# First Evaluation of Roux-en-Y Gastric Bypass as a Novel Surgical Treatment for Diabetes and Glucose Metabolism Regulation in Cats

**Authors:** Linfeng Li, Guoxiang Yuan, Qianbo Xiong, Wen Hao, Lingchen Yang

PMC · DOI: 10.3390/vetsci13030272 · Veterinary Sciences · 2026-03-16

## TL;DR

This study shows that Roux-en-Y gastric bypass surgery can effectively manage diabetes in cats by improving glucose levels and metabolic health.

## Contribution

The study introduces Roux-en-Y gastric bypass as a novel surgical treatment for feline diabetes, demonstrating its efficacy in regulating glucose and metabolic hormones.

## Key findings

- RYGB normalized blood glucose and fructosamine levels in diabetic cats.
- RYGB reduced liver fat and improved pancreatic islet morphology.
- RYGB altered metabolic hormones by decreasing GIP and increasing GLP-1.

## Abstract

Feline diabetes is typically managed with lifelong insulin. This study evaluated Roux-en-Y gastric bypass (RYGB) surgery as a novel treatment for feline diabetes. Using an induced diabetic cat model, researchers compared RYGB to standard insulin therapy. Results demonstrated that RYGB successfully normalized blood glucose and fructosamine levels. RYGB also restored metabolic hormones by decreasing GIP and increasing GLP-1. Furthermore, tissue analysis revealed that RYGB reduced liver fat accumulation and promoted morphological improvements in pancreatic islets. Ultimately, RYGB offers a promising alternative therapy with long-term remission potential for diabetic cats.

Objective: To evaluate the efficacy of Roux-en-Y gastric bypass (RYGB) in improving glucose regulation and metabolic parameters in feline diabetes mellitus (FDM). Methods: FDM was experimentally induced via partial pancreatectomy, splenectomy, and dexamethasone administration. Following insulin stabilization, the RYGB cohort underwent gastric bypass, while the medical management group received glargine insulin. Untreated diabetic controls were monitored for 12 weeks. Blood glucose (GLU), fructosamine (FRU), biochemical profiles, and metabolic hormones were evaluated pre- and post-intervention. Hepatic and pancreatic tissues were collected for histopathological examination. Results: GLU and FRU concentrations in the RYGB group were significantly lower than in diabetic controls (p < 0.05), remaining comparable to the insulin-treated group (p > 0.05). Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were significantly reduced post-RYGB (p < 0.05), closely matching insulin therapy outcomes (p > 0.05). Hormonal assays demonstrated decreased gastric inhibitory polypeptide (GIP) and elevated glucagon-like peptide-1 (GLP-1) in RYGB cats. Histopathologically, the RYGB group exhibited attenuated hepatic steatosis and a higher density of pancreatic islet cells with abundant cytoplasm compared to the control groups. Conclusions: RYGB effectively restores glycemic control and metabolic hormone balance in FDM, promoting morphological improvements in pancreatic islets and offering a highly promising alternative therapy for diabetic felines.

## Linked entities

- **Proteins:** GIP (gastric inhibitory polypeptide), GCG (glucagon)
- **Chemicals:** glargine (PubChem CID 118984454), dexamethasone (PubChem CID 5743)
- **Diseases:** diabetes (MONDO:0005015)

## Full-text entities

- **Genes:** GLP-1 [NCBI Gene 101097825], INS [NCBI Gene 493804], SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, GIP (gastric inhibitory polypeptide) [NCBI Gene 2695], INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, GIP [NCBI Gene 101080591], GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}
- **Diseases:** Pancreas (MESH:D010190), FDM (MESH:D003920), mesenteric defect (MESH:D008639), lipid metabolism disturbances (MESH:D052439), cardiovascular dysfunction (MESH:D002318), polydipsia (MESH:D059606), hepatic lipidosis (MESH:D008064), lethargy (MESH:D053609), Obesity (MESH:D009765), T2DM (MESH:D003924), diabetic complications (MESH:D048909), injury to (MESH:D014947), insulin resistance (MESH:D007333), dyslipidemia (MESH:D050171), malabsorption (MESH:D008286), beta-cell dysfunction (MESH:D007340), multiorgan failure (MESH:D051437), vomiting (MESH:D014839), fatty liver (MESH:D005234), Inflammatory (MESH:D007249), edema (MESH:D004487), -cell dysfunction (MESH:D002292), liver dysfunction (MESH:D017093), jaundice (MESH:D007565), hyperglycemia (MESH:D006943), hepatic dysfunction (MESH:D008107), diabetic nephropathy (MESH:D003928), polyuria (MESH:D011141), weight loss (MESH:D015431), gastric restriction (MESH:D002313), impaired glucose metabolism (MESH:D044882), impaired glucose regulation (MESH:C565631), metabolic derangements (MESH:D008659), endocrinopathy (MESH:C567425), deteriorating renal function (MESH:D058186), hepatopathy (MESH:D020754), pancreatic amyloid deposition (MESH:D058225)
- **Chemicals:** lipid (MESH:D008055), xylene (MESH:D014992), propofol (MESH:D015742), TG (MESH:D014280), dexamethasone (MESH:D003907), glargine (MESH:D000069036), eosin (MESH:D004801), paraformaldehyde (MESH:C003043), ethanol (MESH:D000431), Glucose Metabolism Hormone (-), sodium chloride (MESH:D012965), GLU (MESH:D005947), water (MESH:D014867), hematoxylin (MESH:D006416), dexmedetomidine hydrochloride (MESH:D020927), C-peptide (MESH:D002096), Blood Glucose (MESH:D001786), H&amp;E (MESH:D006371), dexamethasone sodium phosphate (MESH:C004180), FRU (MESH:D019270), paraffin (MESH:D010232), isoflurane (MESH:D007530), Cr (MESH:D003404)
- **Species:** Homo sapiens (human, species) [taxon 9606], Felis catus (cat, species) [taxon 9685]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13030486/full.md

## Figures

10 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13030486/full.md

## References

32 references — full list in the complete paper: https://tomesphere.com/paper/PMC13030486/full.md

---
Source: https://tomesphere.com/paper/PMC13030486