Educational nutrition messaging at breakfast reduces snack intake and influences snack preferences in adult men and women.

Breakfast skipping is associated with increased risk of weight gain and obesity in young adults, possibly due to increased snacking later in the day. Recent research suggests that providing and animal versus a plant source of protein at breakfast can reduce snack intake later in the day. In addition, providing nutrition information via a nutrition label, front-of-pack information, or via text messaging has been shown to help individuals make healthier food choices. The objective of this study was to determine if educational nutrition messaging and protein source influenced snack intake 2 h following the breakfast meal. Participants (n = 33) were randomly assigned to one of two groups: educational nutrition messaging (EM; n = 16) or no messaging (NM; n = 17) group. The study was conducted using a randomized, cross-over design in which each participant received each of two breakfast beverages, whey protein- (WP) and pea protein (PP)- based. Appetite was assessed at 0, 15, 30, 60, 90, and 120 min after each test breakfast using visual analog scales. Participants were then provided with a selection of healthy and unhealthy snacks for 60 min. There was no effect of protein source on appetite or snack intake. However, participants presented with EM had reduced snack intake over the snacking period compared to NM (P = 0.058) and, of the snacks consumed, the EM group consumed a higher percentage of healthy versus unhealthy snacks compared to NM (P < 0.0001), resulting in lower calorie intake. Taken together these data suggest that protein source, as part of a higher protein breakfast, does not affect appetite response or snack intake, but EM may help play a role in reducing snack intake between meals.

An experimental analysis of the affect regulation model of binge eating.

There is research suggesting that binge eating may serve an affect regulation function. However, experimental evidence supporting this model in adults is sparse and studies have been mixed regarding whether negative affect impacts objective energy intake. This study examined the impact of a real-time interpersonal stressor on laboratory test meal intake between individuals endorsing recent objective binge eating (≥1×/week) and those denying disordered eating. Generalized linear modeling was used to compare individuals with recent binge eating (BE group; n = 52) to those denying recent eating pathology (HC group; n = 51) on test meal intake following a stressor (stressful condition) or neutral stimulus (non-stressful condition). Moderated mediation analyses were used to examine whether negative affect mediated the impact of condition on intake differently between BE and HC groups. The BE group did not have significantly higher energy intake than the HC group in the stressful verses non-stressful condition. However, the BE group was more likely to engage in extreme intake (i.e., over- or under-consumption) than the HC group in the stressful versus non-stressful condition (p = 0.02). Changes in negative affect did not significantly mediate the relationship between condition and intake extremes for the BE group. The results indicate that both over- and under-consumption are triggered by stress among individuals with recent binge eating. Continued research investigating both binge eating and restriction as a means of affect regulation in binge-eating samples is encouraged.

Effect of total lens epithelial cell destruction on intraocular lens fixation in the human capsular bag.

PURPOSE: To evaluate the effect of complete destruction of lens epithelial cells (LECs) in the capsular bag on intraocular lens (IOL) stability. SETTING: School of Biological Sciences, University of East Anglia, Norwich, United Kingdom. DESIGN: Comparative evaluation. METHODS: An in vitro organ culture model using the bag-zonule-ciliary body complex isolated from fellow human donor eyes was prepared. A capsulorhexis and fiber extraction were performed, and an Acrysof IOL was implanted. Preparations were secured by pinning the ciliary body to a silicone ring and maintaining it in 6 mL Eagle minimum essential medium supplemented with 5% v/v fetal calf serum and 10 ng/mL transforming growth factor-ß2 for 3 weeks or more. One bag of each pair was treated with 1 µM thapsigargin to destroy all LECs. Observations of LEC growth were captured by phase-contrast microscopy, IOL stability by video microscopy, and endpoint analysis through scanning electron microscopy and immunocytochemistry. RESULTS: The LECs in control capsular bags migrated centrally, closing the bag and fixating the IOL between the anterior and posterior capsules, as seen clinically. These events were not observed in the thapsigargin-treated group. After a period of controlled orbital movement, the IOL in the control group stabilized quicker than in the treated bags. There was no IOL rotation in the bag; however, the IOLs in the treated group rocked with axial movement. CONCLUSIONS: The LECs appeared to aid stabilization of current IOL designs in the capsular bag. The results have clinical implications for IOL design and for strategies to prevent posterior capsule opacification. FINANCIAL DISCLOSURE: No author has a financial or proprietary interest in any material or method mentioned.

Activation of the innate immune response and interferon signalling in myotonic dystrophy type 1 and type 2 cataracts.

Myotonic dystrophy (DM) is caused by a triplet repeat expansion in the non-coding region of either the DMPK (DM1) or CNBP (DM2) gene. Transcription of the expanded region causes accumulation of double-stranded RNA (dsRNA) in DM cells. We sought to determine how expression of triplet repeat RNA causes the varied phenotype typical of DM. Global transcription was measured in DM and non-DM cataract samples using Illumina Bead Arrays. DM samples were compared with non-DM samples and lists of differentially expressed genes (P≤ 0.05) were prepared. Gene set enrichment analysis and the Interferome database were used to search for significant patterns of gene expression in DM cells. Expression of individual genes was measured using quantitative real-time polymerase chain reaction. DMPK and CNBP expression was confirmed in native lens cells showing that a toxic RNA gain of function mechanism could exist in lens. A high proportion, 83% in DM1 and 75% in DM2, of the significantly disregulated genes were shared by both forms of the disease, suggesting a common mechanism. The upregulated genes in DM1 and DM2 were highly enriched in both interferon-regulated genes (IRGs) and genes associated with the response to dsRNA and the innate immune response. The characteristic fingerprint of IRGs and the signalling pathways identified in lens cells support a role for dsRNA activation of the innate immune response in the pathology of DM. This new evidence forms the basis for a novel hypothesis to explain the complex mechanism of DM.

Regional differences in store-operated Ca2+ entry in the epithelium of the intact human lens.

PURPOSE: An elevated level of Ca(2+) is an important factor in cataract, yet precisely how Ca(2+) enters the lens is unknown. Lens epithelial cells contain a range of G-protein-coupled receptors and receptor tyrosine kinases that induce increases in intracellular Ca(2+). Receptor-associated Ca(2+) influx is, therefore, likely to be an important route for Ca(2+) influx to the lens. The authors investigated stimulated and passive Ca(2+) influx in in situ human lens epithelium. METHODS: Ca(2+) changes in equatorial (E) and central anterior (CA) epithelial cells were monitored with the use of a Ca(2+) indicator (Fluo4) and confocal microscopy. Gene expression was monitored by RT-PCR and immunoblotting. RESULTS: Adenosine triphosphate (ATP) induced Ca(2+) responses that were smaller in CA than E. Ca(2+) store depletion, using ATP (100 microM) or thapsigargin (1 microM), revealed greater relative store capacity and Ca(2+) influx in E. Ca(2+) influx was blocked by La(3+) (0.5 microM) in both regions. Unstimulated Ca(2+) influx was greater in E than CA. Greater expression of Orai1 and STIM1 was detected in E than in CA. CONCLUSIONS: Greater Ca(2+) store capacity and Ca(2+) influx in E compared with CA reflects underlying differences in proliferation and differentiation between the regions. The relatively small resting Ca(2+) influx in CA epithelium suggests that store-operated Ca(2+) entry (SOCE) is the main route of Ca(2+) influx in these cells. Greater resting influx and SOCE in E cells suggests that these are a major route for Ca(2+) influx into the lens. Increased expression of Orai1 and STIM1 in E could account for the differences in Ca(2+) entry. Receptor activation will modulate Ca(2+) influx, and inappropriate activity may contribute to cortical cataract.