TY - JOUR
T1 - The heart is better protected against myocardial infarction in the fed state compared to the fasted state
AU - Liepinsh, Edgars
AU - Makrecka, Marina
AU - Kuka, Janis
AU - Makarova, Elina
AU - Vilskersts, Reinis
AU - Cirule, Helena
AU - Sevostjanovs, Eduards
AU - Grinberga, Solveiga
AU - Pugovics, Osvalds
AU - Dambrova, Maija
N1 - Funding Information:
This study was supported by the European Social Fund (No. 2009/0147/1DP/1.1.2.1.2/09/IPIA/VIAA/009 ) and the Latvian National Research Program BIOMEDICINE .
PY - 2014/1
Y1 - 2014/1
N2 - Objective. A variety of calorie restriction diets and fasting regimens are popular among overweight people. However, starvation could result in unexpected cardiovascular effects. Therefore, it is necessary to evaluate the short-term effects of diets on cardiovascular function, energy metabolism and potential risk of heart damage in case of myocardial infarction. The objective of the present study was to investigate whether the increased level of glucose oxidation or reduction of fatty acid (FA) load in the fed state provides the basis for protection against myocardial infarction in an experimental rat model of ischemia-reperfusion. Materials/Methods We tested the effects of the availability of energy substrates and their metabolites on the heart functionality and energy metabolism under normoxic and ischemia-reperfusion conditions. Results In a fasted state, the heart draws energy exclusively from FAs, whereas in a fed state, higher concentration of circulating insulin ensures a partial switch to glucose oxidation, while the load of FA on heart and mitochondria is reduced. Herein, we demonstrate that ischemic damage in hearts isolated from Wistar rats and diabetic Goto-Kakizaki rats is significantly lower in the fed state compared to the fasted state. Conclusions Present findings indicate that postprandial or fed-state physiology, which is characterised by insulin-activated glucose and lactate utilisation, is protective against myocardial infarction. Energy metabolism pattern in the heart is determined by insulin signalling and the availability of FAs. Overall, our study suggests that even overnight fasting could provoke and aggravate cardiovascular events and high-risk cardiovascular patients should avoid prolonged fasting periods.
AB - Objective. A variety of calorie restriction diets and fasting regimens are popular among overweight people. However, starvation could result in unexpected cardiovascular effects. Therefore, it is necessary to evaluate the short-term effects of diets on cardiovascular function, energy metabolism and potential risk of heart damage in case of myocardial infarction. The objective of the present study was to investigate whether the increased level of glucose oxidation or reduction of fatty acid (FA) load in the fed state provides the basis for protection against myocardial infarction in an experimental rat model of ischemia-reperfusion. Materials/Methods We tested the effects of the availability of energy substrates and their metabolites on the heart functionality and energy metabolism under normoxic and ischemia-reperfusion conditions. Results In a fasted state, the heart draws energy exclusively from FAs, whereas in a fed state, higher concentration of circulating insulin ensures a partial switch to glucose oxidation, while the load of FA on heart and mitochondria is reduced. Herein, we demonstrate that ischemic damage in hearts isolated from Wistar rats and diabetic Goto-Kakizaki rats is significantly lower in the fed state compared to the fasted state. Conclusions Present findings indicate that postprandial or fed-state physiology, which is characterised by insulin-activated glucose and lactate utilisation, is protective against myocardial infarction. Energy metabolism pattern in the heart is determined by insulin signalling and the availability of FAs. Overall, our study suggests that even overnight fasting could provoke and aggravate cardiovascular events and high-risk cardiovascular patients should avoid prolonged fasting periods.
KW - Fasted
KW - Fatty acids
KW - Fed
KW - Glucose
KW - Insulin
UR - http://www.scopus.com/inward/record.url?scp=84890116705&partnerID=8YFLogxK
U2 - 10.1016/j.metabol.2013.09.014
DO - 10.1016/j.metabol.2013.09.014
M3 - Article
C2 - 24140100
AN - SCOPUS:84890116705
SN - 0026-0495
VL - 63
SP - 127
EP - 136
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 1
ER -