No abstract

The relationship between dietary fat content and milk composition, production and litter growth was studied in rats fed during pregnancy and lactation purified diets of equal energy density containing 2.5 or 20 g fat/100 g diet. A subsample of rats (HL-EP group) fed the high lipid (HL) diet but pair-fed on an energy basis with the low lipid (LL) diet group was also studied in a separate experiment. Food intake, dam body weight and litter weight were recorded daily. Rats were milked on d 14 of lactation. Milk lipid, lactose and protein concentration and milk production were measured. Lactating rats fed the HL diet had significantly higher energy intakes (P < 0.01) and milk production (P < 0.05) than rats fed the LL diet. Milk lipid concentration and daily milk volume and lipid production were significantly higher in the HL group. The HL-EP dams had significantly higher milk lipid, protein and lactose concentrations (P < 0.05) and tended to have higher daily lipid and energy outputs (P = 0.08) than LL rats. Birth weights of pups were similar among groups, but from d 6 on, the pups from the HL and HL-EP groups were significantly heavier (P < 0.05) than pups from the LL group. This investigation presents evidence that the milk fat concentration and the daily output of fat, protein and lactose of lactating rats are altered by dietary fat manipulations, which in turn affect growth of the litter.

No abstract

We propose that the International Council for the Control of Iodine Deficient Disorders recommend that iodine intake be increased to at least 3 mg/day of I2 in specific pathologies to obtain the potential extrathyroidal benefits described in the present review.

This study analyzes the uptake and antiproliferative effect of two different chemical forms of iodine, iodide (I K ) and molecular iodine (I 2 ), in MCF-7 cells, which are inducible for the Na C =I K symporter (NIS) and positive for pendrin (PDS). The mouse fibroblast cell line NIH3T3 was used as control. Our results show that in MCF-7 cells, IK uptake is sustained and dependent on NIS, whereas I 2 uptake is transient with a maximal peak at 10 min and a final retention of 10% of total uptake. In contrast, no I K was taken up by NIH3T3 cells, and although I 2 was captured with the same time pattern as in MCF-7 cells, its uptake was significantly lower, and it was not retained within the cell. The uptake of I 2 is independent of NIS, PDS, Na C , and energy, but it is saturable and dependent on protein synthesis, suggesting a facilitated diffusion system. Radioiodine was incorporated into protein and lipid fractions only with I 2 treatment. The administration of non-radiolabeled I 2 and 6-iodo-5-hydroxy-8,11,14-eicosatrienoic acid (6-iodolactone, an iodinated arachidonic acid), but not KI, significantly inhibited proliferation of MCF-7 cells. Proliferation of NIH3T3 cells was not inhibited by 20 mM I 2 . In conclusion, these results demonstrate that I 2 uptake does not depend on NIS or PDS; they suggest that in mammary cancer cells, I 2 is taken up by a facilitated diffusion system and then covalently bound to lipids or proteins that, in turn, inhibit proliferation.