Obesity and metabolic syndrome (MetS) have become a growing problem for public health and clinical practice, given their increased prevalence due to the rise of sedentary lifestyles and excessive caloric intake from processed food rich in fat and sugar. There are several definitions of MetS, but most of them describe it as a cluster of cardiovascular and metabolic alterations such as abdominal obesity, reduced high-density lipoprotein (HDL) and elevated low-density lipoprotein (LDL) cholesterol, elevated triglycerides, glucose intolerance, and hypertension. Diagnosis requires three out of these five criteria to be present. Despite the increasing prevalence of MetS, the understanding of its pathophysiology and relationship with disease is still limited. Indeed, the pathological consequences of MetS components have been reported individually, but investigations that have studied the effect of the combination of MeS components on organ pathological remodeling are almost nonexistent. On the other hand, animal models are a powerful tool in understanding the mechanisms that underlie pathological processes such as MetS. In the first part of the review, we will briefly overview the advantages, disadvantages and pathological manifestations of MetS in porcine, canine, rodent, and rabbit diet-induced experimental models. Then, we will focus on the different dietary regimes that have been used in rabbits to induce MetS by means of high-fat, cholesterol, sucrose or fructose-enriched diets and their effects on physiological systems and organ remodeling. Finally, we will discuss the use of dietary regimes in different transgenic strains and special rabbit breeds.

Background: Our aim was to determine the differences in short-term heart rate variability (HRV) between patients with metabolic syndrome (MS) and healthy controls. Methods: We searched electronic databases for primary works with short-term HRV recordings (≤30 min) that made comparisons between individuals with MS versus healthy controls. This systematic review and meta-analysis (MA) was performed according to PRISMA guidelines and registered at PROSPERO (CRD42022358975). Results: Twenty-eight articles were included in the qualitative synthesis and nineteen met the criteria for the MA. Patients with MS showed decreased SDNN (−0.36 [−0.44, −0.28], p < 0.001), rMSSD (−7.59 [−9.98, −5.19], p < 0.001), HF (−0.36 [−0.51, −0.20], p < 0.00001) and LF (−0.24 [−0.38, −0.1], p = 0.001). In subsequent subanalyses, we found a decrease in SDNN (−0.99 (−1.45, −0.52], p < 0.001), rMSSD (−10.18 [−16.85, −3.52], p < 0.01) and HF (−1.04 [−1.97, −0.1] p < 0.05) in women. In men, only LF showed a significant lower value (−0.26 [−0.5, −0.02], p < 0.05). We could not perform MA for non-linear variables. Conclusions: Patients with MS showed changes in time-domain analyses, with lower values in SDNN and rMSSD. Regarding frequency-domain analyses, MS patients showed a decrease in HF and LF When sex was used as a grouping variable, the MA was only possible in one of both sexes (men or women) in rMSSD and LF/HF. Lastly, when data for both men and women were available, subanalyses showed a different behavior compared to mixed analyses for SDNN, HF and LF, which might point towards a different impact of MS in men and women.

Background: Our aim was to determine the impact that metabolic syndrome (MS) produces in long-term heart rate variability (HRV), quantitatively synthesizing the results of published studies to characterize the cardiac autonomic dysfunction in MS. Methods: We searched electronic databases for original research works with long-term HRV recordings (24 h) that compared people with MS (MS+) versus healthy people as a control group (MS−). This systematic review and meta-analysis (MA) was performed according to PRISMA guidelines and registered at PROSPERO (CRD42022358975). Results: A total of 13 articles were included in the qualitative synthesis, and 7 of them met the required criteria to be included in the MA. SDNN (−0.33 [−0.57, 0.09], p = 0.008), LF (−0.32 [−0.41, −0.23], p < 0.00001), VLF (−0.21 [−0.31, −0.10], p = 0.0001) and TP (−0.20 [−0.33, −0.07], p = 0.002) decreased in patients with MS. The rMSSD (p = 0.41), HF (p = 0.06) and LF/HF ratio (p = 0.64) were not modified. Conclusions: In long-term recordings (24 h), SDNN, LF, VLF and TP were consistently decreased in patients with MS. Other parameters that could be included in the quantitative analysis were not modified in MS+ patients (rMSSD, HF, ratio LF/HF). Regarding non-linear analyses, the results are not conclusive due to the low number of datasets found, which prevented us from conducting an MA.

A chronic model of acute myocardial infarction was developed to study the mechanisms involved in adverse postinfarction ventricular remodeling. In an acute myocardial infarction (AMI), the left circumflex coronary artery of New Zealand White rabbits (n = 9) was occluded by ligature for 1 h, followed by reperfusion. A specific care protocol was applied before, during, and after the intervention, and the results were compared with those of a sham operated group (n = 7). After 5 weeks, programmed stimulation and high-resolution mapping were performed on isolated and perfused hearts using the Langendorff technique. The infarct size determined by 2,3,5-triphenyltetrazolium chloride inside of the area at risk (thioflavin-S) was then determined. The area at risk was similar in both groups (54.33% (experimental infarct group) vs. 58.59% (sham group), ns). The infarct size was 73.16% as a percentage of the risk area. The experimental infarct group had a higher inducibility of ventricular arrhythmias (100% vs. 43% in the sham group, p = 0.009). A reproducible chronic experimental model of myocardial infarction is presented in which the extent and characteristics of the lesions enable the study of the vulnerability to develop ventricular arrhythmias because of the remodeling process that occurs during cardiac tissue repair.

Metabolic syndrome (MetS) has been associated with an increased prevalence of cardiac arrhythmias and sudden cardiac death caused by ventricular fibrillation (VF), but the exact underlying mechanisms are not known. Our aim here was to study the effects that diet‐induced MetS produces on ventricular remodelling and its potential electrophysiological arrhythmogenic mechanisms. Thirty‐five male NZW rabbits were assigned to a control (n = 16) or MetS group (n = 19), fed for 28 weeks with a high‐fat and high‐sucrose diet. Echocardiography and electrocardiography were performed before diet and at weeks 14 and 28. Hearts were isolated and perfused in a Langendorff system and epicardial optical mapping was performed using two EMCCD cameras focused on the left (LV) and right (RV) ventricles. mRNA expression levels for ion channel proteins were examined by quantitative RT‐PCR. A mixed‐model ANOVA and unpaired t test were used for statistical analysis. MetS animals showed LV hypertrophy and electrophysiological abnormalities (increased PQ, QRS, QTc and T wave). In isolated hearts, MetS animals had shorter optical APD90 (action potential duration at 90% repolarization), increased restitution slope and alternans, and faster frequency of activation during VF in the RV, whereas no difference was observed in the LV. The mRNA expression for KvLQT1 and KChIP2 increased in the RV. MetS produced LV hypertrophy, and altered atrioventricular and ventricular conduction and repolarization abnormalities. In isolated hearts, the physiological gradients of refractoriness and frequency of activation during VF were abolished in MetS animals, with fast activation rates in both ventricles, which could be explained, at least in part, by upregulation of KvLQT1 and KChIP2 in the RV. image Key points: Metabolic syndrome (MetS) has been associated with ventricular arrhythmias and sudden cardiac death, but the exact underlying mechanisms are not known. Previous studies have addressed the effects that individual components of MetS exert, individually, upon electrical cardiac remodelling, but the results obtained in some cases prove inconclusive or contradictory. We investigated the effects of diet‐induced MetS on ventricular remodelling and its potential electrophysiological arrhythmogenic mechanisms. We found that diet‐induced MetS produced altered activation–repolarization abnormalities as well as fast‐activation non‐stable flattening of the spatial distribution of dominant frequencies driving ventricular fibrillation, which might be explained, at least in part, due to increased expression of potassium channels in the right ventricle.