BACKGROUND & AIMS: BACKGROUND:Alone among autonomic neurones, enteric neurones are known to be vulnerable to age related cell death; over 50% may be lost in aging rodents. A previous study demonstrated unexpectedly that neurones of the myenteric plexus from rats fed a restricted diet appeared not to suffer from extensive cell death in contrast with previous studies of ad libitum fed animals. AIMS:To compare myenteric neurone numbers in the ileum of young and aging male Sprague-Dawley rats fed either ad libitum or a restricted diet. METHODS:Neurones were counted in whole mount preparations of rat ileum stained immunohistochemically for the pan-neuronal marker PGP9.5, for choline acetyltransferase, or for nitric oxide synthase, or with NADH or NADPH histochemistry. RESULTS:Neurone numbers in the rat myenteric plexus were substantially affected by the dietary regimen: ad libitum feeding (50-60 g per day of standard rat chow) resulted in the death of about 50% of myenteric neurones in 24 month Sprague-Dawley rats, while numbers were unchanged when the daily dietary intake was halved between the ages of six and 24 months. Animals fed a double restricted diet (15 g per day) showed no cell loss at 30 months, as well as the predicted increase in longevity. Neurone loss was largely complete by 16 months in ad libitum fed animals. Numbers of cholinergic (possibly motor) neurones, as demonstrated by choline acetyltransferase immunohistochemistry, were substantially reduced in ad libitum fed aging rats but not in animals fed a restricted diet. Loss of cholinergic neurones after ad libitum feeding was confirmed by reduced numbers of neurones of a size range matching that of cholinergic neurones. CONCLUSIONS:Ad libitum feeding of adult rats has adverse effects on the survival of myenteric neurones, neurone loss commencing before 16 months of age. Cholinergic neurones appear to be particularly vulnerable to the effects of diet. Restricting dietary intake from six months of age prevents neurone loss almost entirely up to 30 months of age in these rats.

背景与目标： 背景：已知在自主神经元中，肠神经元易受年龄相关的细胞死亡的影响。老化的啮齿动物可能损失超过50％。先前的研究出乎意料地证明，与先前的随意喂养动物的研究相比，饮食有限的大鼠的肌间神经丛神经元似乎没有遭受广泛的细胞死亡。
目的：比较随意喂养或限制饮食的年轻和衰老雄性Sprague-Dawley大鼠回肠中的肠神经元数量。
方法：对整组大鼠回肠的神经营养素进行免疫组织化学染色，以泛神经元标记PGP9.5，胆碱乙酰转移酶，一氧化氮合酶或NADH或NADPH组织化学染色。
结果：大鼠的肌间神经丛中的神经元数量受到饮食方案的严重影响：随意喂养（每天标准大鼠食物50-60 g）在24个月的Sprague-Dawley大鼠中导致约50％的肌层神经元死亡，而在6至24个月的年龄中将每日饮食摄入量减少一半时，这一数字没有变化。进食双重限制饮食（每天15克）的动物在30个月时未见细胞丢失，并且预期的寿命会增加。在随意喂养的动物中，神经元的丧失在16个月前基本完成。胆碱乙酰基转移酶免疫组织化学证实，胆碱能神经元（可能是运动神经元）的数目在随意喂养的衰老大鼠中显着减少，但在饮食不严格的动物中则没有。随意喂食后胆碱能神经元的丧失被大小范围与胆碱能神经元相匹配的神经元数目减少所证实。
结论：成年大鼠随意喂食会对肌层神经元的存活产生不利影响，神经元的损失开始于16个月大之前。胆碱能神经元似乎特别容易受到饮食的影响。从六个月大时开始限制饮食摄入，可在这些大鼠中几乎完全阻止直到三十个月大时神经元的丧失。

BACKGROUND & AIMS: :Excessive uptake of fatty acids and glucose by adipose tissue triggers adipocyte dysfunction and infiltration of immune cells. Altered metabolic homeostasis in adipose tissue promotes insulin resistance, type 2 diabetes, hypertension, and cardiovascular disease. Inflammatory and metabolic processes are mediated by certain proteolytic enzymes that share a common cellular target, protease-activated receptor 2 (PAR2). This study showed that human and rat obesity correlated in vivo with increased expression of PAR2 in adipose tissue, primarily in stromal vascular cells (SVCs) including macrophages. PAR2 was expressed more than other PARs on human macrophages and was increased by dietary fatty acids (palmitic, stearic, and myristic). A novel PAR2 antagonist, GB88 (5-isoxazoyl-Cha-Ile-spiroindene-1,4-piperidine), given orally at 10 mg/kg/d (wk 8-16) reduced body weight by ∼10% in obese rats fed a high-carbohydrate high-fat (HCHF) diet for 16 wk, and strongly attenuated adiposity, adipose tissue inflammation, infiltrated macrophages and mast cells, insulin resistance, and cardiac fibrosis and remodeling; while reversing liver and pancreatic dysfunction and normalizing secretion of PAR2-directed glucose-stimulated insulin secretion in MIN6 β cells. In summary, PAR2 is a new biomarker for obesity, and its expression is stimulated by dietary fatty acids; PAR2 is a substantial contributor to inflammatory and metabolic dysfunction; and a PAR2 antagonist inhibits diet-induced obesity and inflammatory, metabolic, and cardiovascular dysfunction.

背景与目标： ：脂肪组织摄入过多的脂肪酸和葡萄糖会触发脂肪细胞功能障碍和免疫细胞浸润。脂肪组织中代谢稳态的改变会促进胰岛素抵抗，2型糖尿病，高血压和心血管疾病。炎症和代谢过程由共享共同细胞靶标，蛋白酶激活受体2（PAR2）的某些蛋白水解酶介导。这项研究表明，人和大鼠的肥胖症在体内与PAR2在脂肪组织（主要是在包括巨噬细胞的基质血管细胞（SVC））中表达的增加有关。 PAR2在人类巨噬细胞上的表达高于其他PAR，并且通过膳食脂肪酸（棕榈酸，硬脂酸和肉豆蔻酸）增加。以10 mg / kg / d（wk 8-16）口服给予的新型PAR2拮抗剂GB88（5-isoxazoyl-Cha-Ile-spirindindene-1,4-piperidine）在体重减轻的肥胖大鼠中体重减轻了约10％ 16周的高碳水化合物高脂（HCHF）饮食，可大大减轻肥胖，脂肪组织炎症，巨噬细胞和肥大细胞浸润，胰岛素抵抗以及心脏纤维化和重塑。同时逆转肝和胰腺功能障碍，并使MIN6β细胞中PAR2指导的葡萄糖刺激的胰岛素分泌正常化。总之，PAR2是肥胖的一种新的生物标志物，它的表达受到饮食脂肪酸的刺激。 PAR2是导致炎症和代谢功能障碍的重要因素。 PAR2拮抗剂可抑制饮食引起的肥胖症以及炎症，代谢和心血管功能障碍。

BACKGROUND & AIMS: ETHNOPHARMACOLOGICAL RELEVANCE:Homalium zeylanicum (Gardner) Benth. is a medicinal plant traditionally used in controlling diabetes which thus far has been assessed by the authors only to a very limited extent. PURPOSE:To fill the research gap in the literature review, we investigated the antihyperglycemic effects of hydro alcohol fraction of bark of H. zeylanicum (HAHZB) by modulating oxidative stress and inflammation in high-fat diet fed-streptozotocin (HFD/STZ)-induced type-2 diabetic rats. MATERIALS AND METHODS:To understand the antioxidant capacity of HAHZB, oxygen radical absorbance capacity (ORAC) and cell-based antioxidant protection in erythrocytes (CAP-e) were performed. GC-MS/MS analysis was performed to assess the bioactive components in HAHZB. HFD/STZ-induced diabetic rats were treated orally with HAHZB (300 and 400 mg/kg) for 28 days. After the end of the experiment, marker profiling and histopathological observation of blood and pancreas were examined. The study also highlights interaction between diabetes, oxidative stress and inflammation by examining the increased pro-inflammatory cytokines e.g. TNF-α and C-reactive protein (CRP) promotes DNA damage e.g. oxidation of 8-hydroxy-2-deoxyguanosine (8-OHdG) in chronic hyperglycaemia. RESULTS:In ex vivo cellular antioxidant capacity of -CAP-e and ORAC assays, HAHZB showed remarkable free radical scavenging ability in a dose dependent manner. GC-MS/MS analysis identified 28 no. of compounds and out of which, oleic acid (1.03%), ethyl tridecanoate (11.77%), phytol (1.29), 9,12-octadecadienoic acid, methyl ester, (E,E)-(5.97%), stigmasterol (1.30%) and β-sitosterol (2.86%) have antioxidant, anti-inflammatory and anti-diabetic activities. HAHZB 400 mg/kg significantly (p < 0.001) improved the lipid profile (TC: 74.66 ± 0.59, HDL-C: 22.08 ± 0.46, LDL-C: 38.06 ± 0.69, and TG: 171.92 ± 1.01 mg/dL) as well as restoring antidiabetic markers (SG: 209.62 ± 1.05 mg/dL, SI: 15.07 ± 0.11 μIU/mL, HOMA-IR: 7.79 ± 0.04 %, and HbA1C: 8.93 ± 0.03 %) and renal functional markers (Tg: 291.26 ± 0.57 pg/mL, BUN: 23.79 ± 0.14 mg/dL, and Cr: 1.34 ± 0.04 mg/dL) in diabetic rats. Oxidative stress markers of pancreas (MDA: 3.65 ± 0.17 nM TBARS /mg protein, SOD: 3.14 ± 0.28 U/mg protein, CAT: 7.88 ± 0.23 U/mg protein, GSH: 12.63 ± 0.28 µM/g of tissue) were restored to normal as evidenced by histological architecture of pancreatic islet cells. The increased level of pro-inflammatory cytokines and oxidative DNA damage were significantly restored (TNF-α: 54.48 ± 3.19 pg/mL, CRP: 440.22 ± 7.86 ng/mL, and 8-OHdG: 63.65 ± 1.84 ng/mL) by HAHZB in diabetic rats. CONCLUSION:The present findings confirm that the presence of bioactive compounds in HAHZB exert therapeutic protective effect by decreasing oxidative, inflammation and pancreatic β-cell damage in oxidative stress induced diabetic rats.

背景与目标： 人类药理学联系：oma骨（Gardner）Benth。是传统上用于控制糖尿病的药用植物，迄今为止，作者仅对其进行了非常有限的评估。
目的：为填补文献综述的研究空白，我们通过调节高脂饮食饲喂链脲佐菌素（HFD / STZ）-中的氧化应激和炎症，研究了玉米树皮（HAHZB）的树皮中乙醇部分的降血糖作用。诱导的2型糖尿病大鼠。
材料与方法：为了解HAHZB的抗氧化能力，进行了氧自由基吸收能力（ORAC）和红细胞中基于细胞的抗氧化保护（CAP-e）。进行了GC-MS / MS分析，以评估HAHZB中的生物活性成分。用HHZB（300和400 mg / kg）口服治疗HFD / STZ诱导的糖尿病大鼠28天。实验结束后，检查了血液和胰腺的标志物谱以及组织病理学观察。这项研究还通过检查增加的促炎细胞因子例如糖尿病，糖尿病，氧化应激和炎症来强调糖尿病，氧化应激和炎症之间的相互作用。 TNF-α和C反应蛋白（CRP）促进DNA损伤，例如慢性高血糖症中8-羟基-2-脱氧鸟苷（8-OHdG）的氧化
结果：在-CAP-e和ORAC检测的离体细胞抗氧化能力中，HAHZB以剂量依赖性方式表现出显着的自由基清除能力。 GC-MS / MS分析确定为28号。化合物，其中油酸（1.03％），十三烷酸乙酯（11.77％），植物醇（1.29），9,12-十八碳二烯酸，甲酯，（E，E）-（5.97％），豆甾醇（1.30 ％）和β-谷固醇（2.86％）具有抗氧化，抗炎和抗糖尿病的作用。 HAHZB 400 mg / kg也显着（p <0.001）改善了血脂水平（TC：74.66±0.59，HDL-C：22.08±0.46，LDL-C：38.06±0.69，TG：171.92±1.01 mg / dL）作为恢复性抗糖尿病标志物（SG：209.62±1.05 mg / dL，SI：15.07±0.11μIU/ mL，HOMA-IR：7.79±0.04％，HbA1C：8.93±0.03％）和肾功能标志物（Tg：291.26±0.57） pg / mL，BUN：糖尿病大鼠中的23.79±0.14 mg / dL，Cr：1.34±0.04 mg / dL）。恢复了胰腺的氧化应激指标（MDA：3.65±0.17nM TBARS / mg蛋白，SOD：3.14±0.28U / mg蛋白，CAT：7.88±0.23U / mg蛋白，GSH：12.63±0.28μM/ g组织）胰腺胰岛细胞的组织学结构证明其正常。 HAHZB可以显着恢复增加的促炎细胞因子水平和氧化DNA损伤（TNF-α：54.48±3.19 pg / mL，CRP：440.22±7.86 ng / mL，8-OHdG：63.65±1.84 ng / mL）在糖尿病大鼠中。
结论：本研究结果证实，HAHZB中生物活性化合物的存在可通过减少氧化应激诱导的糖尿病大鼠的氧化，炎症和胰腺β细胞损伤而发挥治疗保护作用。

BACKGROUND & AIMS: :Diets containing unheated casein (CD; control) or a casein-glucose mixture (CGD) previously heated at 140 degrees for 2 h were fed to two groups of young rats for 21 d. Differences in body weight, feed consumption, thymus, and spleen growth, protein metabolism and in vivo immune response were then determined. For this last experiment, animals were inoculated with sheep erythrocytes (SRBC) on day 15 to provide an immunological challenge. No changes were seen in body weight, feed consumption or feed conversion ratios. Neither were significant differences found in spleen weight, protein content, DNA content, DNase (EC 3.1.4.6) activity or lymphocyte count, suggesting that spleen cell growth remained similar in all the animals studied. The CGD induced marked increases in thymus DNA content whilst the protein:DNA ratio became lower. Spleen RNA content was similar in all rats, but thymus RNA content was 29% lower in the CGD group, although this difference did not reach statistical significance. This fact might be a consequence of the low RNase (EC 2.7.7.16) activity and RNase:RNA ratios in the thymus glands of CGD-fed animals. Further, the number of splenic plasma cells secreting anti-SRBC antibodies (direct plaque-forming cells) was significantly decreased in the same group. It might be concluded that both diets are adequate for rat growth and that the differences observed in the thymus of CGD-fed rats may be directed towards preserving tissue function. Nevertheless, the CGD did cause immunological disturbances affecting the humoral immune response.

背景与目标： 将含有未加热的酪蛋白（CD；对照）或酪蛋白-葡萄糖混合物（CGD）的先前已在140度下加热2小时的饮食喂食到两组幼鼠，持续21天。然后确定体重，饲料消耗，胸腺和脾脏生长，蛋白质代谢和体内免疫反应的差异。对于最后一个实验，在第15天用羊红细胞（SRBC）接种动物以提供免疫学攻击。体重，饲料消耗或饲料转化率未见变化。脾脏重量，蛋白质含量，DNA含量，DNase（EC 3.1.4.6）活性或淋巴细胞计数均未发现显着差异，表明脾脏细胞生长在所有研究的动物中均相似。 CGD诱导胸腺DNA含量显着增加，而蛋白质：DNA比例降低。在所有大鼠中，脾脏RNA含量均相似，但CGD组的胸腺RNA含量低29％，尽管这种差异并未达到统计学意义。此事实可能是CGD喂养的动物的胸腺中RNase（EC 2.7.7.16）活性低和RNase：RNA比低的结果。此外，同一组中分泌抗SRBC抗体的脾浆细胞（直接噬菌斑形成细胞）数量明显减少。可以得出结论，两种饮食都足以使大鼠生长，并且在CGD喂养的大鼠的胸腺中观察到的差异可能是为了保持组织功能。尽管如此，CGD确实会引起影响体液免疫反应的免疫学紊乱。

BACKGROUND & AIMS: :The objective of the present study was to examine the associations between the portion sizes of food groups consumed with measures of adiposity using data from the National Diet and Nutrition Survey of British adults. Seven-day weighed dietary records, physical activity diaries and anthropometric measurements were used. Foods eaten were assigned to thirty different food groups and analyses were undertaken separately for men and women. The median daily portion size of each food group consumed was calculated. The potential mis-reporting [corrected] of dietary energy intake (EI) was identified using the following equation: EI--estimated energy requirements/EER [corrected] x 100 = percentage of under-reporting (UR) of energy needs. Multinomial logistic regression (adjusted for age, social class, physical activity level and UR) was used to determine the portion sizes of food groups most strongly associated with obesity status. Few positive associations between the portion sizes of food groups consumed and obesity status were found. However, UR was prevalent, with a median UR of predicted energy needs of 34 and 33 % in men and women, respectively. After the adjustment was made for UR, more associations between the food groups and obesity status became apparent in both sexes. The present study suggests that the true effect of increased portion size of foods on obesity status may be masked by high levels of UR. Alternatively, these data may indicate that an increased risk of obesity is not associated with specific foods/food groups but rather with an overall increase in the range of foods and food groups being consumed.

背景与目标： ：本研究的目的是使用英国成年人的国家饮食和营养调查所提供的数据，通过肥胖测量来检验食用的食物组的份量之间的关联。使用7天称重的饮食记录，体力活动日记和人体测量值。食用的食物被分配到30个不同的食物组中，并且分别对男性和女性进行了分析。计算每个食用食物组的中位数每日份量。饮食能量摄入（EI）的潜在错误报告[校正]使用以下公式确定：EI-估计能量需求/ EER [校正] x 100 =能量需求报告不足（UR）的百分比。使用多项式逻辑回归（根据年龄，社会阶层，体育活动水平和UR进行调整）来确定与肥胖状况最相关的食物组的份量。在食用的食物类别的份量与肥胖状况之间几乎没有正相关。但是，UR普遍存在，男性和女性的预期能量需求中值UR分别为34％和33％。在对UR进行调整后，两性之间的食物组与肥胖状况之间的联系更加明显。本研究表明，高比例的尿素可能掩盖了食物份量增加对肥胖状况的真正影响。或者，这些数据可能表明肥胖的风险增加与特定食品/食物类别无关，而与所食用的食品和食物类别范围的总体增加有关。

BACKGROUND & AIMS: :This study investigated the inhibitory effect of arctigenin, a novel anti-inflammatory lignan, on prostate cancer in obese conditions both in vitro and in vivo. In vitro obese models were established by co-culture of mouse adipocytes 3T3-L1 with androgen-sensitive LNCaP human prostate cancer cells, or by culturing LNCaP cells in adipocytes-conditioned medium. Arctigenin significantly inhibited LNCaP proliferation, along with decreased androgen receptor (AR) and increased Nkx3.1 cellular expression. Male severe combined immunodeficiency mice were subcutaneously implanted with human prostate cancer LAPC-4 xenograft tumors for in vivo study. Mice were fed high-fat (HF) diet and orally given arctigenin at 50 mg/kg body weight daily or vehicle control for 6 weeks. Tumor bearing HF control mice showed a significant increase in serum free fatty acids (FFAs) and decrease in subcutaneous/peritoneal fat depots compared to non-tumor bearing control mice. Arctigenin intervention significantly reduced tumor growth by 45%, associated with decreased circulating FFAs and adipokines/cytokines including IGF-1, VEGF, and MCP-1, along with decreased AR, Ki67, and microvessel density and increased Nkx3.1 expression in tumors. These results indicate the strong ability of arctigenin to co-target obesity and tumor itself in inhibition of prostate tumor growth at a lower concentration compared to most phytochemicals.

背景与目标： ：这项研究在体外和体内研究了肥胖状态下前列腺素对新型抗炎木脂素arctigenin的抑制作用。通过将小鼠脂肪细胞3T3-L1与雄激素敏感性LNCaP人前列腺癌细胞共培养，或通过在脂肪细胞条件培养基中培养LNCaP细胞，可以建立体外肥胖模型。 Arctigenin显着抑制LNCaP增殖，同时降低雄激素受体（AR）和增加Nkx3.1细胞表达。将雄性重度联合免疫缺陷小鼠皮下植入人前列腺癌LAPC-4异种移植肿瘤，以进行体内研究。给小鼠饲喂高脂饮食，并以50μmg/ kg体重的口服剂量或媒介物对照口服给予Arctigenin，持续6周。与无肿瘤的对照小鼠相比，具有肿瘤的HF对照小鼠表现出血清游离脂肪酸（FFA）的显着增加和皮下/腹膜脂肪贮藏库的减少。 Arctigenin干预可将肿瘤生长显着降低45％，与循环中的FFA和包括IGF-1，VEGF和MCP-1在内的脂肪因子/细胞因子降低有关，同时AR，Ki67和微血管密度降低，Nkx3.1表达增加。这些结果表明，与大多数植物化学物质相比，arctigenin具有较强的共同抑制肥胖症和肿瘤本身的能力，能够以较低的浓度抑制前列腺肿瘤的生长。

BACKGROUND & AIMS: BACKGROUND:No studies have evaluated associations between patterns of diet-related practices as determined by latent class analysis (LCA) and gastro-esophageal reflux disease (GERD). We aimed to assess this relationship in a large sample of Iranian adults. METHODS:In a cross-sectional study in 4763 adults, diet-related practices were assessed in four domains, 'meal pattern', 'eating rate', 'intra-meal fluid intake', and 'meal-to-sleep interval', using a pretested questionnaire. LCA was applied to identify classes of diet-related practices. We defined GERD as the presence of heartburn sometimes, often or always. KEY RESULTS:The prevalence of GERD in the study population was 23.5% (n = 1120). We identified two distinct classes of meal patterns: 'regular' and 'irregular', three classes of eating rates: 'moderate', 'moderate-to-slow', and 'moderate-to-fast', two major classes of fluid ingestion with meals: 'moderate' and 'much intra-meal drinking', and two classes regarding the interval between meals and sleeping: 'short' and 'long meal-to-sleep' interval. After adjustment for potential confounders, subjects with 'irregular meal pattern' had higher odds of GERD compared with subjects with 'regular meal pattern' (OR: 1.21; 1.00-1.46). However, when taking into account BMI, the association disappeared. 'Long meal-to-sleep interval' was inversely associated with GERD compared with 'short meal-to-sleep interval' (OR: 0.73; 95% CI: 0.57-0.95). 'Eating rate' and 'intra-meal fluid intake' were not significantly associated with GERD. CONCLUSIONS & INFERENCES:Our data suggest certain associations between dietary patterns and GERD. These findings warrant evaluation in prospective studies to establish the potential value of modifications in dietary behaviors for the management of GERD.

背景与目标： 背景：尚无研究评估通过潜在类别分析（LCA）和胃食管反流病（GERD）所确定的饮食相关行为方式之间的关联。我们旨在评估大量伊朗成年人中的这种关系。
方法：在一项针对4763名成年人的横断面研究中，从四个方面对与饮食相关的行为进行了评估：“进餐方式”，“进食率”，“进餐内液体摄入量”和“进餐到睡眠间隔”，使用预先测试的问卷。 LCA用于确定饮食相关做法的类别。我们将GERD定义为有时，经常或始终存在胃灼热。
关键结果：研究人群中GERD的患病率为23.5％（n = 1120）。我们确定了两种不同的进餐方式：“常规”和“不规律”，三类进食速率：“中度”，“中度至慢速”和“中度至快速”，两种主要的液体摄入方式用餐：“适度”和“多餐内饮酒”，以及关于用餐和睡眠时间间隔的两类：“短”和“较长的进餐到睡眠”时间间隔。在对潜在混杂因素进行调整之后，与“常规进餐模式”的受试者相比，“常规进餐模式”的受试者的GERD几率更高（OR：1.21； 1.00-1.46）。但是，考虑到BMI，该关联消失了。与“进食间隔短”相比，“进食间隔长”与GERD成反比（OR：0.73； 95％CI：0.57-0.95）。 “进食率”和“餐内液体摄入量”与GERD无关。
结论与推论：我们的数据表明饮食模式与GERD之间存在某些关联。这些发现值得在前瞻性研究中进行评估，以建立饮食行为改变对GERD管理的潜在价值。

BACKGROUND & AIMS: BACKGROUND:The Mediterranean diet is one of the healthier diet models. Mediterranean food patterns are suffering a deterioration that can especially affect children and adolescents. OBJECTIVE:Determine adherence to the Mediterranean diet in adolescents of southern Spain and its relationship with the residence area, sex, age, life satisfaction, anthropometry, and habits of physical activity and sedentary activities. METHODOLOGY:A total of 1973 adolescents (11-18 years) of southern Spain participated in this descriptive cross-sectional study. Cut-off value between rural and urban locations was 10000 inhabitants. Adherence to the Mediterranean diet was calculated from the KIDMED questionnaire. Life satisfaction, physical activity, and sedentary activities also were measured through valid and reliable questionnaires. Body mass index and % body fat were measured using the TANITA BC-420-S body analyzer. RESULTS:30.9% of the adolescents reported an optimal quality diet, percent higher in rural locations (P < 0.05). Adherence was lower in older adolescents (P < 0.001), it was not different between sexes or according to anthropometric variables. Adolescents more satisfied with their lives (P < 0.001), more active (P < 0.001), more studious (P < 0.001), and less sedentary in front of a screen (P < 0.001) showed greater adherence to the Mediterranean food pattern. CONCLUSION:The majority of adolescents need to improve their nutritional quality. Compared with these subjects, the adolescents most adherent to the Mediterranean diet had a healthier lifestyle and they showed greater life satisfaction. :Introducción: La dieta mediterránea es uno de los modelos más saludables de dieta. Los patrones alimentarios mediterráneos están sufriendo un deterioro que puede afectar especialmente a niños y adolescentes. Objetivo: Determinar la adherencia a la dieta mediterránea de los adolescentes del sur de España y su relación con el área de residencia, sexo, edad, satisfacción con la vida, características antropométricas y hábitos de actividad física y sedentaria. Métodos: Un total de 1.973 adolescentes (11-18 años) del sur de España participaron en este estudio descriptivo transversal. El punto de corte entre poblaciones rurales y urbanas fue 10.000 habitantes. La adherencia a la dieta mediterránea fue calculada a partir del cuestionario KIDMED. Satisfacción con la vida, actividad física y sedentarismo también mediante cuestionarios fiables y válidos. Índice de masa corporal y % de grasa corporal fueron medidos utilizando el analizador corporal TANITA BC-420-S. Resultados: El 30,9% de los adolescentes reportó una dieta de calidad óptima, porcentaje superior en poblaciones rurales (P < 0,05). La adherencia fue menor en los adolescentes de mayor edad (P < 0,001), sin diferir entre sexos ni según las variables antropométricas. Los adolescentes más satisfechos con sus vidas (P < 0,001), más activos (P < 0,001), más estudiosos (P < 0,001) y menos sedentarios delante de una pantalla (P < 0,001) mostraron mayor adherencia al patrón alimentario mediterráneo. Conclusión: La mayoría de adolescentes necesitan mejorar su calidad nutricional. En comparación con estos sujetos, los más adheridos a la dieta mediterránea llevaban un estilo de vida más saludable y mostraron mayor satisfacción con sus vidas.

背景与目标： 背景：地中海饮食是较健康的饮食模式之一。地中海的食物类型正在恶化，尤其会影响儿童和青少年。
目的：确定西班牙南部青少年对地中海饮食的依从性及其与居住地区，性别，年龄，生活满意度，人体测量学以及体育锻炼和久坐活动习惯的关系。
方法：总共1973年西班牙南部的青少年（11-18岁）参加了该描述性横断面研究。城乡之间的临界值是10000居民。从KIDMED调查表计算出对地中海饮食的坚持。生活满意度，身体活动和久坐活动也通过有效且可靠的问卷进行了测量。使用TANITA BC-420-S人体分析仪测量体重指数和体脂百分比。
结果：30.9％的青少年报告了最佳质量饮食，在农村地区则更高（P <0.05）。年龄较大的青少年的依从性较低（P <0.001），这在男女之间或根据人体测量学变量无差异。青少年对生活的满意度更高（P <0.001），更加活跃（P <0.001），勤奋好学（P <0.001），屏幕前久坐不动（P <0.001）显示出对地中海食物模式的依从性更高。
结论：大多数青少年需要提高营养质量。与这些受试者相比，最喜欢地中海饮食的青少年的生活方式更健康，生活满意度更高。
：饮食简介：饮食中的营养品。洛杉矶特别行政区营养不良儿童和青少年基金会。对象：确定居住在西班牙，西班牙，西班牙，西班牙，西班牙，西班牙，西班牙，西班牙，西班牙，西班牙，西班牙，墨西哥，西班牙，西班牙，西班牙和西班牙的青少年。 Métodos：总共有1.973个青少年（11月18日至10月18日，西班牙人），横向学习是在España参加的。 El punto de corte entre poblaciones Rurales y urbanas fue 10.000 habitantes。死者复审和死刑复审。满足您的要求，请先确认您的行为，然后再执行中止诉讼。 TANDES BC-420-S的商标为masa下士和fueron medidos utilizando el analizador下士为下装。结果：30.9％的青少年青少年报告说，农村地区的上等饮食者（P <0.05）。埃德市市长青年队参议员（P <0,001），性变量。美国青少年洛杉矶（P <0,001），青少年活动（P <0,001），青少年工作室（P <0,001）和西班牙裔白人（P <0,001）多数都参加了会议。结论：青少年市长需要营养。在墨西哥的最保守的情况下，最有价值的市长和在维斯塔斯的最优秀的市长都应受到赞扬。

BACKGROUND & AIMS: OBJECTIVE:To examine the direction and magnitude of the relation between family meal frequency and dietary and family functioning outcomes in children (aged 2-18 years). DESIGN:Systematic literature review with meta-analysis. METHODS:Independent electronic searches, 1 for each outcome of interest, were conducted across 5 databases: PubMed, Cumulative Index to Nursing and Allied Health Literature, Web of Science, Scopus, and PsycINFO. Studies were included if they were peer-reviewed and published in English in the US through December 2018. MAIN OUTCOME MEASURES:Diet and family functioning. RESULTS:Dietary outcomes showed some evidence of a positive association between family meal frequency and fruits, vegetables, fruits and vegetables, sugar-sweetened beverages, and the Healthy Eating Index. There was less clear evidence of this relation in snacks, fast food, and desserts. A positive association was found between family meal frequency or dinner family meal frequency and family functioning outcomes. All studies included had cross-sectional and longitudinal study designs. CONCLUSIONS AND IMPLICATIONS:There is some evidence to show a positive relation between family meal frequency and dietary outcomes. There is stronger evidence for the relation with family functioning outcomes. Most articles included in the systematic reviews were excluded from meta-analysis owing to inadequate data and high methodological diversity across exposure and outcome variables.

背景与目标： 目的：探讨儿童（2-18岁）家庭进餐频率与饮食和家庭功能结局之间关系的方向和大小。
设计：系统的文献回顾与荟萃分析。
方法：在5个数据库中进行了独立的电子搜索，每个感兴趣的结果1项：PubMed，护理和相关健康文献的累积索引，Web of Science，Scopus和PsycINFO。如果研究在2018年12月之前在美国进行同行评审并以英文发表，则将其包括在内。
主要观察指标：饮食和家庭功能。
结果：饮食结果表明家庭进餐频率与水果，蔬菜，水果和蔬菜，加糖饮料和健康饮食指数之间呈正相关。零食，快餐和甜点中没有这种关系的明确证据。在家庭进餐频率或晚餐家庭进餐频率与家庭功能结局之间发现正相关。纳入的所有研究均具有横断面和纵向研究设计。
结论和意义：有一些证据表明家庭进餐频率与饮食结局之间呈正相关。有更充分的证据表明其与家庭功能结局之间的关系。由于资料不足以及暴露和结果变量之间的方法学差异很大，因此纳入系统评价的大多数文章都被排除在荟萃分析之外。

BACKGROUND & AIMS: :Although health benefits of the Dietary Approaches to Stop Hypertension (DASH) diet are established, it is not understood which food compounds result in these benefits. We used metabolomics to identify unique compounds from individual foods of a DASH-style diet and determined if these Food-Specific Compounds (FSC) are detectable in urine from participants in a DASH-style dietary study. We also examined relationships between urinary compounds and blood pressure (BP). Nineteen subjects were randomized into 6-week controlled DASH-style diet interventions. Mass spectrometry-based metabolomics was performed on 24-hour urine samples collected before and after each intervention and on 12 representative DASH-style foods. Between 66-969 compounds were catalogued as FSC; for example, 4-hydroxydiphenylamine was found to be unique to apple. Overall, 13-190 of these FSC were detected in urine, demonstrating that these unmetabolized food compounds can be discovered in urine using metabolomics. Although linear mixed effects models showed no FSC from the 12 profiled foods were significantly associated with BP, other endogenous and food-related compounds were associated with BP (N = 16) and changes in BP over time (N = 6). Overall, this proof of principle study demonstrates that metabolomics can be used to catalog FSC, which can be detected in participant urine following a dietary intervention.

背景与目标： ：尽管已经建立了饮食控制高血压（DASH）饮食的健康益处，但尚不清楚哪种食物化合物可带来这些益处。我们使用代谢组学方法从DASH式饮食的单个食物中识别出独特的化合物，并确定在DASH式饮食研究的参与者的尿液中是否可以检测到这些特定食物的化合物（FSC）。我们还检查了尿液化合物与血压（BP）之间的关系。 19名受试者被随机分为6周控制的DASH式饮食干预。基于质谱的代谢组学是在每次干预前后收集的24小时尿液样本和12种具有代表性的DASH型食物上进行的。 66-969种化合物被归类为FSC；例如，发现4-羟基二苯胺是苹果特有的。总体上，在尿液中检测到13-190种FSC，表明可以使用代谢组学在尿液中发现这些未代谢的食物化合物。尽管线性混合效应模型显示12种轮廓食品中没有FSC与BP显着相关，但其他内源性和食品相关化合物与BP相关（N = 16）和BP随时间的变化（N = 6）。总体而言，这项原理研究证明表明，代谢组学可用于对FSC进行分类，在饮食干预后参与者的尿液中可检测到FSC。

BACKGROUND & AIMS: :We recently found that the mRNA expression of Slc25a25, a Ca2+-sensitive ATP carrier in the inner mitochondrial membrane, fluctuates in a circadian manner in mouse skeletal muscle. We showed here that the circadian expression of muscle Slc25a25 was damped in Clock mutant, muscle-specific Bmal1-deficient, and global Bmal1-deficient mice. Furthermore, a ketogenic diet (KD) that induces time-of-day-dependent hypothermia (torpor), induced Slc25a25 mRNA expression in skeletal muscle. Hypothermia induced by KD did not affect thermogenic genes such as Sarcolipin and Pgc1a in muscles and Ucp1 in adipose tissues. Sciatic denervation abolished circadian and KD-induced Slc25a25 expression, suggesting that the circadian clock regulates muscle Slc25a25 expression via neural pathways. We measured body temperature (Tb) in sciatic denervated mice fed with KD to determine the functional role of KD-induced Slc25a25 expression. Sciatic denervation abolished Slc25a25 expression and augmented KD-induced hypothermia compared with sham-operated mice, but did not affect Tb in mice given a normal diet. These findings suggest that KD feeding induces expression of the muscle circadian gene Slc25a25 via neural pathways, and that SLC25A25 might be involved in muscle thermogenesis under KD-induced hypothermia in mammals.

背景与目标： ：我们最近发现，线粒体内膜上的Ca2敏感ATP载体Slc25a25的mRNA表达以昼夜节律的方式在小鼠骨骼肌中波动。我们在这里显示，在Clock突变体，肌肉特异性Bmal1缺陷和整体Bmal1缺陷小鼠中，肌肉Slc25a25的昼夜节律表达受到抑制。此外，生酮饮食（KD）诱导时间依赖性低温（torpor），诱导骨骼肌中Slc25a25 mRNA表达。 KD引起的体温过低不会影响热生成基因，例如肌肉中的Sarcolipin和Pgc1a以及脂肪组织中的Ucp1。坐骨神经去神经消除了昼夜节律和KD诱导的Slc25a25表达，表明昼夜节律时钟通过神经途径调节肌肉Slc25a25的表达。我们测量了喂养KD的坐骨神经失神经小鼠的体温（Tb），以确定KD诱导的Slc25a25表达的功能作用。与假手术小鼠相比，坐骨神经失神经消除了Slc25a25的表达，并增加了KD诱导的体温过低，但在正常饮食的小鼠中并未影响Tb。这些发现表明，KD喂养通过神经途径诱导了肌肉生物节律基因Slc25a25的表达，并且SLC25A25可能参与了KD诱导的体温过低引起的哺乳动物的肌肉生热。

BACKGROUND & AIMS: :An amendment to this paper has been published and can be accessed via a link at the top of the paper.

背景与目标： ：已经发布了对本文的修订，可以通过本文顶部的链接进行访问。

BACKGROUND & AIMS: :As an initial subdeficient status of zinc, considered as an essential antioxidant trace element, is frequent in burned patients, we aim to assess the effects of low zinc dietary intakes on burn-induced oxidative stress, in an animal model. After 8 weeks of conditioning diets containing 80 ppm (control group) or 10 ppm of zinc (depleted group), Wistar rats were 20% TBSA burned and sampled 1-10 days after injury. Kinetic evolutions of zinc status, plasma oxidative stress parameters, and antioxidant enzymes were also studied in blood and organs. The zinc-depleted diet induced, before injury, a significant decrease in zinc bone level and the increase of oxidative stress markers without stimulation of antioxidant enzyme activity. After burn, more markedly in zinc depleted animals than in controls, zinc levels decreased in plasma and bone, while increasing in liver. The decrease of thiol groups and GSH/GSSG ratio and the depression of GPx activity in liver are also moderately emphasized. Nevertheless, depleted zinc status could not be considered as determining for oxidative damages after burn injury. Further investigations must also be done to enlighten the mechanism of beneficial effects of zinc supplementation reported in burned patients.

背景与目标： ：由于烧伤患者经常缺锌，认为锌是人体必需的抗氧化剂微量元素，因此在动物模型中，我们旨在评估低锌饮食摄入对烧伤诱导的氧化应激的影响。经过8周的含有80 ppm（对照组）或10 ppm锌（贫化组）的饮食，Wistar大鼠被烧伤20％TBSA，并在受伤后1-10天取样。还研究了血液和器官中锌状态，血浆氧化应激参数和抗氧化酶的动力学演化。缺锌饮食在受伤前会导致锌骨水平显着下降和氧化应激标记物的增加，而不会刺激抗氧化酶的活性。烧伤后，缺锌动物中的锌含量明显高于对照组，血浆和骨骼中的锌含量下降，而肝脏中的锌含量上升。肝脏中硫醇基团和GSH / GSSG比值的降低以及GPx活性的降低也得到了适当的强调。然而，锌的贫化状态不能被认为是烧伤后氧化损伤的决定因素。还必须进行进一步的研究，以启发烧伤患者中锌补充的有益作用机理。

BACKGROUND & AIMS: :A low-protein (LP) diet induces injury from energy depletion in renal epithelial cells. Overexpression of heat-shock proteins has been implicated in the restoration of the cytoskeletal anchorage of Na(+)/K(+)-ATPase. We tested if Hsp70 stabilizes renal Na(+)/K(+)-ATPase attachment to the cytoskeleton from the cortex and the outer stripe of the outer medulla (OSOM) in rats during recovery from a LP diet. Rats were fed with a LP diet (8% protein) for 14 days, and then the rats were recovered with a 24% protein (RP) diet. The control group received a 24% protein (NP) diet. Increased Na(+)/K(+)-ATPase dissociation was demonstrated in soluble fraction from OSOM with lower ATP content as a result of LP diet vs NP. Meanwhile, decreased Hsp70 levels in the same fraction were shown. Translocation of Hsp70 to the cytoskeletal injured fraction associated with stabilization of Na(+)/K(+)-ATPase was shown in OSOM from LP after in vitro co-incubation of the cytoskeletal fraction of LP and non-cytoskeletal fraction of RP. These effects were abolished by the addition of the anti-Hsp70 antibody. Absence of Na(+)/K(+)-ATPase detachment from its cytoskeletal anchorage was demonstrated in proximal duct segments from cortex in LP. Co-immunoprecipitation showed that the amount of Na(+)/K(+)-ATPase co-precipitating with Hsp70 increased in the OSOM as a result of the LP diet. In the cortex tissues from rats fed the LP and the RP diet, the interaction of both proteins were similar to the control groups. Our results indicate that Hsp70 has a critical role in protecting the integrity of the cytoskeletal anchorage of Na(+)/K(+)-ATPase during recovery from ATP-depleted injury resulting from LP in OSOM.

背景与目标： ：低蛋白（LP）饮食会因肾上皮细胞能量消耗而引起伤害。热休克蛋白的过表达与Na（）/ K（）-ATPase的细胞骨架锚定的恢复有关。我们测试了在从LP饮食中恢复过程中，Hsp70是否能稳定大鼠皮质和外延髓外条纹（OSOM）的肾Na（）/ K（）-ATPase与细胞骨架的附着。用低脂饮食（8％蛋白质）喂养大鼠14天，然后用24％蛋白质（RP）饮食恢复大鼠。对照组接受24％蛋白质（NP）饮食。由于LP日粮与NP日粮相比，在OSOM的可溶级分中具有较低的ATP含量，Na（）/ K（）-ATPase解离增加。同时，显示出相同分数的Hsp70水平降低。 Hsp70易位到与Na（）/ K（）-ATPase稳定相关的细胞骨架损伤部分，在LP的细胞骨架部分和RP的非细胞骨架部分体外共孵育后的OSOM中显示。通过加入抗Hsp70抗体消除了这些作用。缺乏Na（）/ K（）-ATPase脱离其细胞骨架锚固在LP皮质近端导管节段中。免疫共沉淀显示，LP饮食可导致OSOM中与Hsp70共沉淀的Na（）/ K（）-ATPase量增加。在饲喂LP和RP日粮的大鼠皮层组织中，两种蛋白质的相互作用与对照组相似。我们的结果表明，Hsp70在保护由OSOM中的LP引起的ATP耗尽损伤的恢复过程中，对保护Na（）/ K（）-ATPase的细胞骨架锚定的完整性具有至关重要的作用。

BACKGROUND & AIMS: :Heart diseases are a leading cause of death. While the link between early exposure to nutritional excess and heart disease risk is clear, the molecular mechanisms involved are poorly understood. In the developmental programming field, increasing evidence is pointing out the critical role of epigenetic mechanisms. Among them, polycomb repressive complex 2 (PRC2) and DNA methylation play a critical role in heart development and pathogenesis. In this context, we aimed at evaluating the role of these epigenetic marks in the long-term cardiac alterations induced by early dietary challenge. Using a model of rats exposed to maternal high-fat diet during gestation and lactation, we evaluated cardiac alterations at adulthood. Expression levels of PRC2 components, its histone marks di- and trimethylated histone H3 (H3K27me2/3), associated histone mark (ubiquitinated histone H2A, H2AK119ub1) and target genes were measured by Western blot. Global DNA methylation level and DNA methyl transferase 3B (DNMT3B) protein levels were measured. Maternal high-fat diet decreased H3K27me3, H2Ak119ub1 and DNA methylation levels, down-regulated the enhancer of zeste homolog 2 (EZH2), and DNMT3B expression. The levels of the target genes, isl lim homeobox 1 (Isl1), six homeobox 1 (Six1) and mads box transcription enhancer factor 2, polypeptide C (Mef2c), involved in cardiac pathogenesis were up regulated. Overall, our data suggest that the programming of cardiac alterations by maternal exposure to high-fat diet involves the derepression of pro-fibrotic and pro-hypertrophic genes through the induction of EZH2 and DNMT3B deficiency.

背景与目标： ：心脏病是导致死亡的主要原因。尽管尽早摄入营养过剩与心脏病风险之间的联系是明确的，但所涉及的分子机制却鲜为人知。在开发程序设计领域，越来越多的证据指出了表观遗传机制的关键作用。其中，多梳抑制复合物2（PRC2）和DNA甲基化在心脏发育和发病机理中起着至关重要的作用。在这种情况下，我们旨在评估这些表观遗传标记在早期饮食挑战引起的长期心脏改变中的作用。使用在妊娠和哺乳期间暴露于母体高脂饮食的大鼠模型，我们评估了成年期的心脏改变。通过蛋白质印迹法测量PRC2组分，其组蛋白标记二甲基和三甲基化组蛋白H3（H3K27me2 / 3），相关组蛋白标记（遍在蛋白化的组蛋白H2A，H2AK119ub1）和靶基因的表达水平。测量了总体DNA甲基化水平和DNA甲基转移酶3B（DNMT3B）蛋白质水平。孕妇高脂饮食降低了H3K27me3，H2Ak119ub1和DNA甲基化水平，下调了zeste同源2（EZH2）和DNMT3B表达的增强子。参与心脏发病的靶基因isl lim homeobox 1（Isl1），六个homeobox 1（Six1）和mads box转录增强因子2多肽C（Mef2c）的水平上调。总体而言，我们的数据表明，通过孕妇暴露于高脂饮食来进行心脏改变的程序涉及通过诱导EZH2和DNMT3B缺乏来抑制促纤维化和促肥大基因。