# Association between estimated glucose disposal rate and cognitive impairment in elderly patients with type 2 diabetes mellitus: a cross-sectional study

**Authors:** Tong Chen, Hui-Na Qiu, Xin-Ping Zhang, Fan Wu, Yan-Lan Liu, Jing-Bo Li, Jing-Na Lin

PMC · DOI: 10.3389/fendo.2026.1690654 · Frontiers in Endocrinology · 2026-02-18

## TL;DR

This study found that better glucose disposal in elderly type 2 diabetes patients is linked to lower risk of cognitive impairment, but only up to a certain threshold.

## Contribution

The study reveals a nonlinear relationship between estimated glucose disposal rate and cognitive impairment in elderly T2DM patients.

## Key findings

- Lower eGDR levels were significantly associated with cognitive impairment in elderly T2DM patients.
- Each unit increase in eGDR reduced the risk of cognitive impairment by 8% after adjusting for covariates.
- A nonlinear relationship was observed, with no significant association when eGDR was ≥6.36 mg/kg/min.

## Abstract

Insulin resistance (IR) is a fundamental pathophysiological characteristic of type 2 diabetes mellitus (T2DM) and is intricately related to neurodegeneration. This study sought to investigate the correlation between estimated glucose disposal rate (eGDR), an easily accessible and effective indicator of IR, and cognitive impairment (CI) in elderly patients with T2DM.

This cross-sectional study included 871 elderly patients with T2DM. The eGDR was calculated from glycated hemoglobin (HbA1c), waist circumference and hypertension status to evaluate the extent of IR in patients. Cognitive function was assessed in all participants utilizing the Montreal Cognitive Assessment (MoCA). Linear and logistic regression analyses were performed to evaluate the association between eGDR and cognitive function. Restricted cubic spline (RCS) analysis and threshold effect analysis were conducted to elucidate the nonlinear relationship between eGDR and CI.

The eGDR levels were significantly lower in the CI group compared to the normal cognition group. Linear regression analysis indicated that eGDR was positively correlated with MoCA scores when expressed as continuous or categorical data after fully adjusting for covariates. Logistic regression analysis revealed that, after adjusting for all covariates, each unit increase in eGDR was associated with an 8% reduction in the risk of CI (OR: 0.92, 95% CI: 0.85-0.99, P < 0.05). Participants in the highest eGDR quartile exhibited a 38% lower risk of CI compared to those in the lowest eGDR quartile (OR: 0.62, 95% CI: 0.39-0.99, P < 0.05). RCS analysis and threshold effect analysis demonstrated a nonlinear relationship between eGDR and CI (P for non-linearity=0.001). When eGDR was<6.36 mg/kg/min, the risk of CI decreased with increasing eGDR levels (OR: 0.72, 95% CI: 0.61-0.86, P < 0.001). However, no significant association was observed when eGDR was≥6.36 mg/kg/min. Sensitivity analysis revealed a significant linear positive correlation between homeostatic model assessment (HOMA)2-IR and the risk of CI.

In elderly patients with T2DM, eGDR is significantly associated with cognitive function, exhibiting a nonlinear relationship with the risk of CI. This finding provides novel insights for the prevention and management of CI.

## Linked entities

- **Diseases:** type 2 diabetes mellitus (MONDO:0005148)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, INSR (insulin receptor) [NCBI Gene 3643] {aka CD220, HHF5}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, APP (amyloid beta precursor protein) [NCBI Gene 351] {aka AAA, ABETA, ABPP, AD1, APPI, CTFgamma}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}
- **Diseases:** brain tumors (MESH:D001932), CI (MESH:D003072), T2DM (MESH:D003924), neuronal damage (MESH:D009410), Type 1 diabetes mellitus (MESH:D003922), dementia (MESH:D003704), CAD (MESH:D003324), cardiovascular disease (MESH:D002318), IR (MESH:D007333), CVD (MESH:D002561), vascular damage (MESH:D057772), epilepsy (MESH:D004827), cerebral microvascular damage (MESH:D017566), anemia (MESH:D000740), vascular dementia (MESH:D015140), hyperglycemic (MESH:D006944), Hypertension (MESH:D006973), hyperinsulinemic-euglycemic (MESH:D044903), hypoglycemic (MESH:C000721848), major depressive disorder (MESH:D003865), impairments in hearing (MESH:D034381), cerebral small vessel disease (MESH:D059345), metabolic disorders (MESH:D008659), cerebral arteriosclerosis (MESH:D002537), endothelial dysfunction (MESH:D014652), Diabetes (MESH:D003920), malignant tumors (MESH:D009369), psychiatric disorders (MESH:D001523), AD (MESH:D000544), MCI (MESH:D060825), neurotoxic (MESH:D020258), DM (MESH:D009223), neuroinflammation (MESH:D000090862), impaired glucose metabolism (MESH:D044882), schizophrenia (MESH:D012559), traumatic brain injury (MESH:D000070642), Hyperglycemia (MESH:D006943), neurodegeneration (MESH:D019636), inflammation (MESH:D007249), hepatic or renal dysfunction (MESH:D008107), Parkinson's disease (MESH:D010300)
- **Chemicals:** alcohol (MESH:D000438), glucose (MESH:D005947), ATP (MESH:D000255), FPG (-), C-peptide (MESH:D002096), cholesterol (MESH:D002784), AGEs (MESH:D017127), TG (MESH:D014280), sugar (MESH:D000073893)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

63 references — full list in the complete paper: https://tomesphere.com/paper/PMC12957066/full.md

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Source: https://tomesphere.com/paper/PMC12957066