An Indigenous-informed scoping review study methodology: advancing the science of scoping reviews.

BACKGROUND: Historically, Indigenous voices have been silent in health research, reflective of colonial academic institutions that privilege Western ways of knowing. However, Indigenous methodologies and methods with an emphasis on the active involvement of Indigenous peoples and centering Indigenous voices are gaining traction in health education and research. In this paper, we map each phase of our scoping review process and weave Indigenous research methodologies into Arksey and O'Malley's (2005) framework for conducting scoping reviews. METHODS: Guided by an advisory circle consisting of Indigenous Knowledge Keepers and allied scholars, we utilized both Indigenous and Western methods to conduct a scoping review. As such, a circle of Knowledge Keepers provided guidance and informed our work, while our methods of searching and scoping the literature remained consistent with PRISMA-ScR guidelines. In keeping with an Indigenous methodology, the scoping review protocol was not registered allowing for an organic development of the research process. RESULTS: We built upon Arksey and O'Malley's 5-stages and added an additional 3 steps for a combined 8-stage model to guide our research: (1) Exploration and Listening, (2) Doing the Groundwork, (3) Identifying and Refining the Research Question, (4) Identifying Relevant Studies, (5) Study Selection, (6) Mapping Data, (7) Collating, Summarizing and Synthesizing the Data, and lastly, (8) Sharing and Making Meaning. Engagement and listening, corresponding to Arksey and O'Malley (2005)'s optional "consultation stage," was embedded throughout, but with greater intensity in stages 1 and 8. CONCLUSION: An Indigenous approach to conducting a scoping review includes forming a team with a wide array of experience in both Indigenous and Western methodologies, meaningful Indigenous representation, and inclusion of Indigenous perspectives to shape the analysis and presentation of findings. Engaging Indigenous peoples throughout the entire research process, listening, and including Indigenous voices and perspectives is vital in reconciliation research, producing both credible and useable information for both Indigenous communities and academia. Our Indigenous methodology for conducting a scoping review can serve as a valuable framework for summarizing Indigenous health-related research.

More than meets the islet: aligning nutrient and paracrine inputs with hormone secretion in health and disease.

The pancreatic islet is responsive to an array of endocrine, paracrine, and nutritional inputs that adjust hormone secretion to ensure accurate control of glucose homeostasis. Although the mechanisms governing glucose-coupled insulin secretion have received the most attention, there is emerging evidence for a multitude of physiological signaling pathways and paracrine networks that collectively regulate insulin, glucagon, and somatostatin release. Moreover, the modulation of these pathways in conditions of glucotoxicity or lipotoxicity are areas of both growing interest and controversy. In this review, the contributions of external, intrinsic, and paracrine factors in pancreatic ß-, α-, and δ-cell secretion across the full spectrum of physiological (i.e., fasting and fed) and pathophysiological (gluco- and lipotoxicity; diabetes) environments will be critically discussed.

Analysis of Hepatitis B Virus Genotype D in Greenland Suggests the Presence of a Novel Quasi-Subgenotype.

A disproportionate number of Greenland's Inuit population are chronically infected with Hepatitis B virus (HBV; 5-10%). HBV genotypes B and D are most prevalent in the circumpolar Arctic. Here, we report 39 novel HBV/D sequences from individuals residing in southwestern Greenland. We performed phylodynamic analyses with ancient HBV DNA calibrators to investigate the origin and relationship of these taxa to other HBV sequences. We inferred a substitution rate of 1.4 × 10-5 [95% HPD 8.8 × 10-6, 2.0 × 10-5] and a time to the most recent common ancestor of 629 CE [95% HPD 37-1138 CE]. The Greenland taxa form a sister clade to HBV/D2 sequences, specifically New Caledonian and Indigenous Taiwanese sequences. The Greenland sequences share amino acid signatures with subgenotypes D1 and D2 and ~97% sequence identity. Our results suggest the classification of these novel sequences does not fit within the current nomenclature. Thus, we propose these taxa be considered a novel quasi-subgenotype.

Gestational Diabetes Adversely Affects Pancreatic Islet Architecture and Function in the Male Rat Offspring.

Fetal exposure to gestational diabetes mellitus (GDM) and poor postnatal diet are strong risk factors for type 2 diabetes development later in life, but the mechanisms connecting GDM exposure to offspring metabolic health remains unclear. In this study, we aimed to determine how GDM interacts with the postnatal diet to affect islet function in the offspring as well as characterize the gene expression changes in the islets. GDM was induced in female rats using a high-fat, high-sucrose (HFS) diet, and litters from lean or GDM dams were weaned onto a low-fat (LF) or HFS diet. Compared with the lean control offspring, GDM exposure reduced glucose-stimulated insulin secretion in islets isolated from 15-week-old offspring, which was additively worsened when GDM exposure was combined with postnatal HFS diet consumption. In the HFS diet-fed offspring of lean dams, islet size and number increased, an adaptation that was not observed in the HFS diet-fed offspring of GDM dams. Islet gene expression in the offspring of GDM dams was altered in such categories as inflammation (e.g., Il1b, Ccl2), mitochondrial function/oxidative stress resistance (e.g., Atp5f1, Sod2), and ribosomal proteins (e.g., Rps6, Rps14). These results demonstrate that GDM exposure induced marked changes in gene expression in the male young adult rat offspring that cumulatively interact to worsen islet function, whole-body glucose homeostasis, and adaptations to HFS diets.

Maternal obesity, diabetes during pregnancy and epigenetic mechanisms that influence the developmental origins of cardiometabolic disease in the offspring.

Since 1980, global obesity has doubled, and the incidence of cardiometabolic diseases such as type 2 diabetes and heart disease is also increasing. While genetic susceptibility and adult lifestyle are implicated in these trends, evidence from clinical cohorts, epidemiological studies and animal model experiments support a role for early-life environmental exposures in determining the long-term health of an individual, which has led to the formulation of the Developmental Origins of Health and Disease (DOHaD) theory. In fact, maternal obesity and diabetes during pregnancy, which are on the rise, are strongly associated with altered fetal growth and development as well as with lifelong perturbations in metabolic tissues. A mounting body of evidence implicates epigenetic mechanisms (e.g. DNA methylation and histone modifications) in the regulation of these effects and their transmission to future generations. This review critically discusses the current evidence (in animal model systems and humans) that implicates maternal obesity and diabetes during pregnancy in perturbing the epigenome of the next generation, and the consequential impact on growth, organ development and ultimately cardiometabolic disease progression. Additionally, this review will address some of the limitations of the DOHaD approach and areas that require further study. For example, future research requires verification of the mechanistic impact of the epigenetic marks and their persistence over the life course. Ultimately, this knowledge is needed to establish optimal screening, prevention and therapeutic approaches for children at risk of cardiometabolic disease development.