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.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
The objective was to examine whether there were causal links between vitamin D status, parathyroid hormone, insulin resistance (IR)/insulin sensitivity (IS) and the metabolic syndrome (MS). A total ...of 72 Caucasian men and women, aged 55.7 ± 7.57 years, with body mass index 33.4 ± 4.02 kg/m(2) and abdominal obesity, were assessed for IR/IS based on three commonly used indices before and after 12 weeks of supervised weight loss. During weight stability, though both lower intact parathyroid hormone (iPTH) and higher vitamin D were independently associated with greater IS/lower IR, this was consistent for iPTH across the surrogate measures tested. Higher iPTH, but not lower vitamin D, increased the risk of MS after adjustment for IR/IS. Weight loss resulted in significant reductions in percent fat (-2.83 ± 2.20%), waist (-9.26 ± 5.11 cm), improvements in all IS indices, reductions in MS and iPTH (-0.28 ± 1.17 pmol/l), but no increase in vitamin D (+2.19 ± 12.17 nmol/l). Following weight loss, ΔiPTH either predicted change in IR/IS or contributed to their variance by 4.1-8.9%. On adjustment for IR/IS, higher ΔiPTH did not significantly predict MS after weight loss, though the odds ratios for the effect were sizeable. The data are suggestive of an intrinsic inverse relationship between iPTH and IS in abdominally obese individuals, independent of vitamin D. There remains the possibility of a direct relationship between iPTH and MS.
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DOBA, EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, IZUM, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, SIK, UILJ, UKNU, UL, UM, UPUK, VKSCE, VSZLJ, ZAGLJ
Use of the Dietary Guideline Index to assess cardiometabolic risk in adolescents Chan She Ping-Delfos, Wendy L; Lawrence J. BeilinauthorSchool of Medicine and Pharmacology, Royal Perth Hospital Unit, The University of Western Australia, Perth, WA, 6000, Australia; Wendy H. OddyauthorTelethon Kids Institute, The University of Western Australia, PO Box 85, West Perth, WA, 6872, Australia ...
2015
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