Association of inflammation with glycemic control, insulin sensitivity, and beta-cell function in diabetic cats.

Beta-cell function, not inflammation, determines glycemic control in diabetic cats.

This retrospective study investigated the relationship between inflammation (measured by acute phase proteins: serum amyloid A, α-1-acid glycoprotein, and haptoglobin) and glycemic control, beta-cell function, and insulin resistance in 69 diabetic cats treated with long-acting insulin or insulin plus exenatide. Serial serum samples were collected at enrollment and months 1, 3, and 6. While glycemic control, beta-cell function, and insulin resistance all improved over the study period, no significant associations were found between acute phase reaction markers and fructosamine concentration (glycemic control quality), beta-cell function measures, or insulin resistance markers. However, beta-cell function demonstrated a strong positive association with glycemic control (P<0.001). Acute phase reaction was also not associated with comorbidities. These findings suggest that in diabetic cats, inflammatory status does not predict poor glycemic control, but preserved beta-cell function is a critical determinant of achieving better glycemic control. This contrasts with human diabetes where inflammation plays a significant role.

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