A systematic review of nudge theories and strategies used to influence adult health behaviour and outcome in diabetes management.

BACKGROUND: Diabetes is a chronic disease associated with a variety of complications, and nudging may be a potential solution to improve diabetes control. Since nudging is a new concept, no review of literature on nudging diabetic patients into improving their health behaviour has been done. Therefore, we aim to collate a list of nudge intervention and determine the context in which nudging is successful. METHODS: We adopted a two-arm search strategy comprising the search of literature databases and snowballing using relevant search terms. We summarized patient characteristics, the nudge intervention, according to nudging strategies, delivery mode and their outcomes. The conditions present in effective nudge interventions were assessed and reported. RESULTS: We retrieved 11,494 studies from our searches and included 33. An additional five studies were added through snowballing. Studies included utilized framing (n=5), reminders (n=10), gamification (n=2), social modelling (n=5) and social influence (n=16). Studies on reminders and gamification were more likely to have a statistically significant outcome. The targeted health behaviours identified were medication adherence, physical activity, diet, blood glucose monitoring, foot care, self-efficacy, HbA1c and quality of life. Of these, studies with adherence to medication, foot care practice and quality of life as targeted health behaviours were more likely to show a statistically significant outcome. CONCLUSION: Nudging has shown potential in changing health behaviour of patients with diabetes in specific context. We identified two possible factors (delivery mode and patient characteristics) that may affect the effectiveness of nudge intervention.

Nuclear factor κB (NF-κB) suppresses food intake and energy expenditure in mice by directly activating the Pomc promoter.

AIMS/HYPOTHESIS: While chronic low-grade inflammation is associated with obesity, acute inflammation reduces food intake and leads to negative energy balance. Although both types of inflammation activate nuclear factor κB (NF-κB) signalling, it remains unclear how NF-κB activation results in opposite physiological responses in the two types of inflammation. The goal of this study was to address this question, and to understand the link between inflammation and leptin signalling. METHODS: We studied the ability of NF-κB to modulate Pomc transcription, and how it impinges on signal transducer and activator of transcription 3 (STAT3)-mediated leptin signalling by using a combination of animal models, biochemical assays and molecular biology. RESULTS: We report that suppression of food intake and physical movement with acute inflammation is not dependent on STAT3 activation in pro-opiomelanocortin (POMC) neurons. Under these conditions, activated NF-κB independently leads to increased Pomc transcription. Electrophoretic mobility shift assay and chromatin immunoprecipitation (ChIP) experiments reveal that NF-κB v-rel reticuloendotheliosis viral oncogene homologue A (avian) (RELA [also known as p65]) binds to the Pomc promoter region between -138 and -88 bp, which also harbours the trans-acting transcription factor 1 (SP1) binding site. We found significant changes in the methylation pattern at this region and reduced Pomc activation under chronic inflammation induced by a high-fat diet. Furthermore, RELA is unable to bind and activate transcription when the Pomc promoter is methylated. Finally, RELA binds to STAT3 and inhibits STAT3-mediated promoter activity, suggesting that RELA, possibly together with forkhead box-containing protein 1 (FOXO1), may prevent STAT3-mediated leptin activation of the Pomc promoter. CONCLUSIONS/INTERPRETATION: Our study provides a mechanism for the involvement of RELA in the divergent regulation of energy homeostasis in acute and chronic inflammation.