Low serum 25 hydroxyvitamin D₃ (vitamin D₃) is known to perturb cellular function in many tissues, including the endocrine pancreas, which are involved in obesity and type II diabetes mellitus (TIIDM). Vitamin D₃ insufficiency has been linked to obesity, whether obesity is assessed by body mass index (BMI) or waist circumference (waist). Central obesity, using waist as the surrogate, is associated with the metabolic syndrome (MetSyn), insulin resistance, TIIDM and atherosclerotic cardiovascular disease (CVD). We tested how vitamin D₃ was related to measures of fat mass, MetSyn markers, haemoglobin A_1c (HbA_1c) and MetSyn in a cross-sectional sample of 250 overweight and obese adults of different ethnicities. There were modest inverse associations of vitamin D₃ with body weight (weight) (r = -0.21, p = 0.0009), BMI (r = -0.18, p = 0.005), waist (r = -0.14, p = 0.03), [but not body fat % (r = -0.08, p = 0.24)], and HbA_1c (r = -0.16, p = 0.01). Multivariable regression carried out separately for BMI and waist showed a decrease of 0.74 nmol/L (p = 0.002) in vitamin D₃ per 1 kg/m² increase in BMI and a decrease of 0.29 nmol/L (p = 0.01) per 1 cm increase in waist, with each explaining approximately 3% of the variation in vitamin D₃ over and above gender, age, ethnicity and season.The similar relationships of BMI and waist with vitamin D₃ may have been due to associations between BMI and waist, or coincidental, where different mechanisms relating hypovitaminosis D₃ to obesity occur concurrently. Previously reviewed mechanisms include that 1) low vitamin D₃, may impair insulin action, glucose metabolism and various other metabolic processes in adipose and lean tissue 2) fat soluble-vitamin D₃ is sequestered in the large adipose compartment, and low in serum, 3) obese people may be sensitive about their body shape, minimising their skin exposure to view and sunlight (not tested). We showed evidence for the first theory but no evidence to support the second.In the current study, serum vitamin D₃ was inversely related to weight, BMI and markers of TIIDM (large waist, raised HbA_1c) but not to adipose mass nor to MetSyn per se.

Background: High fat diets have long been associated with weight gain and obesity, and the weak satiety response elicited in response to dietary lipids is likely to play a role. Suppression of appetite and food intake has consistently been shown to be diminished with high fat relative to either high protein or carbohydrate meals. There is however some evidence that the satiating capacity of lipids may be modulated when physicochemical properties are altered, but studies investigating the effect of lipid saturation on appetite have generated inconsistent findings. This study investigated the effects of changes in fatty acid saturation on post-ingestive satiety and energy intake. Methods: High-fat (HF) test breakfasts (2.0 MJ) containing 26 g lipid were given to 18 healthy, lean men in a 3 treatment randomised cross-over design, each treatment separated by a washout of at least 3 days. The breakfasts were high in saturated (SFA, 65% of total fat), polyunsaturated (PUFA, 76%) or monounsaturated (MUFA, 76%) fatty acids, and comprised 2 savoury muffins. Participants rated appetite sensations using visual analogue scales (VAS) to assess palatability immediately following the meals, and hunger and fullness prior to the HF breakfast and throughout the day. Energy intake was measured by covert weighing of a lunch meal which was served 3.5 h after the breakfast, and from which the participants ate ad libitum. Results: There was no difference in VAS ratings of pleasantness, visual appearance, smell, taste, aftertaste and overall palatability between the 3 high-fat test breakfasts. However, there was also no differential effect of the 3 treatments on ratings of hunger, fullness, satisfaction or prospective food consumption during the 3.5 h following the breakfast meal and over the full 6 h experiment. Energy and macronutrient intake at lunch also did not differ between treatments (mean, sem; SFA: 5275.9 ± 286.5 kJ; PUFA: 5227.7 ± 403.9 kJ; MUFA: 5215.6 ± 329.5 kJ; P > 0.05). The maximum difference in energy intake between treatments was less than 2%. Conclusions: There was no evidence of a difference in post-ingestion satiety between high fat meals which differed in saturation profile in this group of lean, healthy men. Trial Registration: ACTRN12610000193077

Increased consumption of vegetables/herbs/fruit may reduce bone turnover and urinary calcium loss in post-menopausal women because of increased intake of polyphenols and potassium, but comparative human studies are lacking. The main aim was to compare bone turnover markers and urinary calcium excretion in two randomised groups (n = 50) of healthy post-menopausal women consuming ≥9 servings of different vegetables/herbs/fruit combinations (three months). Group A emphasised a generic range of vegetables/herbs/fruit, whereas Group B emphasised specific vegetables/herbs/fruit with bone resorption-inhibiting properties (Scarborough Fair Diet), with both diets controlled for potential renal acid load (PRAL). Group C consumed their usual diet. Plasma bone markers, urinary electrolytes (24 h) and estimated dietary PRAL were assessed at baseline and 12 weeks. Procollagen type I N propeptide (PINP) decreased (−3.2 μg/L, p < 0.01) in the B group only, as did C-terminal telopeptide of type I collagen (CTX) (−0.065 μg/L, p < 0.01) in women with osteopenia compared to those with normal bone mineral density (BMD) within this group. Intervention Groups A and B had decreased PRAL, increased urine pH and significantly decreased urinary calcium loss. Urinary potassium increased in all groups, reflecting a dietary change. In conclusion, Group B demonstrated positive changes in both turnover markers and calcium conservation.