metabolic syndromes not directly correlated with Body MassIndex, and should be analyze besides of it.

Keywords: Metabolic syndrome; BMI; Cardiology

doi:10.1016/j.yjmcc.2007.03.769

Expression and activation of myocardial AMPKα arealtered in sucrose-fed rats with metabolic syndromeKarla Carvajal1, Luz Hernández2, David Cruz-Robles2.1Genetic Biochem. Inst Nal Pediatría, Mexico.

2Biochemistry

and Pathology Department, Inst Nal Cardiol, Mexico

High carbohydrate diet is associated with the development ofmetabolic syndrome. An energy deficit in cardiac muscle hasbeen demonstrated in the sucrose-fed rat (SFR), which is relatedto glucose oxidation and energy transfer impairment. To test thehypothesis that this metabolic remodeling obeys in part tochanges in the AMP-dependent protein kinase (AMPK), whichplays a pivotal role in controlling energy homeostasis, weevaluated heart expression of the enzyme as well as itsphosphorylated state and response during global ischaemia inthe isolated rat heart. Under basal conditions, the α catalyticsubunit is over-expressed in hearts from SFR although basalphosphorylated AMPKα was lower. During a 10 min globalischaemia, activation of AMPKα was significantly diminishedin SFR hearts. This unresponsiveness correlated to an increaseof amplitude in the ischaemic contracture. As well, glycogenutilization during this ischaemic insult was significant reduced,although the basal content of this reserve was not altered.Beside these changes in heart muscle, we observed concomitantdisturbances in AMPK α expression on skeletal muscle andadipose tissue. Contrary to that occurring in heart, total AMPKαexpression was decreased, as well as the phosphorylated state.Our results demonstrate that the metabolic syndrome inducedby sucrose feeding is related to disturbances in AMPKexpression and activity over different organs, and that thismay alter the signaling network controlling energy managementin the heart.

Keywords: Metabolism; Ischemia/reperfusion; Energetics

doi:10.1016/j.yjmcc.2007.03.770

Alterations in levels of O-linked N-acetylglucosaminemodified proteins in the uraemic heartDavid A. Ashford, Sunil Bhandari*, Kathleen Bulmer*, Anne-Marie L. Seymour*. Department of Biology, University ofYork. *University of Hull, UK

Myocardial insulin resistance is a characteristic of patientswith chronic kidney disease and may contribute to the highcardiac mortality in this patient group. However, the me-

chanisms underlying this abnormality remain unclear. The aimof this study was to characterise the relative level of O-linkedN-acetylglucosamine (O-GlcNAc) modification of proteins incontrol and uraemic cardiac tissue. Experimental uraemia wasinduced in male Sprague–Dawley rats via a two stage sub-totalnephrectomy. Left ventricular tissue was harvested after8 weeks, homogenised and O-GlcNAc modified proteinsisolated by binding and precipitation with immobilised wheatgerm agglutinin (a lectin specific for glucosamine). Boundproteins were recovered and separated by 1D- and 2D-PAGE.Gels were probed with an O-GlcNAc-specific antibody (1D)or stained with Sypro Red (2D). 1D-PAGE demonstratedseparation of different populations of O-GlcNAc modifiedproteins. Image analysis of 2D gels gave >1500 matchedspots in control and uraemic samples. Of these 78 showed≥2.5-fold upregulation and 72 showed ≥2.5-fold reduction inthe uraemic heart relative to control. Identification of O-GlcNAc modified proteins was evaluated by excising spotsfrom a control gel, digesting with trypsin and analysing byMALDI-TOF/TOF mass spectrometry. Of 12 spots selected,10 were identified including stress related proteins (e.g. HSP-70 and αBcrystallin), cytoskeletal proteins (actin and desmin)and key mitochondrial enzyme subunits (dihydrolipoamidetransacylase E2).

Keywords: O-linked N-acetylglucosamine; Protein modifica-tion; Experimental uraemia

doi:10.1016/j.yjmcc.2007.03.771

Decreases in serum thioredoxin and hyperglycemia byacidity water footbath after lunch in type II diabeticsMakie Higuchi1, Keiko Maetaka1,2, Yuji Mizuno2. 1Division ofPharmacology, Kyushu University of Nurs and SW, Japan.2Kumamoto Aging Research Institute, Kumamoto, Japan

Effects of acidity water footbath on blood pressure,hyperglycemia and oxidative stress after lunch, and themechanisms were examined in type II diabetics (DM).

Methods: Eight DM subjects were 67±3 years old. Threetypes of 15-min footbath (no water, pH7.4– and pH3.0–40 °Cwater) at the sitting position were taken for each DM in arandomized sequence for 3 days. Autonomic nervous activitieswere assessed by power spectral analysis of heart rate variability.

Results: No decrease in the hyperglycemia until 2.5 h afterlunch, and the slight increases in blood pressure and heart rate insham footbath were significantly improved by pH3.0 footbath.However, the acidity water footbath decreased parasympatheticactivity and tended to increase sympathetic activity. In theelderly DM, the parasympathetic and sympathetic tones atsupine position were markedly low and high, respectively, andthe cardiac autonomic nervous reactivity during posture changefrom supine to standing position was impaired. While, seruminsulin did not change, IGF-1 tended to increase andthioredoxin decreased significantly after the footbath.

S58 ABSTRACTS / Journal of Molecular and Cellular Cardiology 42 (2007) S55–S71