Park Chan Yoon, Shin Yongho, Kim Jeong-Han, Zhu Shuang, Jung Young Sun, Han Sung Nim
Department of Food and Nutrition, College of Human Ecology, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, South Korea.
Department of Agricultural Biotechnology, College of Agriculture and Life Science, Seoul National University, Seoul, South Korea.
Nutr Metab (Lond). 2020 Jun 15;17:44. doi: 10.1186/s12986-020-00463-x. eCollection 2020.
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.
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 , and and liver and adipose tissue 25-hydroxylases ( and ) were determined by real-time PCR.
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 and 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.
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.
肥胖人群中经常观察到维生素D缺乏。肥胖者维生素D水平低的一种推测机制是维生素D（VD）在脂肪组织中被隔离，导致其生物利用度降低。然而，只有少数研究通过量化肥胖者组织中的维生素D水平来研究这一机制。
六周龄的C57BL/6小鼠分别喂食含50、1000或25000IU维生素D3/kg饮食的10%或45%千卡脂肪（对照或高脂饮食）饮食，持续13周。通过放射免疫测定法测定血清25-羟基维生素D（25(OH)D）水平，通过液相色谱-串联质谱法测量肝脏和脂肪组织中的胆钙化醇（VD3）和25-羟基胆钙化醇（25(OH)D3）水平。通过实时聚合酶链反应测定空肠、肝脏和脂肪组织中25-羟化酶（CYP2R1和CYP27A1）的mRNA水平。
血清25(OH)D水平受饮食中维生素D含量的影响，但在高脂饮食和对照组之间观察到不同的影响。当维生素D摄入量处于补充水平时，高脂饮食-高剂量维生素D组的血清25(OH)D水平低于对照-高剂量维生素D组，而喂食低剂量或中剂量维生素D的高脂饮食组和对照组之间没有显著差异。与对照-高剂量维生素D组相比，高脂饮食-高剂量维生素D组肝脏和脂肪组织中VD3的总量显著更高。然而，喂食中剂量维生素D的高脂饮食组和对照组之间在组织VD3总量上没有差异。在空肠中，高脂饮食组中CYP2R1和CYP27A1的mRNA水平显著高于对照组。饮食中脂肪量和维生素D含量对肝脏25-羟化酶的mRNA水平均无差异。
当饮食中的维生素D处于补充水平时，大量的VD3似乎储存在肝脏和脂肪组织中；因此，当补充维生素D时，过多的身体脂肪可能导致血清25(OH)D水平相对较低。
