Background/Objectives: Polycystic ovary syndrome (PCOS) is commonly associated with insulin resistance, dyslipidemia and increased inflammation, which all benefit from dietary intake of monounsaturated and n-3 polyunsaturated fatty acids (MUFA and n-3 PUFA). Our goal was to compare the effects of MUFA-rich almonds vs n-3/n-6 PUFA-rich walnuts on metabolic and endocrine parameters in PCOS. Subjects/Methods: Thirty-one PCOS patients randomly received either walnuts or almonds containing 31 g of total fat per day for 6 weeks. At the beginning and at the end, anthropometric parameters, fasting lipids, phospholipid-fatty acids, inflammatory markers, androgens, oral glucose tolerance tests (OGTT) and frequently sampled intravenous-GTT were obtained. Results: Weight remained stable. Within group, walnuts increased the n-3/n-6 essential PUFA in the diet and plasma phospholipids. Walnuts decreased low-density lipoprotein-cholesterol by 6% from 3.76 ± 0.27 to 3.38 ± 0.22 mmol/l (P ¼ 0.05) and apoprotein B by 11% from 0.72 ± 0.04 to 0.64 ± 0.05 g/l (Po0.03). Although almonds also reduced low-density lipoprotein-cholesterol by 10% and apoprotein B by 9%, these were not significant. Walnuts increased insulin response during OGTT by 26% (Po0.02). Both walnuts and almonds increased adiponectin (walnuts from 9.5 ± 1.6 to 11.3 ± 1.8 mg per 100 ml, P ¼ 0.0241; almonds from 10.1 ± 1.5 to 12.2 ± 1.4 mg/dl, P ¼ 0.0262). Walnuts decreased HgBA1 from 5.7 ± 0.1 to 5.5 ± 0.1% (P ¼ 0.0006) with significant intergroup difference from almonds (P ¼ 0.0470). Walnuts increased sex hormone-binding globulin from 38.3±4.1 to 43.1±4.3 nmol/l (P ¼ 0.0038) and almonds reduced free androgen index from 2.6±0.4 to 1.8±0.3 (P ¼ 0.0470). Conclusion: Nut intake exerted beneficial effects on plasma lipids and androgens in PCOS.

Ferritin (Ft) is a large iron-binding protein (~450 kDa) that is found in plant and animal cells and can sequester up to 4,500 iron (Fe) atoms per Ft molecule. Our previous studies on intestinal Caco-2 cells have shown that dietary factors affect the uptake of Fe from ferritin in a manner different from that of Fe from FeSO 4 , suggesting a different mechanism for cellular uptake. The objective of this study was to determine the mechanism for Ft-Fe uptake using Caco-2 cells. Binding of 59 Fe-labeled Ft at 4° C showed saturable kinetics and Scatchard analysis resulted in a K D of 1.6 μM, strongly indicating a receptor-mediated process. Competitive binding studies with excess unlabelled Ft significantly reduced binding and uptake studies at 37° C showed saturation after 4 h. Enhancing and blocking endocytosis using Mas-7 (a G-protein activator) and hypertonic medium (0.5 M sucrose), respectively, demonstrated that Ft-Fe uptake by Mas-7 treated cells was 140% of control cells, whereas sucrose treatment resulted in a statistically significant reduction in Ft-Fe uptake by 70% as compared to controls. Inhibition of macropinocytosis with 5-(N,N-dimethyl)-amiloride (Na + /H + antiport blocker) resulted in a decrease (by ~20%) in Ft-Fe uptake at high concentrations of Ft, suggesting that enterocytes can use more than one Ft-uptake mechanism in a concentration dependent manner. These results suggest that Ft uptake by enterocytes is carried out via endocytosis when Ft levels are within a physiological range, whereas Ft at higher concentrations may be absorbed using the additional mechanism of macropinocytosis.

Biofortification of staple foods with iron (Fe) in the form of ferritin (Ft) is now possible, both by conventional plant breeding methods and transgenic approaches. Ferritin-iron (Ft-Fe) from plants and animals is absorbed well (25-30%) by human subjects, but little is known about dietary factors affecting its absorption.

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