The metabolic syndrome is recognized as a cluster of disturbances associated with obesity, type 2 diabetes and hypertension. Over the past two decades, the number of people with the metabolic syndrome has increased at an alarming rate. This increase is associated with the global epidemic of both obesity and diabetes. Cardiovascular mortality is increased among diabetics and obesity-related insulin-resistant patients, and obesity is currently recognized as independent risk factor for cardiovascular disease. We aimed to establish the effects of a short period of an altered diet on the heart using a rat model of hyperphagia-induced obesity (diet supplemented with sucrose and condensed milk for 8 weeks = DIO) compared to age-matched controls. Isolated, perfused hearts were subjected to global or regional ischaemia/reperfusion. Function on reperfusion was recorded and infarct size determined. A plasma lipid profile was established via HPLC-based methods and proteins involved in metabolic signalling determined either by western blotting or RT-PCR. 8 weeks of diet resulted in whole-body but not myocardial insulin resistance, increased plasma triglyceride and phospholipid levels as well as increased lipid peroxidation. Despite the similar baseline function, hearts from DIO animals showed significantly poorer postischaemic recovery than controls (41.9 % RPP recovery vs 57.9 %, P < 0.05, n = 7-11/group) but surprisingly, smaller infarct size (24.95 ± 1.97 vs 47.26 ± 4.05 % of the area at risk, P < 0.005, n = 8/group). Basal phosphorylation of PKB/Akt was elevated but IRS-1 and SERCA-2 expression severely downregulated. In conclusion, after only 8 weeks of a slight change in diet, the rat heart shows signs of metabolic remodelling. Some of these changes may be protective but others may be detrimental and eventually lead to maladaptation.

Stroke is the second leading cause of death worldwide, affecting about 240 people a day in South Africa and leaving survivors with residual disabilities. At the moment, there is no clinically approved neuroprotective product for stroke but the consumption of plant polyphenols has been suggested to offer some protection against stroke. In this study, we investigated the effects of long-term consumption of fermented rooibos herbal tea (FRHT) on ischemia/reperfusion (I/R)-induced brain injury in adult male Wistar rats. FRHT was administered to the animals ad libitum for 7 weeks prior to the induction of ischemic injury via a 20-minute bilateral occlusion of the common carotid arteries (BCCAO) followed by reperfusion for 24, 96 and 168 hours respectively. Neurobehavioural deficits, brain oedema, blood-brain barrier (BBB) damage, apoptosis, lipid peroxidation and total antioxidant capacity were subsequently evaluated using standard methods. Our results showed that long-term consumption of FRHT by Wistar rats significantly reduced brain oedema and neuronal apoptosis, but did not attenuate BBB damage following cerebral ischemia. Analysis of whole-brain homogenates showed significantly reduced lipid peroxidation levels, increased total antioxidant capacity and resulted in improved neurobehavioural outcomes in FRHT-treated rats when compared with untreated animals. Taken together, our results tend to suggest that continuous consumption of FRHT could confer some protection against ischemic brain injury (IBI) and is therefore highly recommended for patients with stroke-predisposing conditions.

Resting heat rate was measured in superfused rabbit papillary muscles at 20°C during 40 minutes of anoxia and subsequent reoxygenation. To reveal the nature of the reactions underlying energy output under such conditions, the data obtained were compared with values predicted from data on chemical change. Before and after the anoxic period, muscles were stimulated at 0.2 Hz, during which time the contraction-related heat rate was measured. During anoxia, muscles were kept at rest or stimulated at 1 Hz. Stimulation was switched off intermittently to determine resting heat rate. Before anoxia, resting heat rate was 8.7+±1.1 (mean+SEM) mW g dry wt-'. During anoxia, it decreased to 38% and 50%1 of the preanoxic level in resting and stimulated muscles, respectively (P<.05). In resting muscles, heat rate increased with reoxygenation in approximately 10 to 15 minutes to 1.3 times the preanoxic level, whereas this was 3.7 times in stimulated muscles. Resting heat rate returned within 65 (resting muscles) or 150 (stimulated muscles) minutes to the baseline. The ratio of force-and contraction-related heat rate, ie, the economy of contraction, was not different before and after anoxia. We estimated that the heat produced by muscles during anoxia was not different from the heat to be expected from the hydrolysis of creatine phosphate, the breakdown of nucleotides, and the formation of lactate. The overshoot in resting heat during reoxygenation of resting muscles could be accounted for by the resynthesis of the energy store. The much larger overshoot in resting heat of stimulated muscles was due to the contracture. The finding that the economy of contraction was not altered by anoxia and reoxygenation suggests that both sarcoplasmic reticulum Ca2'-ATPase and myofibrillar ATPase are depressed by anoxia and that the enhancement of cytosolic calcium transients with reoxygenation, reported in other studies on papillary muscle, results from reduced binding of calcium rather than from enhanced release. (Circ Res. 1993;73:1177-1187 KEY WORDs * heat rate * stunning * anoxia * reoxygenation * heart T he leading event in the cascade of cellular responses in heart muscles after anoxia or reoxygenation is energetic in nature. However, rather few direct measurements have been reported on changes in energy output of the myocardium with anoxia and reoxygenation. In the present study, we measured the effects of anoxia and reoxygenation on heat production of isolated isometric cardiac muscle. We used a flow-through chamber, similar to the one described by Daut and Elzinga1 for trabeculas, built to accommodate papillary muscles. The latter preparation was preferred to be continuous with earlier work2-4 reporting data from that preparation on isometric force production, nucleotide composition, phosphocreatine (PCr), and lactate during anoxia and reoxygenation.This information was needed for the present work to explain the changes in heat output found with anoxia and reoxygenation.The following specific questions were pursued: (1) What is the ti...

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In quiescent rabbit papillary muscle at 20 degrees C, the formation of ATP in nitrogen, estimated from the production of lactate, is 21% of that in oxygen. Stimulating the anoxic muscles at 0.2 Hz causes a threefold increase in ATP formation. In this study we want to determine 1) whether glycolytic ATP formation can be increased to a rate that would meet the aerobic ATP demand at rest and 2) what the maximum glycolytic rate attainable through stimulation is. Glycolytic rate is estimated from the amount of lactate produced at various times over 40 min of anoxia. Nucleotides and creatine compounds are also determined. Lactate formation at the onset of anoxia is proportional to stimulus frequency. The amount of lactate formed is correlated to the breakdown of glycogen; glucose is not used. Therefore the amount of glycogen present in the muscle at the onset of anoxia is the main determinant of the amount of ATP formed when oxidative phosphorylation is inhibited. The rate of lactate formation at the onset of anoxia increases from 1.22 mumol.g dry wt-1.min-1 in resting muscles to 18.5 mumol.g dry wt-1.min-1 in 1-Hz-stimulated muscles. This implies that in anoxic myocardium, glycolysis can provide ATP at more than three times the rate found in the muscle at rest in ample oxygen.