Associations between vitamin D status in infants and blood lipids, body mass index and waist circumference.

AIM: To study the relationships between 25-hydroxyvitamin D status and blood lipids, insulin, glucose, body mass index and waist circumference in infants. METHODS: In a cross-sectional study, 255 infants aged 9 months with a blood sample for 25-hydroxyvitamin D were examined. Plasma 25-hydroxyvitamin D concentrations were analysed by chemiluminescent immunoassay. Associations between plasma 25-hydroxyvitamin D and high-density lipoprotein (HDL), low-density lipoprotein, total cholesterol, triglycerides, insulin, glucose, body mass index and waist circumference were analysed. RESULTS: Mean plasma 25-hydroxyvitamin D was 77.2 ± 22.7 nM. At the time of examination, 97% received vitamin D supplementation. 25-Hydroxyvitamin D was negatively associated with HDL (p = 0.003), cholesterol (p = 0.002) and triglycerides (p = 0.010) in multivariate analysis controlled for gender, season, body mass index, length, birth weight and breastfeeding. There were no associations between 25-hydroxyvitamin D and glucose or insulin (all p > 0.05). 25-hydroxyvitamin D was negatively associated with body mass index (p = 0.005) and waist circumference (p = 0.002) controlled for gender, season, breastfeeding, birth weight and length. CONCLUSION: Vitamin D status is negatively associated with blood lipids, body mass index and waist circumference in infants where nearly all received vitamin D supplements. Whether this has long-term health effects remains to be elucidated.

Vitamin D status in infants: relation to nutrition and season.

In a cross-sectional study, the primary objective was to assess the plasma concentration of 25-hydroxyvitamin D (25(OH)D) in healthy 9-month-old infants (n=255). The secondary objective was to evaluate nutritional variables and season in relation to 25(OH)D. The concentration of 25(OH)D was 77.2 ± 22.7 nmol/l (mean ± s.d.), ranging from 12 to 151 nmol/l. During the first 9 months, 97% received vitamin D supplementation (10 µg/day) and 89% had sufficient levels of 25(OH)D (50-250 nmol/l). In multiple regression analysis, controlled for body mass index (BMI) and intake of infant formula, a longer period of exclusive breastfeeding (P=0.026) and breastfeeding at 9 months (P=0.001) were both associated with lower levels. Dietary vitamin D intake was 4.4 ± 3.1 µg/day and in multiple regression analysis, controlled for BMI, intake of infant formula and mean energy intake, it was positively associated with 25(OH)D (P=0.001). There was a significant seasonal difference in 25(OH)D, with higher levels during summer-autumn compared with winter-spring (P=0.021) after control for BMI.

RFamide-related peptides signal through the neuropeptide FF receptor and regulate pain-related responses in the rat.

The mammalian RFamide-related peptide RFRP1 was found to signal through the neuropeptide FF 2 receptor expressed in Xenopus oocytes. The peptide induced a dose-dependent outward current, which was dependent on the simultaneous expression of GIRK1 and GIRK4 potassium channels. In neuropathic rats, RFRP1 administered intrathecally induced tactile antiallodynia and thermal antinociception, whereas in the solitary tract nucleus it produced only mechanical antihyperalgesia. Expression of the RFamide-related peptide mRNA in the rat CNS was distinctly different from that of neuropeptide FF. Most notably, the gene was not expressed in the hindbrain or spinal cord at detectable levels. However, there was a prominent group of RFamide-related peptide mRNA-expressing neurons in the central hypothalamus, in the area in and between the dorsomedial and ventromedial nuclei. The results suggest that RFamide-related peptides are potentially involved in pain regulation through a hypothalamo-medullary projection system, and possibly via action on neuropeptide FF 2 receptors. In neuropathic animals, the pain suppressive effect of RFamide-related peptide varies depending on the submodality of noxious test stimulation and the site of RFamide-related peptide administration.