When commonly consumed mushroom species are exposed to a source of ultraviolet (UV) radiation, such as sunlight or a UV lamp, they can generate nutritionally relevant amounts of vitamin D. The most common form of vitamin D in mushrooms is D₂, with lesser amounts of vitamins D₃ and D₄, while vitamin D₃ is the most common form in animal foods. Although the levels of vitamin D₂ in UV-exposed mushrooms may decrease with storage and cooking, if they are consumed before the ‘best-before’ date, vitamin D₂ level is likely to remain above 10 μg/100 g fresh weight, which is higher than the level in most vitamin D-containing foods and similar to the daily requirement of vitamin D recommended internationally. Worldwide mushroom consumption has increased markedly in the past four decades, and mushrooms have the potential to be the only non-animal, unfortified food source of vitamin D that can provide a substantial amount of vitamin D₂ in a single serve. This review examines the current information on the role of UV radiation in enhancing the concentration of vitamin D₂ in mushrooms, the effects of storage and cooking on vitamin D₂ content, and the bioavailability of vitamin D₂ from mushrooms.

Background: It is speculated that high saturated fat very low carbohydrate diets (VLCARB) have adverse effects on cardiovascular risk but evidence for this in controlled studies is lacking. The objective of this study was to compare, under isocaloric conditions, the effects of a VLCARB to 2 low saturated fat high carbohydrate diets on body composition and cardiovascular risk. Methods: Eighty three subjects, 48 ± 8 y, total cholesterol 5.9 ± 1.0 mmol/L, BMI 33 ± 3 kg/m² were randomly allocated to one of 3 isocaloric weight loss diets (6 MJ) for 8 weeks and on the same diets in energy balance for 4 weeks: Very Low Fat (VLF) (CHO:Fat:Protein; %SF = 70:10:20; 3%), High Unsaturated Fat (HUF) = (50:30:20; 6%), VLCARB (4:61:35; 20%) Results: Percent fat mass loss was not different between diets VLCARB -4.5 ± 0.5, VLF-4.0 ± 0.5, HUF -4.4 ± 0.6 kg). Lean mass loss was 32-31% on VLCARB and VLF compared to HUF (21%) (P < 0.05). LDL-C increased significantly only on VLCARB by 7% (p < 0.001 compared with the other diets) but apoB was unchanged on this diet and HDL-C increased relative to the other 2 diets. Triacylglycerol was lowered by 0.73 ± 0.12 mmol/L on VLCARB compared to -0.15 ± 0.07 mmol/L on HUF and -0.06 ± 0.13 mmol/L on VLF (P < 0.001). Plasma homocysteine increased 6.6% only on VLCARB (P = 0.026). VLCARB lowered fasting insulin 33% compared to a 19% fall on HUF and no change on VLF (P < 0.001). The VLCARB meal also provoked significantly lower post prandial glucose and insulin responses than the VLF and HUF meals. All diets decreased fasting glucose, blood pressure and CRP (P < 0.05). Conclusion: Isocaloric VLCARB results in similar fat loss than diets low in saturated fat, but are more effective in improving triacylglycerols, HDL-C, fasting and post prandial glucose and insulin concentrations. VLCARB may be useful in the short-term management of subjects with insulin resistance and hypertriacylglycerolemia.

Postprandial lipemia after an oral fat challenge was studied in middle-aged men with visceral obesity. The two groups had similar plasma cholesterol levels, but obese subjects had higher levels of plasma triglyceride and reduced amounts of high-density cholesterol. Fasting plasma insulin was fourfold greater in obese subjects because of concomitant insulin resistance, with a calculated HOMA score of 3.1 ± 0.6 vs. 0.8 ± 0.2, respectively. Plasma apolipoprotein B₄₈(apoB₄₈) and retinyl palmitate (RP) after an oral fat challenge were used to monitor chylomicron metabolism. Compared with lean subjects, the fasting concentration of apoB₄₈was more than twofold greater in obese individuals, suggestive of an accumulation of posthydrolyzed particles. After the oral lipid load, the incremental areas under the apoB₄₈and RP curves (IAUC) were both significantly greater in obese subjects (apoB₄₈: 97 ± 17 vs. 44 ± 12 μg · ml⁻¹· h; RP: 3,120 ± 511 vs. 1,308 ± 177 U · ml⁻¹· h, respectively). A delay in the conversion of chylomicrons to remnants probably contributed to postprandial dyslipidemia in viscerally obese subjects. The triglyceride IAUC was 68% greater in obese subjects (4.7 ± 0.6 vs. 2.8 ± 0.8 mM · h, P< 0.06). Moreover, peak postprandial triglyceride was delayed by ∼2 h in obese subjects. The reduction in triglyceride lipolysis in vivo did not appear to reflect changes in hydrolytic enzyme activities. Postheparin plasma lipase rates were found to be similar for lean and obese subjects. In this study, low-density lipoprotein (LDL) receptor expression on monunuclear cells was used as a surrogate marker of hepatic activity. We found that, in obese subjects, the binding of LDL was reduced by one-half compared with lean controls (70.9 ± 15.07 vs. 38.9 ± 4.6 ng LDL bound/μg cell protein, P = 0.02). Because the LDL receptor is involved in the removal of proatherogenic chylomicron remnants, we suggest that the hepatic clearance of these particles might be compromised in insulin-resistant obese subjects. Premature and accelerated atherogenesis in viscerally obese, insulin-resistant subjects may in part reflect delayed clearance of postprandial lipoprotein remnants.