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Interaction of Osteoarthritis and BMI on Leptin Promoter Methylation in Taiwanese Adults

骨关节炎和 BMI 对台湾成人瘦素启动子甲基化的交互作用

  • 影响因子:4.32
  • DOI:10.3390/ijms21010123
  • 作者列表:"Tzi-Peng Yang","Hsiao-Mei Chen","Chao-Chin Hu","Li-Yuan Chen","Fen-Fen Shih","Disline Manli Tantoh","Kuan-Jung Lee","Yi-Chia Liaw","Rong-Tzong Tsai","Yung-Po Liaw
  • 发表时间:2020-01-24
Abstract

Leptin (LEP) regulates glucose metabolism and energy storage in the body. Osteoarthritis (OA) is associated with the upregulation of serum LEP. LEP promoter methylation is associated with obesity. So far, few studies have explored the association of BMI and OA with LEP methylation. We assessed the interaction between body mass index (BMI) and OA on LEP promoter methylation. Data of 1114 participants comprising 583 men and 558 women, aged 30−70 years were retrieved from the Taiwan Biobank Database (2008−2015). Osteoarthritis was self-reported and cases were those who reported having ever been clinically diagnosed with osteoarthritis. BMI was categorized into underweight, normal weight, overweight, and obesity. The mean LEP promoter methylation level in individuals with osteoarthritis was 0.5509 ± 0.00437 and 0.5375 ± 0.00101 in those without osteoarthritis. The interaction between osteoarthritis and BMI on LEP promoter methylation was significant (p-value = 0.0180). With normal BMI as the reference, the mean LEP promoter methylation level was significantly higher in obese osteoarthritic individuals (β = 0.03696, p-value = 0.0187). However, there was no significant association between BMI and LEP promoter methylation in individuals without osteoarthritis, regardless of BMI. In conclusion, only obesity was significantly associated with LEP promoter methylation (higher levels) specifically in osteoarthritic patients.

摘要

瘦素 (LEP) 调节体内葡萄糖代谢和能量储存。骨关节炎 (OA) 与血清 LEP 的上调有关。LEP 启动子甲基化与肥胖相关。迄今为止,很少有研究探讨 BMI 和 OA 与 LEP 甲基化的相关性。我们评估了体重指数 (BMI) 和 OA 对 LEP 启动子甲基化的相互作用。从台湾生物样本库数据库 (1114 & #583; 558) 中检索到 8722 例参与者的数据,包括 2008 例男性和 8722 例女性,年龄 30 & #2015; 70 岁。骨关节炎是自我报告的,病例是那些报告曾被临床诊断为骨关节炎的病例。BMI 分为低体重、正常体重、超重和肥胖。骨关节炎个体的平均 LEP 启动子甲基化水平为 0.5509 & #177; 0.00437,无骨关节炎个体为 0.5375 & #177; 0.00101。骨关节炎和 BMI 对 LEP 启动子甲基化的交互作用显著 (p 值 = 0.0180)。以正常 BMI 为参考,肥胖骨关节炎个体的平均 LEP 启动子甲基化水平显著增高 ( 946; = 0.03696,p 值 = 0.0187)。然而,无论 BMI 如何,在无骨关节炎的个体中,BMI 和 LEP 启动子甲基化之间没有显著相关性。总之,在骨关节炎患者中,只有肥胖与 LEP 启动子甲基化 (较高水平) 显著相关。

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相关文献
影响因子:4.51
发表时间:2020-01-24
来源期刊:Nutrients
DOI:10.3390/nu12010090
作者列表:["Stephen Morehen","Benoit Smeuninx","Molly Perkins","Paul Morgan","Leigh Breen"]

METHODS:Maintaining adequate daily protein intake is important to maintain muscle mass throughout the lifespan. In this regard, the overnight period has been identified as a window of opportunity to increase protein intake in the elderly. However, it is unknown whether pre-sleep protein intake affects next-morning appetite and, consequently, protein intake. Therefore, the purpose of the current study was to investigate the effects of a pre-sleep protein drink on next-morning appetite, energy intake and metabolism. Twelve older individuals (eight males, four females; age: 71.3 ± 4.2 years) took part in a single-blind randomised cross-over study. After a standardised dinner, participants consumed either a 40-g protein drink, isocaloric maltodextrin drink, or placebo water control before bedtime. Next-morning appetite, energy intake, resting metabolic rate (RMR), respiratory exchange rate (RER), and plasma acylated ghrelin, leptin, glucose, and insulin concentrations were assessed. No between-group differences were observed for appetite and energy intake at breakfast. Furthermore, RMR, RER, and assessed blood markers were not significantly different between any of the treatment groups. Pre-sleep protein intake does not affect next-morning appetite and energy intake and is therefore a viable strategy to increase daily protein intake in an older population.

翻译标题与摘要 下载文献
影响因子:4.32
发表时间:2020-01-24
DOI:10.3390/ijms21010123
作者列表:["Tzi-Peng Yang","Hsiao-Mei Chen","Chao-Chin Hu","Li-Yuan Chen","Fen-Fen Shih","Disline Manli Tantoh","Kuan-Jung Lee","Yi-Chia Liaw","Rong-Tzong Tsai","Yung-Po Liaw"]

METHODS:Leptin (LEP) regulates glucose metabolism and energy storage in the body. Osteoarthritis (OA) is associated with the upregulation of serum LEP. LEP promoter methylation is associated with obesity. So far, few studies have explored the association of BMI and OA with LEP methylation. We assessed the interaction between body mass index (BMI) and OA on LEP promoter methylation. Data of 1114 participants comprising 583 men and 558 women, aged 30−70 years were retrieved from the Taiwan Biobank Database (2008−2015). Osteoarthritis was self-reported and cases were those who reported having ever been clinically diagnosed with osteoarthritis. BMI was categorized into underweight, normal weight, overweight, and obesity. The mean LEP promoter methylation level in individuals with osteoarthritis was 0.5509 ± 0.00437 and 0.5375 ± 0.00101 in those without osteoarthritis. The interaction between osteoarthritis and BMI on LEP promoter methylation was significant (p-value = 0.0180). With normal BMI as the reference, the mean LEP promoter methylation level was significantly higher in obese osteoarthritic individuals (β = 0.03696, p-value = 0.0187). However, there was no significant association between BMI and LEP promoter methylation in individuals without osteoarthritis, regardless of BMI. In conclusion, only obesity was significantly associated with LEP promoter methylation (higher levels) specifically in osteoarthritic patients.

翻译标题与摘要 下载文献
影响因子:4.82
发表时间:2020-01-01
DOI:10.1038/s41366-019-0368-2
作者列表:["Wulan, Siti N.","Schrauwen-Hinderling, Vera B.","Westerterp, Klaas R.","Plasqui, Guy"]

METHODS:Background For the same BMI, South Asians have a higher body fat percentage, a higher liver fat content and a more adverse metabolic profile than whites. South Asians may have a lower fat oxidation than whites, which could result in an unfavorable metabolic profile when exposed to increased high-fat foods consumption and decreased physical activity as in current modern lifestyle. Objective To determine substrate partitioning, liver fat accumulation and metabolic profile in South Asian and white men in response to overfeeding with high-fat diet under sedentary conditions in a respiration chamber. Design Ten South Asian men (BMI, 18–29 kg/m^2) and 10 white men (BMI, 22–33 kg/m^2), matched for body fat percentage, aged 20–40 year were included. A weight maintenance diet (30% fat, 55% carbohydrate, and 15% protein) was given for 3 days. Thereafter, a baseline measurement of liver fat content (1H-MRS) and blood parameters was performed. Subsequently, subjects were overfed (150% energy requirement) with a high-fat diet (60% fat, 25% carbohydrate, and 15% protein) over 3 consecutive days while staying in a respiration chamber mimicking a sedentary lifestyle. Energy expenditure and substrate use were measured for 3 × 24-h. Liver fat and blood parameters were measured again after the subjects left the chamber. Results The 24-h fat oxidation as a percentage of total energy expenditure did not differ between ethnicities ( P  = 0.30). Overfeeding increased liver fat content ( P  = 0.02), but the increase did not differ between ethnicities ( P  = 0.64). In South Asians, overfeeding tended to increase LDL-cholesterol ( P  = 0.08), tended to decrease glucose clearance ( P  = 0.06) and tended to elevate insulin response ( P  = 0.07) slightly more than whites. Conclusions Despite a similar substrate partitioning and similar accretion of liver fat, overfeeding with high-fat under sedentary conditions tended to have more adverse effects on the lipid profile and insulin sensitivity in South Asians.

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