Comparing long-term outcomes of children treated with new-onset type 2 diabetes in an outpatient versus inpatient setting: A retrospective chart review.

BACKGROUND: Early identification and management of pediatric type 2 diabetes mellitus (T2DM) is crucial for improving long-term outcomes. This study aimed to assess if the severity of T2DM at presentation, inferred by the location of treatment initiation (inpatient or outpatient), influences long-term clinical outcomes. METHODS: A retrospective chart review was conducted on 116 pediatric T2DM patients. Data on treatment initiation location, initial and subsequent glycated hemoglobin (HbA1c) levels, prescribed insulin, and body mass index were collected from electronic medical records. RESULTS: Of the 116 patients, 69 were initially treated in an inpatient setting, and 47 received outpatient treatment. At treatment initiation, the inpatient group had significantly higher HbA1c levels compared to the outpatient group (p < .001), but 3 years after treatment initiation, no significant difference in HbA1c was observed between the two groups (p = .057). Prescribed insulin dosages were higher in the inpatient group at treatment initiation (p < .001) and remained higher after 3 years (p < 0.003) compared to the outpatient group. CONCLUSIONS: Pediatric patients initially treated in an inpatient setting had poorer glycemic control and higher prescribed insulin dosing at baseline. After 3 years, there was no significant difference in HbA1c levels, but patients treated as inpatients continued to have higher prescribed insulin. These findings suggest that the severity of diabetes at initial presentation may affect long-term clinical outcomes in children with T2DM.

Impact of SARS-CoV2 on youth onset type 2 diabetes new diagnoses and severity.

INTRODUCTION: Initial reports show an increase in youth onset type 2 diabetes during the COVID-19 pandemic. We aim to expand on existing evidence by analyzing trends over a longer period. OBJECTIVES: Our study aims to describe change in the amount, severity, and demographics of youth onset type 2 diabetes diagnoses during the COVID-19 pandemic compared to the five years before. METHODS: We performed a retrospective cross-sectional review of youth (age ≤ 21) diagnosed with type 2 diabetes during the COVID-19 pandemic (1 May 2020-30 April 2021) and the five years before (1 May 2015-30 April 2020) at a tertiary care center. Children were identified by International Classification of Diseases codes. Charts were reviewed to confirm diagnosis. Chi-square, t tests, and Fisher's exact tests were used for analyses. RESULTS: In the prepandemic era annual diagnoses of type 2 diabetes ranged from 41-69 (mean = 54.2), whereas during the pandemic period 159 children were diagnosed, an increase of 293%. The increase resulted in a higher incidence rate ratio during the pandemic than before, 2.77 versus 1.07 (p = .006). New diagnoses increased most, by 490%, in Non-Hispanic Black patients. The average HbA1c at presentation was higher during the pandemic (9.5% ± 2.6) (79.9 mmol/mol ± 28.2) than before (8.7%±2.1) (72.1 mmol/mol ± 23.1) (p = .003). Of those diagnosed during the pandemic, 59% were tested for COVID-19 and three tested positive. CONCLUSIONS: New diagnoses of type 2 diabetes increased during the pandemic, most notably in Non-Hispanic Black youth. There was not a significant correlation found with clinical or biochemical COVID-19 infection in those tested.

Metabolic factors in the development of hepatic steatosis and altered mitochondrial gene expression in vivo.

The objective of the study was to understand the role in vivo of elevated plasma free fatty acids (FFA), insulin, and glucose levels in the development of steatosis and altered mitochondrial gene/protein expression. We studied 4 groups of Sprague-Dawley rats: (1) high-fat diet (HFD), (2) high-dose streptozotocin-induced diabetes (T1DM), (3) low-dose streptozotocin-induced diabetic rats on an HFD (T2DM), and (4) controls. Liver histology and expression of genes/proteins related to mitochondrial fatty acid oxidation and biogenesis were analyzed. Despite an attempt to compensate by increasing expression of genes of fatty acid oxidation (carnitine palmitoyl transferase-1/medium chain acyl-CoA dehydrogenase), the HFD and diabetic groups developed marked steatosis and suffered a significant reduction in mitochondrial biogenesis gene expression (nuclear respiratory factor 1/transcriptional factor A, mitochondrial). In T2DM rats, the combination of high glucose and FFA unexpectedly did not lead to greater fat accumulation than HFD alone. Greater steatosis in HFD vs T2DM (P < .001) correlated with impairment in the gene expression of PPAR-α (ie, fatty acid oxidation) and PGC1α, a major coactivator for mitochondrial biogenesis. Steatosis was not severe in insulin-deficient T1DM rats despite very elevated FFA and glucose levels. Increased carnitine palmitoyl transferase-1/medium chain acyl-CoA dehydrogenase/PPAR-α gene expression suggested inadequate adaptation to high FFA in both T1DM/T2DM rats. Hyperinsulinemia combined with elevated FFA is the key metabolic factor driving hepatic lipogenesis in vivo (HFD rats). Mitochondrial biogenesis (nuclear respiratory factor 1; transcriptional factor A, mitochondrial) is highly susceptible to FFA-induced steatosis. In contrast, hyperglycemia does not have an additive effect (T2DM) and leads to only a modest degree of steatosis in the absence of hyperinsulinemia, even when FFA are extremely elevated as in T1DM rats.