Vitamin D status as measured by plasma 25-hydroxyvitamin D (25(OH)D) is important to human health. Circumpolar people rely on dietary sources and societal changes in the Arctic are having profound dietary effects. The objective of the present study was to determine plasma 25(OH)D status and factors important to plasma 25(OH)D in populations in Greenland. Inuit and non-Inuit aged 50–69 years in the capital in West Greenland (latitude 64°15′N) and in a major town and remote settlements in East Greenland (latitude 65°35′N) were surveyed. Supplement use and lifestyle factors were determined by questionnaires. Inuit food scores were computed from a FFQ of seven traditional Inuit and seven imported food items. 25(OH)D2 and 25(OH)D3 levels were measured in the plasma. We invited 1 % of the population of Greenland, and 95 % participated. 25(OH)D3 contributed 99·7 % of total plasma 25(OH)D. Non-Inuit had the lowest median plasma 25(OH)D of 41 (25th–75th percentile 23–53) nmol/l compared with 64 (25th–75th percentile 51–81) nmol/l in Inuit (P< 0·001). Plasma 25(OH)D was below 20 and 50 nmol/l in 13·8 and 60·1 % of participants, respectively, with Inuit food item scores below 40 % (P< 0·001), and in 0·2 and 25·0 % of participants, respectively, with higher scores (P< 0·001). The Inuit diet was an important determinant of plasma 25(OH)D (P< 0·001) and its effect was modified by ethnicity (P= 0·005). Seal (P= 0·005) and whale (P= 0·015) were major contributors to plasma 25(OH)D. In conclusion, a decrease in the intake of the traditional Inuit diet was associated with a decrease in plasma 25(OH)D levels, which may be influenced by ethnicity. The risk of plasma 25(OH)D deficiency in Arctic populations rises with the dietary transition of societies in Greenland. Vitamin D intake and plasma 25(OH)D status should be monitored.

We investigated the effect of oral high-dose cholecalciferol on plasma and adipose tissue cholecalciferol and its subsequent release, and on plasma 25-hydroxyvitamin D (25(OH)D). Female Wistar rats (n 126) received 37·5 μg cholecalciferol/d for 14 d and were subsequently studied for a further 88 d. Two subgroups of eighteen rats each were fasted for 3 d immediately after treatment (days 14−17) and at the end of the study (days 98−101). During treatment, plasma cholecalciferol increased rapidly to reach a steady-state. Plasma 25(OH)D and adipose tissue cholecalciferol increased linearly for 1 - 2 d after treatment. Serum Ca and inorganic phosphate also increased. Subsequently half-lives of plasma cholecalciferol and 25(OH)D, and perirenal and subcutaneous adipose tissue were: 1·4, 22·5, 97·5 and 80·9 d respectively. Fasting, as compared with ad libitum feeding, caused increased plasma free fatty acids, weight loss up to 14% and increased adipose tissue cholecalciferol (nmol/g wet weight). It did not affect plasma cholecalciferol immediately after cholecalciferol treatment, but raised plasma 25(OH)D. Fasting at the end of the study decreased plasma cholecalciferol and increased plasma 25(OH)D. We conclude that orally-administered cholecalciferol rapidly accumulates in adipose tissue and that it is very slowly released while there is energy balance. Fasting causes preferential loss of triacylglycerols from adipose tissue, as opposed to cholecalciferol, but nevertheless augments plasma 25(OH)D. Adipose tissue may act as a ‘buffer to functional vitamin D status’ by preventing, to a certain extent, unregulated production of 25(OH)D from dietary vitamin D, and by slowly releasing vitamin D under fasting conditions.