What is the clinical evidence from this study?

Study design: Other. Population: Diabetes mellitus (n=24). Intervention: Good hyperglycemic control (insulin) vs. Poor hyperglycemic control. Primary outcome: Left ventricular ejection fraction at day 28 (p=<0.05).

January 1, 2009International Heart Journal21 citationsOpen Access

Impact of Hyperglycemic Control on Left Ventricular Myocardium A Molecular and Cellular Basic Study in a Diabetic Rat Model

Q: What are the key findings of this study?

Good hyperglycemic control in diabetic rats significantly preserved left ventricular ejection fraction (88.8% vs 85.8%, p<0.05) and attenuated myocardial inflammation compared to poor control.

PSPei‐Hsun Sung CSCheuk‐Kwan Sun SKSheung‐Fat Ko

Key Result

Good hyperglycemic control in diabetic rats significantly preserved left ventricular ejection fraction (88.8% vs 85.8%, p<0.05) and attenuated myocardial inflammation compared to poor control.

Structured PICO

Does good hyperglycemic control improve left ventricular function and reduce myocardial inflammation in a diabetic rat model?

Population

24 adult male Sprague Dawley rats, including 16 with streptozocin-induced diabetes and 8 healthy controls, followed for 28 days to assess the impact of hyperglycemic control on left ventricular function.

Intervention

Good hyperglycemic control using subcutaneous insulin (sliding scale 2-10 units/kg based on blood glucose levels) for 28 days.

Comparator

Poor hyperglycemic control (insulin 45 units/kg only if blood glucose > 200 gm/dL) and healthy normal controls.

Outcome

Left ventricular function (LVEF) and molecular/cellular markers of inflammation, apoptosis, and gap junctions (MMP-9, ET-1, PGC-1alpha, eNOS, Cx43, PKC-epsilon) at day 28.surrogate

Good glycemic control in a diabetic rat model preserves left ventricular function and attenuates myocardial inflammation and apoptosis compared to poor glycemic control.

Main Result

Absolute Event Rate: 88.8% vs 85.8%

p-value: p=<0.05

Limitations

Did not investigate the function and anatomy of coronary epicardial vessels
Timeframe of 4 weeks is too short to obtain significant results on long-term impact
Did not determine whether inflammation and cellular-molecular perturbations are elicited by hyperglycemia or an increase in blood osmolarity

Abstract

This experimental study investigated the impact of hyperglycemic control on left ventricular (LV) function using a model of diabetes mellitus (DM) (induced by streptozocin 60 mg/kg). Sixteen adult-Sprague Dawley rats were divided into group 1 (poor hyperglycemic control, n = 8) and group 2 (good hyperglycemic control, n = 8). Diabetic rats and 8 healthy rats serving as controls (group 3) were sacrificed on day 28 after DM induction. The results demonstrated that HbA(1C) on day 28 was higher in group 1 than in groups 2 and 3 (P < 0.0001). The mRNA expressions of MMP-9 and endothelin-1 were elevated in group 1 compared with that in groups 2 and 3 (P < 0.05), whereas PGC-1alpha and eNOS were lower in group 1 than in groups 2 and 3 (P < 0.05). The number of apoptotic nuclei was higher in group 1 than in groups 2 and 3 (P < 0.01). The integrated area (microm(2)) of connexin43 (Cx43), Cx43 protein expression, and LV function were lower in group 1 than in groups 2 and 3 (P < 0.05). Moreover, PKC-epsilon expression in the mitochondrial compartment was decreased in group 1 compared to that in groups 2 and 3 (P < 0.005).

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