RESUMEN
INTRODUCTION: Monitoring, Evaluation and Learning (MEL) is an integral part of research, programme and policy development and implementation. However, MEL methods used to monitor and evaluate interdisciplinary research projects are often informal and under-reported. This article describes the MEL protocol of the UKRI GCRF Action Against Stunting Hub (AASH). METHODS AND ANALYSIS: The AASH conducts interdisciplinary research into childhood stunting in India, Indonesia and Senegal across 23 distinct work packages. Project-specific MEL framework and methods will be implemented. A logframe will be developed to monitor and evaluate the research activities across the field sites including the number of participants recruited, questionnaires, measurements and procedures completed. MEL dashboards using Tableau and Glasscubes will be used to track and report progress, milestones and outcomes of the project. Dashboard outputs will be reported as numbers and percentages, with additional graphs/charts for easy visualisation. A 'learning' framework will be developed to outline appropriate pipelines for the dissemination of the research findings. This includes a theory of change explicating the overarching ambitions of the project in influencing policy, practice and research, and strategic engagement of relevant stakeholders to evaluate knowledge, attitudes and best practices for impactful engagement and dissemination of the research findings. ETHICS AND DISSEMINATION: Ethical approval was granted by the Ethics Committee of the London School of Hygiene & Tropical Medicine (17915/RR/17513); National Institute of Nutrition (ICMR)-Ministry ofâ¯Health and Family Welfare, Government of India (CR/04/I/2021); Health Research Ethics Committee, University of Indonesia and Cipto Mangunkusumo Hospital (KET-887/UN2.F1/ETIK/PPM.00.02/2019); and the National Ethics Committee for Health Research (CNERS), Senegal (Protocole SEN19/78). Findings from this work will be published in peer-reviewed journals, presented in conferences and disseminated to policy makers and research communities.
Asunto(s)
Trastornos del Crecimiento , Investigación Interdisciplinaria , Humanos , India/epidemiología , Indonesia/epidemiología , Trastornos del Crecimiento/epidemiología , Trastornos del Crecimiento/prevención & control , Senegal/epidemiología , Preescolar , Niño , Proyectos de Investigación , Evaluación de Programas y Proyectos de SaludRESUMEN
Fibroblast growth factor 21 (FGF21) has emerged as a pleiotropic hormone and is known for its beneficiary roles in the management of diabetes and hyperglycaemia. However, the role of FGF21 during the transition from prediabetes to diabetes still remains unclear. Hence, the present study is aimed to understand the regulation of glucose homeostasis by FGF21 during the transition from prediabetes to diabetes in WNIN/GR-Ob rats. A total of 36 WNIN/GR-Ob obese male rats (28 days old) were divided into control and high sucrose (HS) groups and were fed ad libitum with their respective diets. These groups were sacrificed at different time points (week 1, 6, and 12) and various physical, biochemical, and molecular mediators were assessed to address FGF21 mediated glucose homeostasis. The study results revealed that rats developed impaired glucose tolerance and insulin resistance by exhibiting delayed glucose clearance from circulation, elevated fasting insulin, increased AUC glucose and HOMA-IR scores significantly; thereby rats demonstrated prediabetes by week 6 and diabetes complications by week 12. In line with the above, differential expression of genes attributed to FGF21 mediated glucose homeostasis, i.e., PPARα, FGF21, ß-klotho, PPARγ, Adiponectin, Akt, and UCP1 suggest that the acute insulin sensitizing effect of FGF21 was significantly impaired during prediabetes to diabetes transition. In addition, increased gene and protein expression of FGF21 during the transition compared to controls could be a compensatory response to possibly counteract the metabolic stress imposed by high sucrose diet in WNIN/GR-Ob rats of the experimental group. Findings from the current study emphasize the potential role of FGF21 in glucose homeostasis and its attenuation might aggravate glucose impairment during the transition from prediabetes to diabetes in high sucrose diet induced WNIN/GR-Ob rats.
Asunto(s)
Glucemia/metabolismo , Diabetes Mellitus/etiología , Sacarosa en la Dieta , Factores de Crecimiento de Fibroblastos/metabolismo , Estado Prediabético/etiología , Animales , Diabetes Mellitus/sangre , Diabetes Mellitus/metabolismo , Modelos Animales de Enfermedad , Glucuronidasa/metabolismo , Homeostasis , Proteínas Klotho , Masculino , Obesidad/complicaciones , PPAR alfa/metabolismo , Estado Prediabético/sangre , Estado Prediabético/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Ratas , Transducción de Señal , Proteína Desacopladora 1/metabolismoRESUMEN
Obesity is a multifactorial disorder, caused mainly due to lifestyle changes, and increased consumption of calorie dense diets is not just limited to developed countries anymore. Chronic physiological stress and oxidative stress are known to be implicated in the etiology of obesity. However, the role of stress response towards obesity manifestation in genetically different rat strains is poorly understood. In the current study we have used obesity susceptible & resistant rat models to understand the role of both glucocorticoid and oxidativestress in the pathophysiology of obesity. Upon challenge with calorie dense diets, WNIN showed an increased glucocorticoid stress, resulting in increased oxidative stress; whereas such a phenomenon was not noticed in F-344 and SD. However, there was an increase in the circulatory melatonin levels in calorie dense fed groups of both F-344 and SD animals, which might have contributed to reduced oxidative stress. The molecular switch in the activation of melatonin could be possibly attributed to the genetic differences among these strains. It will be interesting to explore other molecular mechanisms for melatonin regulation, albeit increased corticosterone is implicated in the enhanced production of melatonin.