Vitamin D status and insulin sensitivity are novel predictors of resting metabolic rate: a cross-sectional analysis in Australian adults.

PURPOSE: Resting metabolic rate (RMR) accounts for two-thirds of the total energy expenditure in sedentary individuals. After accounting for traditional factors, there still remains a considerable unexplained variance in RMR. There is a pandemic of obesity and metabolic syndrome (MetS) which coexists with a high prevalence of vitamin D insufficiency. The aim of this study was to evaluate the potential effects of vitamin D status, insulin sensitivity (IS) and the metabolic syndrome (MetS) on RMR in Australian adults. METHODS: RMR, respiratory quotient (RQ), McAuley's insulin sensitivity index, fat mass (FM), fat-free mass (FFM) and vitamin D status were assessed in Australian adults. The presence of MetS was evaluated by current standard criteria. Predictors of RMR were examined through multiple linear regression based on stepwise and backward regression approaches with attention to multi-collinearity. All analyses were conducted on SPSS version 21. RESULTS: One hundred and twenty-seven participants (45 men, 82 women), aged 53.4 ± 11.7 years and BMI 31.9 ± 5.2 kg/m(2), were included. Forty-one subjects were insufficient in vitamin D status (<50 nmol/L), and 75 participants had the MetS. A parsimonious regression model explained 85.8 % of RMR and was given by: RMR (kJ/d) = 1931 + 83.5 × FFM (kg) + 29.5 × FM (kg) + 5.65 × 25(OH)D (nmol/L) - 17.6 × age (years) - 57.51 × IS. CONCLUSION: Vitamin D status and IS are novel independent predictors of RMR in adults. Future studies could validate a causal role for these factors in human energy metabolism.

Mechanistic roles for calcium and vitamin D in the regulation of body weight.

Low intakes of calcium and inadequate vitamin D status often cluster with higher prevalence rates of obesity. Consequently, there has been much interest in the mechanisms by which calcium and vitamin D could regulate body weight and adiposity. This review has focused on randomized controlled trials (RCTs) that have manipulated these nutrients and studied pathways of energy balance. Overall, there is consistent evidence that calcium and vitamin D increase whole body fat oxidation after single and multiple meals, and that calcium promotes a modest energy loss through increased faecal fat excretion. The evidence is equivocal for a greater diet-induced thermogenesis, increased lipolysis, suppression of key lipogenic enzymes, decreased hunger ratings or reduced energy/macronutrient intake. Emerging evidence suggests a potential improvement in insulin sensitivity following vitamin D that would impinge on food intake and substrate oxidation. However, the very few RCTs on supplemental vitamin D and energy balance have not explored postprandial avenues of the hormone's actions. Future efforts in this area need to define the threshold intake of these nutrients that would maximize metabolic and gastrointestinal outcomes. Such studies would provide a platform for endorsing the non-skeletal role of calcium and vitamin D in human pathophysiology.

Calcium and vitamin D for obesity: a review of randomized controlled trials.

Obesity often coexists with low calcium intake and vitamin D insufficiency. There is emerging evidence of a role for these nutrients in the regulation of body weight. However, it is unclear whether increasing intakes of calcium and/or vitamin D during energy restriction, is a better strategy for weight and fat loss. We searched the literature from 2000 to date for randomized controlled trials (RCTs) on weight loss that had increased calcium or vitamin D per se, or in combination. Primary and secondary studies were included for this analysis. A total of 15 RCTs on calcium with or without vitamin D and seven on vitamin D alone met our criteria. Two studies reported that supplemental calcium significantly increased fat loss during caloric restriction by 1.8 and 2.2 kg, three found differences between 1 and 3.5 kg but were statistically nonsignificant, while nine trials were equivocal (±0.7 kg). The data on vitamin D supplementation during weight loss were too few to make firm conclusions. Current evidence from RCTs did not consistently support the contention that calcium and vitamin D accelerated weight or fat loss in obesity. There were studies that favoured the hypothesis but lacked the statistical power. There is a need for RCTs to examine the influence of vitamin D on body fat.

Second meal effects of dietary calcium and vitamin D.

OBJECTIVE: To determine the second meal effects of calcium and vitamin D on postprandial glucose, insulin, non-esterified fatty acids (NEFA) and glycerol. METHODS: Eight volunteers aged (mean+/-s.e.m.) 55.5+/-1.2 years and body mass index 29.0+/-1.6 kg/m(2), completed a randomized within-subject design that compared a low calcium-low vitamin D breakfast and an isocaloric high calcium-high vitamin D breakfast (HCB). Four hours following each breakfast, a very low calcium standard lunch was ingested. Serial blood collections were made on the hour over a duration of 8 h. Postprandial responses were calculated as the percentage change (Delta) from the fasting value for breakfast meals, and the 4th hour breakfast value for each lunch, respectively. Non-parametric tests of significance were employed. RESULTS: The change in glucose, insulin, serum ionized calcium (iCa(2+)) and intact parathyroid hormone was not different between the two breakfasts, or the two lunches. However, HCB resulted in a lesser suppression of NEFA that significantly carried over to lunch (P=0.036, Wilcoxon test). A similar pattern of change in glycerol did not attain overall statistical significance. DeltaNEFA and Deltaglycerol were related at lunch (Spearman's r=0.52, P=0.04). Relative to breakfast, both lunches resulted in significantly higher glucose and insulin responses (P=0.011, Wilcoxon test). CONCLUSIONS: The data are suggestive of second meal effects of calcium and vitamin D. Our observations of higher glucose and insulin after lunch may include the involvement of second meal factors as well.