联素血症及抵抗素水平升高。