# Impact of Short‐Term Insulin Pump Therapy on Cardiometabolic Index in Patients With Newly Diagnosed Type 2 Diabetes Mellitus

**Authors:** Xia Chen, Shuya Li, Zeren Chen, Dong Wang, Ling Yang, Xia Deng, Haoxiang Li

PMC · DOI: 10.1002/edm2.70192 · Endocrinology, Diabetes & Metabolism · 2026-03-05

## TL;DR

Short-term insulin pump therapy in new type 2 diabetes patients improves blood sugar and insulin resistance while lowering a key cardiometabolic index.

## Contribution

Demonstrates the impact of short-term CSII on cardiometabolic index and its correlation with insulin resistance in newly diagnosed T2DM patients.

## Key findings

- Short-term CSII treatment significantly reduced cardiometabolic index (CMI) in T2DM patients.
- CMI was positively correlated with insulin resistance (HOMA-IR) and negatively with β-cell function (HOMA-β).
- CMI was independently associated with fasting C-peptide levels before and after treatment.

## Abstract

This study aims to investigate the changes in cardiometabolic index (CMI) levels in newly diagnosed type 2 diabetes mellitus (T2DM) patients before and after undergoing short‐term continuous subcutaneous insulin infusion (CSII) intensive treatment and analyse its correlation with insulin resistance.

This study retrospectively collected data from 604 patients who were initially diagnosed with T2DM and received short‐term CSII treatment during their hospitalisation in the Endocrinology Department of the Affiliated Hospital of Jiangsu University. Clinical data, blood glucose, insulin, C‐peptide, blood biochemistry, and other indicators were collected before and after treatment, and CMI was calculated.

Short‐term CSII treatment significantly improved blood glucose levels, insulin resistance, and pancreatic β‐cell function in T2DM patients, while downregulating the CMI index (p = 0.002). Correlation analysis showed a positive correlation between CMI and HOMA‐IR (p < 0.001) and a negative correlation between CMI and HOMA‐β (p = 0.008). Stepwise linear regression model analysis revealed that CMI was independently associated with fasting C‐peptide (FCP) before treatment (β = 0.291, p < 0.001); after treatment, CMI was associated with FCP (β = 0.160, p < 0.001) and HOMA‐IR (β = 0.159, p < 0.001).

After short‐term intensive CSII treatment, the CMI level in newly diagnosed T2DM patients significantly decreased, indicating that intensive CSII treatment may have certain significance in improving cardiometabolic function.

The study reveals that CMI levels significantly decrease after short‐term CSII therapy in T2DM, with CMI positively correlated with insulin resistance, indicating the therapy's significance in improving patients' cardiometabolic function.

## Linked entities

- **Diseases:** type 2 diabetes mellitus (MONDO:0005148), T2DM (MONDO:0005148)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, APOC3 (apolipoprotein C3) [NCBI Gene 345] {aka APOCIII, Apo-C3, ApoC-3}, LPL (lipoprotein lipase) [NCBI Gene 4023] {aka HDLCQ11, LIPD}, REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}
- **Diseases:** trauma (MESH:D014947), inflammation (MESH:D007249), CMI (MESH:D024821), dyslipidemia (MESH:D050171), coronary heart disease (MESH:D003327), mental disorders (MESH:D001523), renal failure (MESH:D051437), Alzheimer's disease (MESH:D000544), endothelial dysfunction (MESH:D014652), diabetes (MESH:D003920), malignancies (MESH:D009369), lactic acidosis (MESH:D000140), respiratory failure (MESH:D012131), gestational diabetes mellitus (MESH:D016640), Organ dysfunction (MESH:D009102), autoimmune diseases (MESH:D001327), obesity (MESH:D009765), hyperthyroidism (MESH:D006980), metabolic abnormalities (MESH:D008659), adrenal diseases (MESH:D000307), Cushing's syndrome (MESH:D003480), systemic lupus erythematosus (MESH:D008180), diabetic foot (MESH:D017719), rheumatoid arthritis (MESH:D001172), hyperglycemic (MESH:D006944), hypothyroidism (MESH:D007037), atherosclerosis (MESH:D050197), myocardial infarction (MESH:D009203), CVDs (MESH:D002318), infection (MESH:D007239), hypoglycemia (MESH:D007003), cerebrovascular disease (MESH:D002561), Insulin Resistance (MESH:D007333), T2DM (MESH:D003924), peripheral arterial disease (MESH:D058729), heart failure (MESH:D006333), diabetic peripheral neuropathy (MESH:D010523), hyperaldosteronism (MESH:D006929), diabetic ketoacidosis (MESH:D016883), Type 1 diabetes mellitus (MESH:D003922), diabetic coma (MESH:D003926), liver failure (MESH:D017093), diabetic nephropathy (MESH:D003928), abdominal obesity (MESH:D056128), impaired glucose tolerance (MESH:D018149), pheochromocytoma (MESH:D010673), Chronic complications (MESH:D002908)
- **Chemicals:** TG (MESH:D014280), C-peptide (MESH:D002096), cholesterol (MESH:D002784), blood glucose (MESH:D001786), 2hPPG (-), lipid (MESH:D008055), glucose (MESH:D005947)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

23 references — full list in the complete paper: https://tomesphere.com/paper/PMC12963456/full.md

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Source: https://tomesphere.com/paper/PMC12963456