Key result
Four weeks of high fat diet feeding in rats induced glucose intolerance and impaired myocardial contractile function during dipyridamole-induced hyperaemia, but did not alter myocardial perfusion.
Why the study?
Does a high fat diet-induced glucose intolerance impair myocardial function and perfusion during hyperaemia in male Wistar rats?
Does a high fat diet-induced glucose intolerance impair myocardial function and perfusion during hyperaemia in male Wistar rats?
Short-term high fat diet-induced glucose intolerance in rats impairs hyperaemia-induced increases in myocardial contractile function, but preserves myocardial perfusion.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for early contractile impairment in diet-induced glucose intolerance; human studies needed before clinical relevance.
BACKGROUND: Glucose intolerance is a major health problem and is associated with increased risk of progression to type 2 diabetes mellitus and cardiovascular disease. However, whether glucose intolerance is related to impaired myocardial perfusion is not known. The purpose of the present study was to study the effect of diet-induced glucose intolerance on myocardial function and perfusion during baseline and pharmacological induced hyperaemia. METHODS: Male Wistar rats were randomly exposed to a high fat diet (HFD) or control diet (CD) (n = 8 per group). After 4 weeks, rats underwent an oral glucose tolerance test. Subsequently, rats underwent (contrast) echocardiography to determine myocardial function and perfusion during baseline and dipyridamole-induced hyperaemia (20 mg/kg for 10 min). RESULTS: Four weeks of HFD feeding resulted in glucose intolerance compared to CD-feeding. Contractile function as represented by fractional shortening was not altered in HFD-fed rats compared to CD-fed rats under baseline conditions. However, dipyridamole increased fractional shortening in CD-fed rats, but not in HFD-fed rats. Basal myocardial perfusion, as measured by estimate of perfusion, was similar in CD- and HFD-fed rats, whereas dipyridamole increased estimate of perfusion in CD-fed rats, but not in HFD-fed rats. However, flow reserve was not different between CD- and HFD-fed rats. CONCLUSIONS: Diet-induced glucose intolerance is associated with impaired myocardial function during conditions of hyperaemia, but myocardial perfusion is maintained. These findings may result in new insights into the effect of glucose intolerance on myocardial function and perfusion during hyperaemia.
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Brom et al. (2012) studied Diet-induced glucose intolerance (n=16). High fat diet vs. Control diet was evaluated on Myocardial function (fractional shortening) and perfusion during baseline and dipyridamole-induced hyperaemia. Four weeks of high fat diet feeding in rats induced glucose intolerance and impaired myocardial contractile function during dipyridamole-induced hyperaemia, but did not alter myocardial perfusion.
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