@article{StieglitzMirbabaieDeubeletal.2023, author = {Stieglitz, Stefan and Mirbabaie, Milad and Deubel, Annika and Braun, Lea-Marie and Kissmer, Tobias}, title = {The potential of digital nudging to bridge the gap between environmental attitude and behavior in the usage of smart home applications}, series = {International Journal of Information Management}, volume = {72}, journal = {International Journal of Information Management}, publisher = {Elsevier}, address = {Oxford}, issn = {0268-4012}, doi = {10.1016/j.ijinfomgt.2023.102665}, year = {2023}, abstract = {Despite energy efficiency measures, global energy demand has gradually increased due to global economic growth and changes in consumer behavior. Even if people are aware of the problem and want to change their energy consumption, they have difficulty acting on their attitudes. This is called the attitude-behavior gap. To narrow this gap and reduce energy consumption and CO2 emissions, behavioral interventions beyond technological advances must be considered. A promising intervention is nudging, which uses insights from behavioral economics to gently nudge individuals toward more sustainable choices. In this study, we investigate how modifying digital choice architectures with nudges can be used to influence consumer energy conservation behavior in smart home applications (SHAs). We conducted an online experiment with 391 participants to test the effectiveness of the following three digital nudges in an SHA: self-commitment, reminder, and social norm nudge. While the results of a structural equation model indicated no effect on bridging the gap between attitude and behavior, we found the potential to promote energy conservation with two nudge types. Thus, this paper makes substantial contribution to persuasive and information systems-enabled sustainability for a better world in the form of digital nudges for emerging technologies.}, language = {en} } @article{KehmJaehnertDeubeletal.2020, author = {Kehm, Richard and J{\"a}hnert, Markus and Deubel, Stefanie and Flore, Tanina and K{\"o}nig, Jeannette and Jung, Tobias and Stadion, Mandy and Jonas, Wenke and Sch{\"u}rmann, Annette and Grune, Tilman and H{\"o}hn, Annika}, title = {Redox homeostasis and cell cycle activation mediate beta-cell mass expansion in aged, diabetes-prone mice under metabolic stress conditions: role of thioredoxin-interacting protein (TXNIP)}, series = {Redox Biology}, volume = {37}, journal = {Redox Biology}, publisher = {Elsevier}, address = {Amsterdam}, issn = {2213-2317}, doi = {10.1016/j.redox.2020.101748}, pages = {11}, year = {2020}, abstract = {Overnutrition contributes to insulin resistance, obesity and metabolic stress, initiating a loss of functional beta-cells and diabetes development. Whether these damaging effects are amplified in advanced age is barely investigated. Therefore, New Zealand Obese (NZO) mice, a well-established model for the investigation of human obesity-associated type 2 diabetes, were fed a metabolically challenging diet with a high-fat, carbohydrate restricted period followed by a carbohydrate intervention in young as well as advanced age. Interestingly, while young NZO mice developed massive hyperglycemia in response to carbohydrate feeding, leading to beta-cell dysfunction and cell death, aged counterparts compensated the increased insulin demand by persistent beta-cell function and beta-cell mass expansion. Beta-cell loss in young NZO islets was linked to increased expression of thioredoxin-interacting protein (TXNIP), presumably initiating an apoptosis-signaling cascade via caspase-3 activation. In contrast, islets of aged NZOs exhibited a sustained redox balance without changes in TXNIP expression, associated with higher proliferative potential by cell cycle activation. These findings support the relevance of a maintained proliferative potential and redox homeostasis for preserving islet functionality under metabolic stress, with the peculiarity that this adaptive response emerged with advanced age in diabetesprone NZO mice.}, language = {en} } @article{KehmRueckriemenWeberetal.2019, author = {Kehm, Richard and R{\"u}ckriemen, Jana and Weber, Daniela and Deubel, Stefanie and Grune, Tilman and H{\"o}hn, Annika}, title = {Endogenous advanced glycation end products in pancreatic islets after short-term carbohydrate intervention in obese, diabetes-prone mice}, series = {Nutrition \& Diabetes}, volume = {9}, journal = {Nutrition \& Diabetes}, publisher = {Nature Publ. Group}, address = {London}, issn = {2044-4052}, doi = {10.1038/s41387-019-0077-x}, pages = {5}, year = {2019}, abstract = {Diet-induced hyperglycemia is described as one major contributor to the formation of advanced glycation end products (AGEs) under inflammatory conditions, crucial in type 2 diabetes progression. Previous studies have indicated high postprandial plasma AGE-levels in diabetic patients and after long-term carbohydrate feeding in animal models. Pancreatic islets play a key role in glucose metabolism; thus, their susceptibility to glycation reactions due to high amounts of dietary carbohydrates is of special interest. Therefore, diabetes-prone New Zealand Obese (NZO) mice received either a carbohydrate-free, high-fat diet (CFD) for 11 weeks or were additionally fed with a carbohydrate-rich diet (CRD) for 7 days. In the CRD group, hyperglycemia and hyperinsulinemia were induced accompanied by increasing plasma 3-nitrotyrosine (3-NT) levels, higher amounts of 3-NT and inducible nitric oxide synthase (iNOS) within pancreatic islets. Furthermore, N-epsilon-carboxymethyllysine (CML) was increased in the plasma of CRD-fed NZO mice and substantially higher amounts of arg-pyrimidine, pentosidine and the receptor for advanced glycation end products (RAGE) were observed in pancreatic islets. These findings indicate that a short-term intervention with carbohydrates is sufficient to form endogenous AGEs in plasma and pancreatic islets of NZO mice under hyperglycemic and inflammatory conditions.}, language = {en} }