Celiac disease (CD) is a chronic autoimmune disorder of the small intestine, whose only effective treatment is a gluten-free diet (GFD). It is characterized by the atrophy of the intestinal villi that leads to altered nutrient absorption. This study describes the nutritional imbalances which may be found in adults with CD following a GFD. During the first year of treatment, deficiencies will overcome as the intestinal mucosa recovers. Thus, biochemical data will show this progression, together with the decrease in symptoms. In contrast, in the long term, when a strict GFD is followed and mucosal recovery is achieved, analyzing nutrient intake makes more sense. Macronutrient consumption is characterized by its low complex carbohydrate and fiber intakes, and high fat (especially SFA) and sugar intakes. This profile has been related to the consumption of GFP and their nutritional composition, in addition to unbalanced dietary habits. The most notable deficiencies in micronutrients are usually those of iron, calcium and magnesium and vitamin D, E and some of group B. It is necessary to follow up patients with CD and to promote nutritional education among them, since it could help not only to achieve a gluten free but also a balanced diet.

Early adaptive responses to hypoxia are essential for cell survival, but their nature and underlying mechanisms are poorly known. We have studied the post-transcriptional changes in the proteome of mammalian cells elicited by acute hypoxia and found that phosphorylation of eukaryotic elongation factor 2 (eEF2), a ribosomal translocase whose phosphorylation inhibits protein synthesis, is under the precise and reversible control of O(2) tension. Upon exposure to hypoxia, phosphorylation of eEF2 at Thr(56) occurred rapidly (<15 min) and resulted in modest translational arrest, a fundamental homeostatic response to hypoxia that spares ATP and thus facilitates cell survival. Acute inhibitory eEF2 phosphorylation occurred without ATP depletion or AMP kinase activation. Furthermore, eEF2 phosphorylation was mimicked by prolyl hydroxylase (PHD) inhibition with dimethyloxalylglycine or by selective PHD2 siRNA silencing but was independent of hypoxia-inducible factor α stabilization. Moreover, overexpression of PHD2 blocked hypoxic accumulation of phosphorylated eEF2. Therefore, our findings suggest that eEF2 phosphorylation status (and, as a consequence, translation rate) is controlled by PHD2 activity. They unravel a novel pathway for cell adaptation to hypoxia that could have pathophysiologic relevance in tissue ischemia and cancer.

The treatment of Celiac disease consists in a strict lifelong gluten-free (GF) diet. As the ingestion of small amounts can have damaging complications, there has been an ongoing discussion regarding the safe threshold for dietary residual gluten. The aim was to analyze the evolution of gluten content in cereal-based GF foodstuffs (n = 3141) from 1998 to 2016 measured by the enzyme-linked immunosorbent assay (ELISA) technique. Eight categories were defined: flours, breakfast cereals/bars, bakery, pasta, breads, dough, snacks, and yeasts, and these were divided into GF labeled-foods (GF-L) or reportedly GF foodstuffs, but not certified (GF-NC). Gluten-detection was decreased over time in line with the evolving European regulations about food information and gluten content claims. This decline started sooner in GF-L products than in GF-NC. As a whole, gluten was detected in 371 samples, with breakfast cereals/bars being the most contaminated group. Snacks and yeasts changed from being high gluten-detected samples to being totally GF over the years. The downside is that, of contaminated samples, those in the low levels of gluten detection range have decreased while flour samples containing over 100 mg/kg gluten have risen in the 2013–2016 period. Obtained data confirm that GF cereal-based foods are becoming safer but gluten control must be maintained.