Abstract
BackgroundVitamin 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.MethodsSix-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.ResultsSerum 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.ConclusionA 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.
Highlights
Vitamin D deficiency has been often observed in obese persons
When vitamin D (VD) intake was at a supplementary level, high-fat diet-induced obesity resulted in a greater amount of VD3 storage in liver and epididymal adipose tissue compared with the non-obese control, and this could contribute to low serum 25(OH)D levels
At supplementary level of VD intake, high fat dietinduced obesity resulted in lower serum 25(OH)D levels than the lean control
Summary
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. It has been reported that the prevalence of VD deficiency was 35% higher in obese persons and 24% higher in overweight persons compared with non-obese persons [7] Several mechanisms such as low ultraviolet B (UVB) exposure of obese people and VD sequestration or dilution into adipose tissue have been proposed for the higher prevalence of VD deficiency among the obese, the causes of their low 25(OH)D levels are still inconclusive. VD sequestration or volumetric dilution might explain the VD deficiency observed in the obese, few studies have directly demonstrated these hypotheses by quantifying VD levels in adipose tissue and comparing VD levels between obese and non-obese subjects due to the difficulty in measuring fat-soluble VD from small quantities of fat tissue [11,12,13]. Environmentally controllable animal studies are needed to provide evidence for how obesity affects the storage of VD in soft tissues and VD metabolism
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