Child-targeted on-pack communications in Belgian supermarkets: associations with nutritional value and type of brand.

Persuasive on-pack marketing strategies, such as colourful images and games, affect children's preferences and requests. The purpose of this study was to describe the prevalence of these child-directed (i.e. aimed at children) strategies on food packages at a Belgian retailer. Although previous research already demonstrated the frequency of most of these techniques directed at children, this paper extends to food pricing and facing strategies (i.e. the number of items from the same product aligned next to each other in the supermarket shelves) which were unstudied till now. Moreover, the association between the use of these strategies, the products' (un)healthiness and their type of brand (national vs. private) is investigated. The content analysis found that 372 food products contained one or more child-directed marketing strategies on-pack, all these communications were coded; the products could be classified in 15 food categories. On average, 3.9 (Min = 1; Max = 8) food promotion techniques were used per package. Unhealthiness of products was rated according to Food Standards Agency (FSA) Nutrient Profile UK. We found that 89.2% of all products with child-directed strategies were considered to be unhealthy. The presence of marketing strategies was associated with higher product unhealthiness, but did not differ much between types of brand. Overall, these findings suggest that (unhealthy) foods aimed at children typically feature many on-pack persuasive communications, which implies that policy makers should (continue to) monitor this. These findings highlight the need for further research to investigate the impact of on-pack communications on children's consumption.

Knockdown of the type 3 iodothyronine deiodinase (D3) interacting protein peroxiredoxin 3 decreases D3-mediated deiodination in intact cells.

The type 3 iodothyronine deiodinase (D3) is the primary deiodinase that inactivates thyroid hormone. Immunoprecipitation of D3, followed by fluorescent two-dimensional difference gel electrophoresis and mass spectrometry, identified peroxiredoxin 3 (Prx3) as a D3-associated protein. This interaction was confirmed using reverse coimmunoprecipitation, in which pull-down of Prx3 resulted in D3 isolation, and by fluorescence resonance energy transfer between cyan fluorescent protein-D3 and yellow fluorescent protein-Prx3. Prx3 overexpression did not change D3 activity in transfected HEK 293 cells; however, Prx3 knockdown resulted in a 50% decrease in D3-mediated whole-cell deiodination. Notably, D3 activity of cell lysates with dithiothreitol as an exogenous reducing factor and D3 protein levels were not decreased with Prx3 knockdown, indicating that the observed reduction in whole-cell deiodination was not simply due to a decrease in D3 enzyme levels. Prx3 knockdown did not change D3's affinity for T3 because saturation of D3-mediated whole-cell deiodination occurred between 20 and 200 nm T3 both with and without Prx3. Furthermore, the decrease in D3 activity in whole cells was not attributable to nonspecific oxidative stress because pretreatment with the antioxidant N-acetyl cysteine did not reverse the effects of Prx3 knockdown. Thioredoxin, the cofactor needed for Prx3 regeneration, supported D3 microsomal activity; however, Prx3 knockdown did not change D3 activity in this system. In conclusion, knockdown of Prx3 decreases D3 activity in whole cells, whereas absolute levels of D3 are unchanged, consistent with Prx3 playing a rate-limiting role in the regeneration of the D3 enzyme.

The dioxin-like PCB 77 but not the ortho-substituted PCB 153 interferes with chicken embryo thyroid hormone homeostasis and delays hatching.

The effects of the dioxin-like polychlorinated biphenyl (PCB) 77 and the ortho-substituted PCB 153 on thyroid hormone availability were investigated during the last week of embryonic development in chicken. High doses of these PCBs (1microg PCB 77 and 20microg PCB 153) were injected into chicken eggs at day 4 of incubation. Blood and tissue samples were collected from day 14 of incubation until 1 day after hatching. We did not observe influences of PCB 153 on thyroid hormone (TH) levels. Treatment with PCB 77, on the other hand, decreased plasma total T(4) concentrations but increased hepatic T(4) levels at day 14 of incubation. Later in development, at stages near the process of hatching, severe decreases of T(4) and T(3) levels were observed in the PCB 77 group, both in plasma and tissues. PCB 77 severely reduced the TH peak that normally coincides with the stage of internal pipping. This reduction was accompanied by a considerable delay in the moment of hatching. We conclude that the dioxin-like PCB 77, but not the ortho-substituted PCB 153, can decrease TH availability towards the end of embryonic development and hence disturb the process of hatching.

Type 1 iodothyronine deiodinase is a sensitive marker of peripheral thyroid status in the mouse.

Mice with one thyroid hormone receptor (TR) alpha-1 allele encoding a dominant negative mutant receptor (TR alpha1(PV/+)) have persistently elevated serum T3 levels (1.9-fold above normal). They also have markedly increased hepatic type 1 iodothyronine deiodinase (D1) mRNA and enzyme activity (4- to 5-fold), whereas other hepatic T3-responsive genes, such as Spot14 and mitochondrial alpha-glycerol phosphate dehydrogenase (alpha-GPD), are only 0.7-fold and 1.7-fold that of wild-type littermates (TR alpha1+/+). To determine the cause of the disproportionate elevation of D1, TR alpha1+/+ and TR alpha1(PV/+) mice were rendered hypothyroid and then treated with T3. Hypothyroidism decreased hepatic D1, Spot14, and alpha-GPD mRNA to similar levels in TR alpha1+/+ and TR alpha1(PV/+) mice, whereas T3 administration caused an approximately 175-fold elevation of D1 mRNA but only a 3- to 6-fold increases in Spot14 and alpha-GPD mRNAs. Interestingly, the hypothyroidism-induced increase in cerebrocortical type 2 iodothyronine deiodinase activity was 3 times greater in the TR alpha1(PV/+) mice, and these mice had no T3-dependent induction of type 3 iodothyronine deiodinase. Thus, the marked responsiveness of hepatic D1 to T3 relative to other genes, such as Spot14 and alpha-GPD, explains the relatively large effect of the modest increase in serum T3 in the TR alpha1(PV/+) mice, and TR alpha plays a key role in T3-dependent positive and negative regulation of the deiodinases in the cerebral cortex.