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Effects of high fat diet-induced obesity on vitamin D metabolism and tissue distribution in vitamin D deficient or supplemented mice.

高脂饮食诱导肥胖对维生素d 缺乏或补充小鼠维生素d 代谢和组织分布的影响。

  • 影响因子:3.69
  • DOI:10.1186/s12986-020-00463-x
  • 作者列表:"Park CY","Shin Y","Kim JH","Zhu S","Jung YS","Han SN
  • 发表时间:2020-06-15
Abstract

Background:Vitamin D deficiency has been often observed in obese persons. One of the mechanisms suggested for low vitamin D status in obesity was decreased bioavailability of vitamin D (VD) due to sequestration in adipose tissue. However, only few studies have investigated this mechanism via quantifying vitamin D levels from tissues from the obese. Methods:Six-wk-old C57BL/6 mice were fed 10 or 45% kcal fat (CON or HFD) diets containing 50, 1000 or 25,000 IU vitamin D3/kg diet (LVd, CVd or HVd) for 13 wks. Serum 25-hydroxyvitamin D (25(OH)D) levels were determined by radioimmunoassay and liver and adipose tissue cholecalciferol (VD3) and 25-hydrocholecalciferol (25(OH)D3) levels were measured by LC-MS/MS. mRNA levels of jejunal Mttp, Cd36, Sr-b1, Npc1l1, and Abca1 and liver and adipose tissue 25-hydroxylases (Cyp2r1 and Cyp27a1) were determined by real-time PCR. Results:Serum 25(OH)D levels were affected by dietary vitamin D content but differential effects were observed between HFD and CON groups. When vitamin D intake was at a supplementary level, the HFD-HVd group had lower serum 25(OH)D levels than the CON-HVd group, while there was no significant difference between the HFD and CON groups fed LVd or CVd. Total amount of VD3 in liver and adipose tissue were significantly higher in HFD-HVd group compared with the CON-HVd group. However, no difference in total amount of tissue VD3 was observed between the CON and HFD groups fed CVd. In jejunum, mRNA levels of Mttp and Abca1 were significantly higher in HFD groups than CON groups. There was no difference in mRNA levels of liver 25-hydroxylases by both dietary fat amount and vitamin D content. Conclusion:A significant amount of VD3 seemed to be stored in the liver and adipose tissue when dietary vitamin D is at a supplementation level; thus excess body adiposity could contribute to relatively low serum 25(OH)D level when vitamin D was supplemented.

摘要

背景: 在肥胖者中经常观察到维生素d 缺乏。肥胖低维生素d 状态的机制之一是由于脂肪组织中的滞留导致维生素d (VD) 的生物利用度降低。然而,只有很少的研究通过量化来自肥胖组织的维生素d 水平来研究这一机制。 方法: 采用六周大的 C57BL/6 小鼠灌胃 10 或 45% 大卡脂肪 (CON 或 HFD) 基础饲粮中添加 50 、 1000 或 25,000  IU 维生素 D3/kg 日粮 (LVd, CVd 或 HVd) 13 周。用放射免疫法测定血清 25-羟基维生素d (25(OH)D) 水平以及肝脏和脂肪组织胆钙化醇 (VD3) 和 25-氢胆钙化醇 (25(OH)D3) 通过 LC-MS/MS 测量水平。通过 real-time PCR 测定空肠 Mttp 、 Cd36 、 Sr-b1 、 Npc1l1 和 Abca1 以及肝脏和脂肪组织 25-羟化酶 (Cyp2r1 和 Cyp27a1) 的 mRNA 水平。 结果: 血清 25(OH)D 水平受膳食维生素d 含量的影响,但 HFD 组和 CON 组之间存在差异效应。当维生素d 摄入处于补充水平时,HFD-HVd 组血清 25(OH)D 水平低于 CON-HVd 组,而 HFD 组和 CON 组喂养 LVd 或 CVd 之间无显著差异。HFD-HVd 组肝脏和脂肪组织中 VD3 的总量明显高于 CON-HVd 组。然而,在喂食 CVd 的 CON 和 HFD 组之间未观察到组织 VD3 总量的差异。在空肠,Mttp 和 Abca1 的 mRNA 水平在 HFD 组明显高于 CON 组。无论是膳食脂肪量还是维生素 D 含量,肝脏 25-羟化酶的 mRNA 水平均无差异。 结论: 当膳食维生素d 处于补充水平时,肝脏和脂肪组织中似乎储存了大量的 VD3; 因此,当补充维生素d 时,过量的身体肥胖可能导致血清 25(OH)D 水平相对较低。

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发表时间:2020-01-24
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DOI:10.3390/nu12010090
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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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