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首页> 外文期刊>Nutrition Metabolism >Effects of high fat diet-induced obesity on vitamin D metabolism and tissue distribution in vitamin D deficient or supplemented mice
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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

机译: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

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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 Mttp, Cd36, Sr-b1, Npc1l1, and Abca1 and liver and adipose tissue 25-hydroxylases (Cyp2r1 and Cyp27a1) 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 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. 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.
机译:维生素D缺乏缺乏在肥胖的人中经常观察到。由于在脂肪组织中螯合,因此在肥胖症中肥胖的低维生素D状态的一种机制是降低了维生素D(VD)的生物利用度。然而,只有很少的研究通过量化来自肥胖组织的维生素D水平来研究这种机制。含有50,000或25,000℃的10或45%KCAL脂肪(CON或HFD)饮食,含有50%,1000或25,000℃的饮食(LVD,CVD或HVD),为13周,含有50%或45%的KCAL脂肪(CON或HFD)。通过放射免疫测定和肝脏和脂肪组织胆碱(VD3)和25-羟基丙酮(25(OH)D3)水平测定血清25-羟基羟乙二醇蛋白D(25(OH)D)水平。通过LC-MS / MS测量水平。通过实时PCR测定Jejunal MTTP,CD36,SR-B1,NPC1L1和ABCA1和肝脏和脂肪组织25-羟基酶(CYP2R1和CYP27A1)的mRNA水平。血清25(OH)D水平受膳食维生素D含量的影响,但在HFD和CON组之间观察到差异效应。当维生素D摄入量在补充水平时,HFD-HVD组具有比CON-HVD组更低的血清25(OH)D水平,而HFD和CON组在喂养LVD或CVD之间没有显着差异。与CON-HVD组相比,HFD-HVD组肝脏和脂肪组织中的VD3总量显着高。然而,在CON和HFD组之间观察到CVD的CON和HFD组之间没有观察到组织VD3的总量差异。在Jejunum,HFD组MTTP和ABCA1的mRNA水平比CON组显着高。通过膳食脂肪量和维生素D含量,肝25-羟基酶mRNA水平没有差异。当膳食维生素D处于补充水平时,大量VD3似乎储存在肝脏和脂肪组织中;因此,当补充维生素D时,过量的体脂可能有助于相对低的血清25(OH)D水平。

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