Eggs for Improving Nutrition, cognitive development and reducing linear growth retardation among Infants and young Children (ENRICH) : Protocol of an egg supplementation trial among children aged 9-18 months in Hyderabad, India

SKB, SRC and BK: conceptualised, designed the study and wrote first draft. LFA, TD, DPP, MC, KS and PA: developed detailed protocols, planned data collection, critical input to manuscript. RM, HD-K, CH, SFR, RPullakhandam, RPalika, RRK, RNK, MLJ and PH: concept, design, critical inputs to manuscript.Peer reviewe

Epigenetic studies in children at risk of stunting and their parents in India, Indonesia and Senegal : A UKRI GCRF Action Against Stunting Hub protocol paper

ASR provided research and organisational support within the Action Against Stunting Hub (AASH) epigenetics theme and drafted and revised the manuscript. MN led the AASH epigenetic theme in Senegal and oversees the implementation of the epigenetic protocol and contributed to the development of the protocol and critically revised the manuscript. RRK led the AASH epigenetic theme in India and oversaw the implementation of the epigenetic protocol, contributed to the development of the protocol and critically revised the manuscript. MKH led the AASH epigenetic theme in Indonesia and oversaw the implementation of the epigenetic protocol, contributed to the development of the protocol and critically revised the manuscript. DYD was responsible for monitoring evaluation and learning on the hub, critically reviewed the protocol and revised the manuscript. LFA managed the implementation of the study in India, critically reviewed the protocol and revised the manuscript. NLZ managed the implementation of the study in Indonesia, critically reviewed the protocol and revised the manuscript. AD managed the implementation of the study in Senegal, critically reviewed the protocol and revised the manuscript. DY, TCA and MN are epigenetic researchers in Indonesia, critically reviewed the protocol and reviewed the manuscript. MG, DS, SSV and MM are epigenetic researchers in India, critically reviewed the protocol and reviewed the manuscript. GWH advised on the statistical aspects of the protocol and the power calculation and reviewed the manuscript. UF is the AASH project lead in Indonesia, contributed to study design and coordination of the study and thematic linkages; supervised drafting of the manuscript. BF is the AASH project lead in Senegal, contributed to study design and coordination of the study and thematic linkages and supervised drafting of the manuscript. BK is the AASH project lead in India, contributed to study design and coordination of the study and thematic linkages and supervised drafting of the manuscript. PH is the AASH project deputy lead and epigenetic theme lead who designed the study, drafted and revised the manuscript, carried out the statistical calculations.Peer reviewe

Eggs for Improving Nutrition, cognitive development and reducing linear growth retardation among Infants and young Children (ENRICH): protocol of an egg supplementation trial among children aged 9-18 months in Hyderabad, India.

INTRODUCTION: Evidence on the impact of nutrient-rich animal source foods such as eggs for improving child growth and cognition is inconsistent. This study aims to examine the impact of an egg intervention in children, along with behaviour change communication (BCC) to the mother, on linear growth and cognition, and nutritional status in children aged 9-18 months. METHODS AND ANALYSIS: A 9-month open-labelled randomised controlled trial will be conducted in three urban slums in Hyderabad, India, as a substudy of an observational cohort study (n=350) following pregnant women and their children until 18 months of age in a population at risk of stunting. The children born to women enrolled during the third trimester of pregnancy will be block randomised in a 1:4 ratio into the intervention (n=70) and control (n=280) groups. Children in the intervention group will be supplemented with one egg per day starting from 9 months until 18 months of age. BCC designed to enhance adherence to the intervention will be used. The control group will be a part of the observational cohort and will not receive any intervention from the study team. The primary outcome will be length-for-age z-scores, and the secondary outcomes will include cognition, blood biomarkers of nutritional status including fatty acid profile and epigenetic signatures linked with linear growth and cognition. Multivariate intention-to-treat analyses will be conducted to assess the effect of the intervention. ETHICS AND DISSEMINATION: The study is approved by the Institutional ethics committees of ICMR-National Institute of Nutrition, Hyderabad, India and London School of Hygiene and Tropical Medicine, UK. The results will be published in peer-reviewed journals and disseminated to policy-makers. Findings will also be shared with study participants and community leaders. TRIAL REGISTRATION NUMBER: CTRI/2021/11/038208

Attenuation of FGF21 signalling might aggravate the impairment of glucose homeostasis during the high sucrose diet induced transition from prediabetes to diabetes in WNIN/GR-Ob rats

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, β-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

Obese Locus in WNIN/Obese Rat Maps on Chromosome 5 Upstream of Leptin Receptor

<div><p>WNIN/Obese (WNIN/Ob) rat a new mutant model of metabolic syndrome was identified in 1996 from an inbred Wistar rat strain, WNIN. So far several papers are published on this model highlighting its physical, biochemical and metabolic traits. WNIN/Ob is leptin resistant with unaltered leptin or its receptor coding sequences - the two well-known candidate genes for obesity. Genotyping analysis of F₂ progeny (raised from WNIN/Ob × Fisher - 344) in the present study localized the mutation to a recombinant region of 14.15cM on chromosome 5. This was further corroborated by QTL analysis for body weight, which narrowed this region to 4.43 cM with flanking markers D5Rat256 & D5Wox37. Interval mapping of body weight QTL shows that the LOD score peak maps upstream of leptin receptor and shows an additive effect suggesting this as a novel mutation and signifying the model as a valuable resource for studies on obesity and metabolic syndrome. </p> </div

Genetic map distances (cM) were estimated between the markers using F₂ progeny genotype data (n=68).

<p>Genetic map distances (cM) were estimated between the markers using F₂ progeny genotype data (n=68).</p

Boxplot showing distribution of body weights in the three phenotypes of F₂ progeny rats, Lean(n=77), Carrier(n=151) and Obese(n=71).

<p>Boxplot showing distribution of body weights in the three phenotypes of F₂ progeny rats, Lean(n=77), Carrier(n=151) and Obese(n=71).</p