High dietary sucrose triggers hyperinsulinemia, increases myocardial beta-oxidation, reduces glycolytic flux and delays post-ischemic contractile recovery

Autor: Karine Couturier, P. Gachon, D. Gonsolin, Roland Favier, Yves Boirie, Sébastien Peltier, Luc Demaison, Valérie Novel-Chaté, Salvatore Pepe, Christiane Keriel, Xavier Leverve, Stéphanie Rondel, Patrice Faure, Blandine Garait
Přispěvatelé: Bioénergétique fondamentale et appliquée, Université Joseph Fourier - Grenoble 1 (UJF)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratory of Experimental Surgery, Université Libre de Bruxelles [Bruxelles] (ULB), Laboratoire de Biochimie (DBI), CHU Grenoble, Laboratoire de Nutrition Humaine (UMPE), Institut National de la Recherche Agronomique (INRA), Laboratory of Cardiac Surgical Research, Monash University [Clayton], Hamant, Sarah, Université libre de Bruxelles (ULB)
Jazyk: angličtina
Rok vydání: 2007
Předmět:
Blood Glucose
Male
MESH: Oxidation-Reduction
Sucrose
MESH: Myocardial Contraction
MESH: Organ Size
Clinical Biochemistry
Wistar
Myocardial Ischemia
030204 cardiovascular system & hematology
chemistry.chemical_compound
0302 clinical medicine
Dietary Sucrose
Pyruvic Acid
Hyperinsulinemia
Insulin
Glycolysis
MESH: Animals
0303 health sciences
General Medicine
Organ Size
Lipids
MESH: Myocardial Reperfusion Injury
MESH: Hyperinsulinism
MESH: Glycolysis
MESH: Myocardial Ischemia
Oxidation-Reduction
MESH: Triglycerides
medicine.medical_specialty
MESH: Myocardium
MESH: Rats
Ischemia
Myocardial Reperfusion Injury
MESH: Insulin
In Vitro Techniques
MESH: Dietary Sucrose
Contractility
03 medical and health sciences
Insulin resistance
Internal medicine
Hyperinsulinism
medicine
[SDV.BBM] Life Sciences [q-bio]/Biochemistry
Molecular Biology
Animals
[SDV.BBM]Life Sciences [q-bio]/Biochemistry
Molecular Biology
Lactic Acid
Rats
Wistar
Molecular Biology
MESH: Pyruvic Acid
Triglycerides
030304 developmental biology
Myocardium
Body Weight
Cell Biology
MESH: Rats
Wistar
medicine.disease
Myocardial Contraction
MESH: Lipids
MESH: Male
Rats
MESH: Body Weight
Endocrinology
chemistry
MESH: Blood Glucose
MESH: Lactic Acid
Metabolic syndrome
Zdroj: Molecular and Cellular Biochemistry
Molecular and Cellular Biochemistry, Springer Verlag, 2007, 295 (1-2), pp.217-28. ⟨10.1007/s11010-006-9291-7⟩
ISSN: 0300-8177
1573-4919
DOI: 10.1007/s11010-006-9291-7⟩
Popis: International audience; Although the causal relationship between insulin resistance (IR) and hypertension is not fully resolved, the importance of IR in cardiovascular dysfunction is recognized. As IR may follow excess sucrose or fructose diet, the aim of this study was to test whether dietary starch substitution with sucrose results in myocardial dysfunction in energy substrate utilization and contractility during normoxic and post-ischemic conditions. Forty-eight male Wistar rats were randomly allocated to three diets, differing only in their starch to sucrose (S) ratio (13, 2 and 0 for the Low S, Middle S and High S groups, respectively), for 3 weeks. Developed pressure and rate x pressure product (RPP) were determined in Langendorff mode-perfused hearts. After 30 min stabilization, hearts were subjected to 25 min of total normothermic global ischemia, followed by 45-min reperfusion. Oxygen consumption, beta-oxidation rate (using 1-13C hexanoate and Isotopic Ratio Mass Spectrometry of CO2 produced in the coronary effluent) and flux of non-oxidative glycolysis were also evaluated. Although fasting plasma glucose levels were not affected by increased dietary sucrose, high sucrose intake resulted in increased plasma insulin levels, without significant rise in plasma triglyceride and free fatty acid concentrations. Sucrose-rich diet reduced pre-ischemic baseline measures of heart rate, RPP and non-oxidative glycolysis. During reperfusion, post-ischemic recovery of RPP was impaired in the Middle S and High S groups, as compared to Low S, mainly due to delayed recovery of developed pressure, which by 45 min of reperfusion eventually resumed levels matching Low S. At the start of reperfusion, delayed post-ischemic recovery of contractile function was accompanied by: (i) reduced lactate production; (ii) decreased lactate to pyruvate ratio; (iii) increased beta-oxidation; and (iv) depressed metabolic efficiency. In conclusion, sucrose rich-diet increased plasma insulin levels, in intact rat, and increased cardiac beta-oxidation and coronary flow-rate, but reduced glycolytic flux and contractility during normoxic baseline function of isolated perfused hearts. Sucrose rich-diet impaired early post-ischemic recovery of isolated heart cardiac mechanical function and further augmented cardiac beta-oxidation but reduced glycolytic and lactate flux.
Databáze: OpenAIRE
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