ABSTRACT
Purpose: The COVID-19 pandemic has shown a rise in pediatric diabetes. Studies have indicated an increased likelihood of children with COVID-19 infection developing diabetes. Our objective was to assess not only for an increase in pediatric diabetes at our hospital and identify possible risk factors but also to correlate psychosocial changes resulting from the pandemic with new-onset diabetes during this time. Methods: We analyzed data from 58 children aged 1-18 years admitted to our hospital with new-onset diabetes between March 2020 and December 2021, including inflammatory biomarkers and SARS-CoV-2 antibodies (Ab), as well as results of a lifestyle questionnaire. Results: Average monthly hospital admissions for new-onset diabetes rose from 10 to 18 with the start of the pandemic. Of the 58 children in our analysis, 33% had positive SARS-CoV-2 IgG Ab, 31% had type 1 diabetes mellitus (T1DM), and 62% had type 2 diabetes mellitus (T2DM). More than half (54%) were in DKA. Those with T2DM were older, majority African American, had higher median BMI percentiles, and lower Vitamin D levels. There were no significant correlations between any psychosocial risk factors and either diabetes type or SARS-CoV2 Ab status. Conclusions: Despite the increased incidence of new-onset diabetes among children in Mississippi during the pandemic, this study was unable to demonstrate significant correlations between COVID-19 infection and new-onset diabetes. This study highlighted the correlation between increased BMI and type 2 diabetes, which speaks to the significant problem of obesity and diabetes in Mississippi and the need for further research.
ABSTRACT
Body growth is rapid in infancy but subsequently slows and eventually ceases due to a progressive decline in cell proliferation that occurs simultaneously in multiple organs. We previously showed that this decline in proliferation is driven in part by postnatal down-regulation of a large set of growth-promoting genes in multiple organs. We hypothesized that this growth-limiting genetic program is orchestrated by microRNAs (miRNAs). Bioinformatic analysis identified target sequences of the miR-29 family of miRNAs to be overrepresented in age-down-regulated genes. Concomitantly, expression microarray analysis in mouse kidney and lung showed that all members of the miR-29 family, miR-29a, -b, and -c, were strongly up-regulated from 1 to 6 weeks of age. Real-time PCR confirmed that miR-29a, -b, and -c were up-regulated with age in liver, kidney, lung, and heart, and their expression levels were higher in hepatocytes isolated from 5-week-old mice than in hepatocytes from embryonic mouse liver at embryonic day 16.5. We next focused on 3 predicted miR-29 target genes (Igf1, Imp1, and Mest), all of which are growth-promoting. A 3'-untranslated region containing the predicted target sequences from each gene was placed individually in a luciferase reporter construct. Transfection of miR-29 mimics suppressed luciferase gene activity for all 3 genes, and this suppression was diminished by mutating the target sequences, suggesting that these genes are indeed regulated by miR-29. Taken together, the findings suggest that up-regulation of miR-29 during juvenile life drives the down-regulation of multiple growth-promoting genes, thus contributing to physiological slowing and eventual cessation of body growth.
