# Rising Trends in Pediatric Type 2 Diabetes: A Comprehensive Bibliometric Analysis of Global Research (1998-2023)

**Authors:** Raju Vaishya, Anoop Misra, Brij Mohan Gupta, Ghouse Modin Naseesab Mamdapur, Abhishek Vaish

PMC · DOI: 10.31729/jnma.v63i2091.9223 · 2025-11-30

## TL;DR

This paper analyzes global research trends in pediatric Type 2 Diabetes from 1998 to 2023, showing rapid growth but uneven contributions from different regions.

## Contribution

The study provides a comprehensive bibliometric analysis of global research trends in pediatric Type 2 Diabetes over 25 years.

## Key findings

- Annual publication growth in pediatric Type 2 Diabetes research was 20.02% from 1998 to 2023.
- The USA led in research output (42%), while Finland had the highest citation impact.
- India and South Asia contributed little, indicating a need for region-specific studies.

## Abstract

Pediatric Type 2 Diabetes is a growing global concern, driven by rising childhood obesity and lifestyle factors. The study aimed to analyze global publication trends, key contributors, and collaborative networks in Pediatric Type 2 Diabetes research. A bibliometric analysis of 1,555 Scopus-indexed publications was conducted. Study types, citation metrics, and collaboration networks were evaluated. There was 20.02% annual growth (5 papers in 1998 to 99 in 2023). The USA (42%) led globally, followed by the UK, Canada, and Germany; Finland had the highest citation impact. Original research (70.6%) dominated, mainly on clinical and epidemiological themes. P. Zeitler was the most prolific author, while G. Imperatore’s works were the most cited. Strong collaborations existed between the USA and the UK, with the University of Colorado Anschutz Medical Campus as the leading institution. Pediatric Type 2 Diabetes research shows rapid expansion but limited contributions from India and South Asia, highlighting a need for region-specific studies.

## Linked entities

- **Diseases:** Type 2 Diabetes (MONDO:0005148)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, INSR (insulin receptor) [NCBI Gene 3643] {aka CD220, HHF5}
- **Diseases:** hypertension (MESH:D006973), insulin resistance (MESH:D007333), T1D (MESH:D003922), T2D (MESH:D003924), Digestive and Kidney Diseases (MESH:D007674), P-cell dysfunction (MESH:D002292), dyslipidemia (MESH:D050171), IR (MESH:C537629), Diabetes (MESH:D003920), pre (MESH:D058246), TLS (MESH:C535338), overweight (MESH:D050177), obese (MESH:D009765), IMPACTFUL (MESH:D004834), CPP (MESH:C000719203)
- **Chemicals:** saxagliptin (MESH:C502994), dapagliflozin (MESH:C529054), linagliptin (MESH:D000069476), sitagliptin (MESH:D000068900), exenatide (MESH:D000077270), metformin (MESH:D008687)

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12906719/full.md

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Source: https://tomesphere.com/paper/PMC12906719