Measurement of Insulin Resistance in Cats With Chronic Kidney Disease.

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.