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1.
Diabetes Metab Syndr ; 18(2): 102944, 2024 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-38281447

RESUMO

BACKGROUND AND AIM: South Asian migrants have a higher prevalence of chronic diseases than Caucasians. Despite much literature that has explored challenges in chronic disease management amongst the South Asian population in the past decades, their chronic disease management is still suboptimal. Understanding their determinants of disease management behaviour using the Theoretical Domains Framework will inform the development of a culturally sensitive intervention relevant to consumer-end-users. This study aimed to synthesise qualitative and quantitative studies on chronic disease management among adult South Asian immigrants. METHODS: A mixed-methods systematic review was conducted using electronic databases. The Mixed Methods Appraisal Tool assessed the quality of the included studies. Quantitative data were transformed into qualitative data and analysed thematically. Subthemes were mapped in the Theoretical Domains Framework presenting barriers and facilitators under each theme. RESULTS: 18293 studies were identified, of which 37 studies were included. The barriers and facilitators identified were categorised into four overarching themes: patient-provider interaction and relationship (e.g., complex language use by health professionals), the impact of migration (e.g., weather conditions had an impact on engagement with physical activity), heritage-based practices (e.g., an obligation to consume energy-dense food in social gatherings), and chronic disease management strategies (e.g., lack understanding of appropriate disease management strategies). CONCLUSION: This review provides a comprehensive understanding of the complexity of chronic disease management among South Asian migrants and insights into developing multifaceted interventions to address barriers to chronic disease management, guiding the healthcare professionals in helping overcome South Asians perceived barriers to managing chronic disease in the host countries.


Assuntos
Doença Crônica , Estilo de Vida , População do Sul da Ásia , Migrantes , Adulto , Humanos
2.
J Biol Chem ; 296: 100714, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33930463

RESUMO

Overconsumption of sucrose and other sugars has been associated with nonalcoholic fatty liver disease (NAFLD). Reports suggest hepatic de novo lipogenesis (DNL) as an important contributor to and regulator of carbohydrate-induced hepatic lipid accumulation in NAFLD. The mechanisms responsible for the increase in hepatic DNL due to overconsumption of carbohydrate diet are less than clear; however, literatures suggest high carbohydrate diet to activate the lipogenic transcription factor carbohydrate response element-binding protein (ChREBP), which further transcribes genes involved in DNL. Here, we provide an evidence of an unknown link between nuclear factor kappa-light chain enhancer of activated B cells (NF-κB) activation and increased DNL. Our data indicates high carbohydrate diet to enforce nuclear shuttling of hepatic NF-κB p65 and repress transcript levels of sorcin, a cytosolic interacting partner of ChREBP. Reduced sorcin levels, further prompted ChREBP nuclear translocation, leading to enhanced DNL and intrahepatic lipid accumulation both in vivo and in vitro. We further report that pharmacological inhibition of NF-κB abrogated high carbohydrate diet-mediated sorcin repression and thereby prevented ChREBP nuclear translocation and this, in turn, attenuated hepatic lipid accumulation both in in vitro and in vivo. Additionally, sorcin knockdown blunted the lipid-lowering ability of the NF-κB inhibitor in vitro. Together, these data suggest a heretofore unknown role for NF-κB in regulating ChREBP nuclear localization and activation, in response to high carbohydrate diet, for further explorations in lines of NAFLD therapeutics.


Assuntos
Fatores de Transcrição de Zíper de Leucina e Hélice-Alça-Hélix Básicos/metabolismo , Núcleo Celular/efeitos dos fármacos , Carboidratos da Dieta/farmacologia , Lipogênese/efeitos dos fármacos , Fígado/metabolismo , Fator de Transcrição RelA/metabolismo , Transporte Ativo do Núcleo Celular/efeitos dos fármacos , Núcleo Celular/metabolismo , Células Hep G2 , Humanos
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