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Published on: September 18, 2017
Preserved postischemic heart function in sucrose-fed type 2 diabetic OLETF rats
Hong Chen1, Hideaki Higashino, Zdravko A Kamenov
1Department of Pharmacology, Second Military Medical University, 800 Xiang Yin Road, Shanghai 200433, China. hchen100@hotmail.com
Insights
Diabetic hearts show impaired function and ischemia tolerance. Sucrose feeding in type 2 diabetic rats improved heart function post-ischemia, possibly due to reduced cardiac norepinephrine release.
Area of Science:
- Cardiology
- Endocrinology
- Diabetology
Background:
- Cardiovascular disease is a major complication of diabetes mellitus.
- Diabetic heart dysfunction and ischemia tolerance remain areas of debate.
- Understanding these mechanisms is crucial for managing diabetic patients.
Purpose of the Study:
- To investigate ischemic heart function in type 2 diabetic rats.
- To explore the relationship between hyperglycemia and cardiac norepinephrine release.
- To assess the impact of sucrose feeding on diabetic heart ischemia tolerance.
Main Methods:
- Utilized Otsuka Long-Evans Tokushima Fatty (OLETF) and Long-Evans Tokushima Otsuka (LETO) rats.
- Administered sucrose to a group of OLETF rats (OLETF-S) to exacerbate hyperglycemia.
- Isolated and perfused hearts using a working heart preparation, subjected to ischemia-reperfusion, and measured hemodynamics and norepinephrine overflow.
Main Results:
- OLETF rats exhibited marked hyperglycemia, further worsened by sucrose feeding.
- Baseline cardiac output was reduced in OLETF rats but preserved in OLETF-S rats.
- OLETF hearts showed poor post-ischemic function, while OLETF-S hearts were resistant to ischemia, with lower norepinephrine release.
Conclusions:
- OLETF rat hearts are vulnerable to ischemia, but sucrose feeding confers resistance.
- Reduced cardiac norepinephrine release may protect sucrose-fed diabetic hearts from post-ischemic damage.
- This study sheds light on the complex interplay between hyperglycemia, cardiac function, and ischemia in diabetes.
Abstract:
Cardiovascular disease is one of the most important causes of morbidity and mortality in diabetes mellitus, but there has been controversy over functional impairment of diabetic hearts and their tolerance to ischemia. We studied ischemic heart function in type 2 diabetic rats with different degrees of hyperglycemia and its relationship with cardiac norepinephrine release. Otsuka Long-Evans Tokushima Fatty rats (OLETF) and age-matched Long-Evans Tokushima Otsuka normal rats (LETO) were used. One group of OLETF rats was given 30% sucrose in drinking water (OLETF-S). Hearts were isolated and perfused in a working heart preparation and subjected to 30 min ischemia followed by 40 min reperfusion at age of 12 months. Hemodynamics and coronary norepinephrine overflow were examined. Fasting plasma glucose in OLETF increased markedly at 12 months and sucrose administration exacerbated hyperglycemia in diabetic rats (LETO 6.6 +/- 0.5, OLETF 8.3 +/- 0.7, OLETF-S 15.0 +/- 1.7 mmol/L, P < 0.01). Basic cardiac output in OLETF was decreased as compared with LETO and OLETF-S (LETO 29.4 +/- 2.5, OLETF 24.0 +/- 2.4, OLETF-S 27.0 +/- 0.9 ml/min/g, P < 0.05) and remained very low after ischemia, while in OLETF-S it was well preserved (OLETF 4.2 +/- 2.1, OLETF-S 13.7 +/- 2.6 ml/min/g, P < 0.01). Correspondently, cardiac norepinephrine released during ischemia and reperfusion was lower in OLETF-S (OLETF 2.3 +/- 1.0, OLETF-S 0.7 +/- 0.1 pmol/ml, P < 0.01). Thus, OLETF hearts were more vulnerable to ischemia but sucrose feeding rendered their hearts resistant to ischemia. Less norepinephrine release may play a role in preventing postischemic functional deterioration in sucrose-fed diabetic hearts.
