Bastan Idil, Cayiroglu Cem Turker, Kaya Kartal Yeliz, Sel Tevhide
Department of Internal Medicine, Faculty of Veterinary Medicine, Ankara University, Ankara, Turkey.
Department of Biochemistry, Faculty of Veterinary Medicine, Ankara University, Ankara, Turkey.
Vet Med Sci. 2025 May;11(3):e70383. doi: 10.1002/vms3.70383.
BACKGROUND: Chronic renal failure in cats is frequently associated with several well-known consequences, including uremia, hypertension, anaemia and secondary hyperparathyroidism. In contrast to extensive studies on insulin resistance and impaired glucose homeostasis in humans with chronic kidney disease (CKD), there is a lack of research addressing these metabolic alterations in cats with CKD. Understanding the metabolic changes associated with CKD in cats is essential for effective clinical management and for enhancing our knowledge of the disease's pathophysiology. Therefore, this study aimed to evaluate insulin secretion, glucose concentrations and homoeostasis model assessment of insulin resistance (HOMA-IR) in non-diabetic cats diagnosed with stage 3-4 CKD. METHODS: Ten clinically healthy cats (healthy controls) and fifteen non-diabetic cats with CKD) were included in the study. Fasting blood glucose, insulin, urea, creatinine, phosphor, calcium, sodium, chlorine, potassium, albumin and total protein levels were analysed in all the patients. The HOMA-IR index was calculated to show the existence of insulin resistance. RESULTS: Serum samples from 25 cats were analysed, including 15 with CKD and 10 healthy controls. Cats with CKD exhibited significantly lower serum insulin concentrations (6.05 ± 2.45pg/mL) compared to healthy cats (19.08 ± 5.01pg/mL; p < 0.001). Glucose concentrations in cats with CKD (149.89 ± 61.49) were notably higher than those in healthy controls (93.02 ± 7.39; p < 0.001). The HOMA-IR score was significantly lower in cats with CKD (0.31 ± 0.15) compared to the control group (0.62 ± 0.16; p < 0.001). LIMITATIONS: The limitations of this study include a small sample size, the absence of histopathological assessments and the failure to fully characterise the inflammatory status of the subjects. CONCLUSION: Our findings indicate that, unlike in humans, insulin levels and HOMA-IR are lower in cats with CKD, suggesting a potential mechanism of β-cell dysfunction and reduced insulin secretion contributing to hyperglycaemia. Future research focused on oxidative stress in conjunction with pro-inflammatory cytokines, inflammatory mediators and serum fPLI concentrations may be crucial for understanding the pathogenesis of hypoinsulinaemia in cats with CKD.
背景：猫的慢性肾衰竭常伴有多种众所周知的后果，包括尿毒症、高血压、贫血和继发性甲状旁腺功能亢进。与对慢性肾脏病（CKD）患者胰岛素抵抗和葡萄糖稳态受损的广泛研究相比，针对患有CKD的猫的这些代谢改变的研究较少。了解与猫CKD相关的代谢变化对于有效的临床管理以及增进我们对该疾病病理生理学的认识至关重要。因此，本研究旨在评估诊断为3 - 4期CKD的非糖尿病猫的胰岛素分泌、血糖浓度和胰岛素抵抗稳态模型评估（HOMA-IR）。 方法：本研究纳入了10只临床健康的猫（健康对照组）和15只患有CKD的非糖尿病猫。分析了所有患者的空腹血糖、胰岛素、尿素、肌酐、磷、钙、钠、氯、钾、白蛋白和总蛋白水平。计算HOMA-IR指数以显示胰岛素抵抗的存在。 结果：分析了25只猫的血清样本，包括15只患有CKD的猫和10只健康对照。与健康猫（19.08±5.01pg/mL；p<0.001）相比，患有CKD的猫血清胰岛素浓度显著降低（6.05±2.45pg/mL）。患有CKD的猫的血糖浓度（149.89±61.49）明显高于健康对照组（93.02±7.39；p<0.001）。与对照组（0.62±0.16；p<0.001）相比，患有CKD的猫的HOMA-IR评分显著降低（0.31±0.15）。 局限性：本研究的局限性包括样本量小、缺乏组织病理学评估以及未能充分表征受试者的炎症状态。 结论：我们的研究结果表明，与人类不同，患有CKD的猫的胰岛素水平和HOMA-IR较低，提示β细胞功能障碍和胰岛素分泌减少可能是导致高血糖的潜在机制。未来针对氧化应激与促炎细胞因子、炎症介质和血清fPLI浓度的研究可能对于理解患有CKD的猫低胰岛素血症的发病机制至关重要。
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