Role of physical activity and cardiorespiratory fitness in metabolically healthy obesity: a narrative review

Obesity has been associated with a multitude of metabolic disorders, often clustering with risk factors of cardiovascular disease and type 2 diabetes mellitus, hypertension, dyslipidaemia. Overall, obesity is a worldwide, growing health concern. However, a subgroup of obese individuals with a low burden of metabolic abnormalities have been identified and described as metabolically healthy obese (MHO). Whether the MHO phenotype is protective against obesity-related metabolic disorders in the long-term is presently unclear, and current research examining the potential transition has yielded inconsistent results. In this current narrative review, we aim to provide insights on the role of physical activity (PA) and cardiorespiratory fitness (CRF) in MHO. Lifestyle factors such as PA and CRF may influence the MHO phenotype. Limited studies have characterised energy expenditure and CRF in MHO and metabolically unhealthy obese. However, higher levels of PA, less sedentary behaviour and higher CRF have been observed in MHO individuals. Considering the multiple benefits of PA, it is high time to advocate this lifestyle change beyond its influence on energy balance in a weight loss programme to improve cardiovascular and metabolic risk factors irrespective of body weight and fat mass changes. Improved CRF via increased PA, especially exercise participation, while avoiding weight gain is not only a realistic goal, but should be the primary intervention for MHO populations to prevent the transition to an abnormal metabolic state

Recent Progress in the Diagnosis and Management of Type 2 Diabetes Mellitus in the Era of COVID-19 and Single Cell Multi-Omics Technologies

Type 2 diabetes mellitus (T2DM) is one of the world’s leading causes of death and life-threatening conditions. Therefore, we review the complex vicious circle of causes responsible for T2DM and risk factors such as the western diet, obesity, genetic predisposition, environmental factors, and SARS-CoV-2 infection. The prevalence and economic burden of T2DM on societal and healthcare systems are dissected. Recent progress on the diagnosis and clinical management of T2DM, including both non-pharmacological and latest pharmacological treatment regimens, are summarized. The treatment of T2DM is becoming more complex as new medications are approved. This review is focused on the non-insulin treatments of T2DM to reach optimal therapy beyond glycemic management. We review experimental and clinical findings of SARS-CoV-2 risks that are attributable to T2DM patients. Finally, we shed light on the recent single-cell-based technologies and multi-omics approaches that have reached breakthroughs in the understanding of the pathomechanism of T2DM

Dietary red palm oil supplementation reduces myocardial infarct size in an isolated perfused rat heart model

<p>Abstract</p> <p>Background and Aims</p> <p>Recent studies have shown that dietary red palm oil (RPO) supplementation improves functional recovery following ischaemia/reperfusion in isolated hearts. The main aim of this study was to investigate the effects of dietary RPO supplementation on myocardial infarct size after ischaemia/reperfusion injury. The effects of dietary RPO supplementation on matrix metalloproteinase-2 (MMP2) activation and PKB/Akt phosphorylation were also investigated.</p> <p>Materials and methods</p> <p>Male Wistar rats were divided into three groups and fed a standard rat chow diet (SRC), a SRC supplemented with RPO, or a SRC supplemented with sunflower oil (SFO), for a five week period, respectively. After the feeding period, hearts were excised and perfused on a Langendorff perfusion apparatus. Hearts were subjected to thirty minutes of normothermic global ischaemia and two hours of reperfusion. Infarct size was determined by triphenyltetrazolium chloride staining. Coronary effluent was collected for the first ten minutes of reperfusion in order to measure MMP2 activity by gelatin zymography.</p> <p>Results</p> <p>Dietary RPO-supplementation decreased myocardial infarct size significantly when compared to the SRC-group and the SFO-supplemented group (9.1 ± 1.0% <it>versus </it>30.2 ± 3.9% and 27.1 ± 2.4% respectively). Both dietary RPO- and SFO-supplementation were able to decrease MMP2 activity when compared to the SRC fed group. PKB/Akt phosphorylation (Thr 308) was found to be significantly higher in the dietary RPO supplemented group when compared to the SFO supplemented group at 10 minutes into reperfusion. There was, however, no significant changes observed in ERK phosphorylation.</p> <p>Conclusions</p> <p>Dietary RPO-supplementation was found to be more effective than SFO-supplementation in reducing myocardial infarct size after ischaemia/reperfusion injury. Both dietary RPO and SFO were able to reduce MMP2 activity, which suggests that MMP2 activity does not play a major role in protection offered by RPO. PKB/Akt phosphorylation may, however, be involved in RPO mediated protection.</p

Dietary red palm oil supplementation decreases infarct size in cholesterol fed rats

BACKGROUND AND AIMS: The effect of red palm oil (RPO) supplementation on infarct size after ischaemia/reperfusion in a cholesterol enriched diet-induced hyperlipidemic animal model has not been reported. Previous studies reported results on the effect of RPO in a normal diet, whilst evidence of protection has been linked to improved functional recovery, prosurvival kinase, anti-apoptosis and NO-cGMP. Therefore, we aimed to investigate the effects of dietary RPO supplementation in a cholesterol-enriched diet-induced hyperlipidemic rat model and to investigate the involvement of matrix metalloproteinase 2 (MMP2) inhibition as a possible mechanism of protection. MATERIALS AND METHODS: Male Wistar rats were fed either a standard rat chow diet (Norm) or a 2% cholesterol-enriched diet (Chol) for nine weeks. Additionally, two more groups received the same treatment, however, at the week 4, diet was supplemented with RPO for the last five weeks (Norm+RPO and Chol+RPO), respectively. After the feeding period hearts were isolated, perfused according to Langendorff and subjected to 30 minutes of normothermic global ischaemia followed by two hours of reperfusion. Infarct size was measured by 2,3,5-triphenyltetrazolium chloride staining at the end of reperfusion. RESULTS: Cholesterol-enriched diet increased myocardial infarct size from 23.5±3.0% to 37.2±3.6% (p<0.05) when compared to normal diet. RPO supplementation significantly reduced infarct size either in Norm+RPO or in Chol+RPO (to 9.2±1.0% and 26.9±3.0%), respectively. Infarct size in Chol+RPO was comparable to the Norm group. MMP2 activity before ischaemia was significantly reduced in the Chol+RPO group when compared to the Chol group. However, the MMP2 activity of the hearts of the RPO fed rats was significantly increased when compared to the normal diet group after ischaemia. CONCLUSIONS: For the first time it was shown that dietary RPO supplementation attenuated the increased susceptibility of the hearts in cholesterol fed rats to ischaemia/reperfusion injury. This was shown by reduced infarct size. For the first time we also show that red palm oil supplementation altered pre-ischaemic levels of MMP-2, which may indicate that myocardial MMP2 may be implicated as a possible role player in RPO mediated protection against ischaemia/reperfusion injury in hearts of cholesterol supplemented rats.This work was supported by a Collaborative Research Grant between Hungary (ZA-35/2006) and South Africa (NRF: 62212) and by grants from the National Office for Research and Technology (Jedlik-NKFP-A1-2006-029, Med-Food, Baross DA-TECH-07-2008-0041, TAMOP-4.2.2-08/1/2008-0013, TAMOP-4.2.1/B-09/1/KONV-2010-0005). T. Csont holds a "János Bolyai Felowship" from the Hungarian Academy of Sciences

The Effects of Exercise Training and High Triglyceride Diet in an Estrogen Depleted Rat Model

Cardiovascular morbidity and mortality of premenopausal women are significantly lower compared to men of similar age. However, this protective effect evidently decreases after the onset of menopause. We hypothesized that physical exercise could be a potential therapeutic strategy to improve inflammatory processes and cardiovascular antioxidant homeostasis, which can be affected by the loss of estrogen and the adverse environmental factors, such as overnutrition. Ovariectomized (OVX, n= 40) and sham-operated (SO, n= 40) female Wistar rats were randomized to exercising (R) and non-exercising (NR) groups. Feeding parameters were chosen to make a standard chow (CTRL) or a high triglyceride diet (HT) for 12 weeks. Aortic and cardiac heme oxygenase (HO) activity and HO-1 concentrations significantly decreased in all of the NR OVX and SO HT groups. However, the 12-week physical exercise was found to improve HO-1 values. Plasma IL-6 concentrations were higher in the NR OVX animals and rats fed HT diet compared to SO CTRL rats. TNF-α concentrations were significantly higher in the NR OVX groups. 12 weeks of exercise significantly reduced the concentrations of both TNF-α and IL-6 compared to the NR counterparts. The activity of myeloperoxidase enzyme (MPO) was significantly increased as a result of OVX and HT diet, however voluntary wheel-running exercise restored the elevated values. Our results show that estrogen deficiency and HT diet caused a significant decrease in the activity and concentration of HO enzyme, as well as the concentrations of TNF-α, IL-6, and the activity of MPO. However, 12 weeks of voluntary wheel-running exercise is a potential non-pharmacological therapy to ameliorate these disturbances, which determine the life expectancy of postmenopausal women

Novel features of the rat model of inflammatory bowel disease based on 2,4,6-trinitrobenzenesulfonic acidinduced acute colitis

The 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced acute inflammatory bowel disease (IBD) model in the rat is discussed, focusing on the details of the TNBS instillation and highlighting the advantages and limitations of this model. For determination of the time-dependent action of 50% ethanol and different doses of TNBS, male Wistar rats were treated with 50% ethanol or 10 mg or 30 mg of TNBS dissolved in 50% ethanol. The TNBS-induced inflammation peaked 48-72 h after installation and the colitis caused by 30 mg of TNBS was more severe than that caused by 10 mg of TNBS. To test the effectiveness of sulfasalazine (SASP), male rats were treated with 10 mg of TNBS or with 10 mg of TNBS and SASP, and 72 h later the extent of mucosal damage was determined. Orally administered 50 mg/kg/day SASP proved to reduce the TNBS-induced colonic inflammation in rats significantly. The TNBS-induced colitis model facilitates a better understanding of the immunopathological mechanisms of IBD. Optimization of the dose of TNBS and oral SASP as positive control in TNBS-induced colitis in rats furnishes an appropriate test system for new anti-IBD drugs

Sexual dimorphism of cardiovascular ischemia susceptibility is mediated by heme oxygenase

We investigated the gender differences in heme-oxygenase (HO) enzyme, which produces endogenous vascular protective carbon monoxide (CO). We studied (1) the activity and expression of HO enzymes in the left ventricle (LV) and aorta, (2) basal increase in basal blood pressure provoked by arginine vasopressine (AVP) in vivo, (3) the heart perfusion induced by AVP, (4) the ST segment depression provoked by adrenaline and 30 seconds later phentolamine, and (5) the aorta ring contraction induced by AVP in female and male Wistar rats. We found that HO activity and the expression of HO-1 and HO-2 were increased in female rat aorta and LV. We demonstrated that the basal blood pressure and administration of AVP provoked blood pressure response are increased in the males; the female myocardium was less sensitive towards angina. Both differences could be aggravated by the inhibition of HO. The aorta rings were more susceptible towards vasoconstriction by AVP in males; isolated heart perfusion decrease was higher in males. The HO inhibition aggravated the heart perfusion in both sexes. In conclusion, the increased HO activity and expression in females might play a role in the sexual dimorphism of cardiovascular ischemia susceptibility during the reproductive age. © 2013 Anikó Pósa et al