Barriers and facilitators of lifestyle management among adult South Asian migrants living with chronic diseases: A mixed-methods systematic review.

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.

Julolidine-based small molecular probes for fluorescence imaging of RNA in live cells.

Intracellular RNA imaging with organic small molecular probes has been an intense topic, although the number of such reported dyes, particularly dyes with high quantum yields and long wavelength excitation/emission, is quite limited. The present work reports the design and synthesis of three cationic julolidine-azolium conjugates (OX-JLD, BTZ-JLD and SEZ-JLD) as turn-on fluorescent probes with appreciably high quantum yields and brightness upon interaction with RNA. A structure-efficiency relationship has been established for their potential for the interaction and imaging of intracellular RNA. Given their chemical structure, the free rotation between the donor and the acceptor gets restricted when the probes bind with RNA resulting in strong fluorescence emission towards a higher wavelength upon photoexcitation. A detailed investigation revealed that the photophysical properties and the optical responses of two probes, viz. BTZ-JLD and SEZ-JLD, towards RNA are very promising and qualify them to be suitable candidates for biological studies, particularly for cellular imaging applications. The probes allow imaging of intracellular RNA with prominent staining of nucleoli in live cells under a range of physiological conditions. The results of the cellular digest test established the appreciable RNA selectivity of BTZ-JLD and SEZ-JLD inside the cellular environment. Moreover, a comparison between the relative intensity profile of SEZ-JLD before and after the RNA-digestion test inside the cellular environment indicated that the interference of cellular viscosity in fluorescence enhancement is insignificant, and hence, SEZ-JLD can be used as a cell membrane permeable cationic molecular probe for deep-red imaging of intracellular RNA with a good degree of selectivity.

Dietary management of type 2 diabetes mellitus among South Asian immigrants: A mixed-methods study.

AIMS: There is a high prevalence of South Asian immigrants in Australia living with type 2 diabetes mellitus, with the dietary management of the condition presenting as a key challenge. However, their current dietary patterns and barriers to diabetes self-management are unclear. Therefore, this study aims to (i) investigate current dietary patterns and (ii) explore barriers and facilitators to dietary management in this population. METHODS: A concurrent mixed-methods study comprising three 24-h dietary recalls and a semi-structured interview for each self-identified South Asian immigrant adult with diabetes recruited across Victorian primary care clinics and social media to address the aforementioned two aims. Dietary recall data were converted into food groups using Foodworks, and data analysed in SPSS. Qualitative data were thematically analysed using NVivo. RESULTS: Among 18 participants recruited, 14, 16 and 17 participants had grain, fruit and dairy intake lower than daily Australian recommendations, respectively. These findings echoed qualitative data that participants viewed diabetes management as reducing carbohydrate intake. Participants reported difficulties incorporating diabetes-related dietary and lifestyle recommendations into their routine and a lack of knowledge about available organisational support. They mentioned challenges in receiving social support from families and friends and relied on support from health professionals. Facilitators included proficiency in nutrition information label reading and self-blood glucose monitoring skills. CONCLUSION: Enhancing the accessibility to organisational support, facilitating the adaption of dietary recommendations into individuals' routines, and strengthening support from health professionals are essential components in intervention development to improve diabetes management for South Asians.

Diet-induced induction of hepatic serine/threonine kinase STK38 triggers proinflammation and hepatic lipid accumulation.

Nonalcoholic fatty liver disease (NAFLD) is one of the most common liver diseases worldwide. Although the involvement of chronic overnutrition, systemic inflammation, and insulin resistance in the development of NAFLD is well-established, however, the associations among these remain to be elucidated. Several studies have reported that chronic overnutrition, such as excessive consumption of fats (high-fat diet, HFD), can cause insulin resistance and inflammation. However, the mechanisms by which HFD exerts inflammation and thereby promotes insulin resistance and intrahepatic fat accumulation remain poorly understood. Here, we show that HFD induces the expression of hepatic serine/threonine kinase 38 (STK38), which further induces systemic inflammation leading to insulin resistance. Notably, ectopic expression of STK38 in mouse liver leads to lean NAFLD phenotype with hepatic inflammation, insulin resistance, intrahepatic lipid accumulation, and hypertriglyceridemia in mice fed on a regular chow diet. Further, depletion of hepatic STK38 in HFD-fed mice remarkably reduces proinflammation, improves hepatic insulin sensitivity, and decreases hepatic fat accumulation. Mechanistically, two critical stimuli are elicited by STK38 action. For one stimulus, STK38 binds to Tank-Binding protein Kinase 1 and induces Tank-Binding protein Kinase 1 phosphorylation to promote NF-κß nuclear translocation that mobilizes the release of proinflammatory cytokines and eventually leads to insulin resistance. The second, stimulus involves intrahepatic lipid accumulation by enhanced de novo lipogenesis via reducing the AMPK-ACC signaling axis. These findings identify STK38 as a novel nutrient-sensitive proinflammatory and lipogenic factor in maintaining hepatic energy homeostasis, and it provides a promising target for hepatic and immune health.

Determining the efficacy of ginger Zingiber officinale as a potential nutraceutical agent for boosting growth performance and health status of Labeo rohita reared in a semi-intensive culture system.

A 120-day feeding trial was conducted in a pilot field setting to study the nutraceutical properties of ginger powder (GP), focusing on the growth performance and health status of Indian major carp L. rohita reared under a semi-intensive culture system. L. rohita fingerlings (average weight: 20.5 g) were divided into five groups and fed a diet with no GP supplementation (control), or a diet supplemented with GP at 5 g (GP5), 10 g (GP10), 15 g (GP15), and 20 g (GP20) per kg of feed. The study was carried out in outdoor tanks (20 m2) following a complete randomized design with three replicates for each experimental group. Dietary supplementation of GP at 15 g·kg-1 (GP15) of feed caused a significant increase in the growth performances of the fish. Results also showed that feeding of GP15 diet led to a significant improvement in the health status of fish as indicated by a marked change in the tested haematological indices (i.e., higher RBC, WBC, Hb, and Ht values), oxidative status (increased SOD and decreased LPO levels), biochemical parameters (increased HDL, decreased cholesterol, and triglycerides levels), and activities of the liver enzymes (decreased AST and ALT). Overall results suggested that dietary supplementation of GP could positively influence the growth and health status of L. rohita fingerlings, and hence could be an important natural nutraceutical for sustainable farming of carp.

Liver-Derived S100A6 Propels ß-Cell Dysfunction in NAFLD.

Nonalcoholic fatty liver disease (NAFLD) is an independent predictor of systemic insulin resistance and type 2 diabetes mellitus (T2DM). However, converse correlates between excess liver fat content and ß-cell function remain equivocal. Specifically, how the accumulation of liver fat consequent to the enhanced de novo lipogenesis (DNL) leads to pancreatic ß-cell failure and eventually to T2DM is elusive. Here, we have identified that low-molecular-weight calcium-binding protein S100A6, or calcyclin, inhibits glucose-stimulated insulin secretion (GSIS) from ß cells through activation of the receptor for the advanced glycation end products and diminution of mitochondrial respiration. Serum S100A6 level is elevated both in human patients with NAFLD and in a high-fat diet-induced mouse model of NAFLD. Although serum S100A6 levels are negatively associated with ß-cell insulin secretory capacity in human patients, depletion of hepatic S100A6 improves GSIS and glycemia in mice, suggesting that S100A6 contributes to the pathophysiology of diabetes in NAFLD. Moreover, transcriptional induction of hepatic S100A6 is driven by the potent regulator of DNL, carbohydrate response element-binding protein (ChREBP), and ectopic expression of ChREBP in the liver suppresses GSIS in a S100A6-sensitive manner. Together, these data suggest elevated serum levels of S100A6 may serve as a biomarker in identifying patients with NAFLD with a heightened risk of developing ß-cell dysfunction. Overall, our data implicate S100A6 as, to our knowledge, a hitherto unknown hepatokine to be activated by ChREBP and that participates in the hepato-pancreatic communication to impair insulin secretion and drive the development of T2DM in NAFLD.

NF-κB p65 regulates hepatic lipogenesis by promoting nuclear entry of ChREBP in response to a high carbohydrate diet.

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.