Function In Metabolic Syndrome Research Articles

The Regulatory Role of microRNA-21 in Coronary Microcirculation in Metabolic Syndrome

Coronary vasculature is essential to supply oxygen and nutrients to the heart and maintain normal cardiac function. Obstruction of large vessels of coronaries (atherosclerosis) is well studied, but coronary microvascular dysfunction (CMD), which is associated with diabetic cardiomyopathy, Takotsubo cardiomyopathy, Ischemia with the non-obstructive coronary artery (INOCA), and HFpEF, is understudied. CMD is characterized by impaired endothelial-dependent vasodilation, but detailed mechanisms have yet to be elucidated. The anti-fibrotic role of microRNA-21 (miR-21) is reported in the HFrEF induced by ischemia/reperfusion or pressure overload, but how miR-21 regulates CMD is not entirely understood. Our recent study shows miR-21 ablation ameliorated impaired vasodilation in isolated coronaries of mice fed on high fat and high sugar (HFHS) diet. In this study, we examined the coronary flow reserve (CFR), the relationship between myocardial blood flow (MBF) and cardiac work (doppler) under hyperemia, cardiac function (echocardiography and exercise exertion test), fibrosis and gene expression of miR-21 knockout and wild-type (WT) mice fed on chow or HFHS diet. Our preliminary data show that MBF and CFR were decreased, cardiac index, stroke volume, and running distance were reduced, and the E/E’ ratio was increased in WT mice fed on the HFHS diet compared to the WT mice fed on the chow diet. The perivascular fibrosis was increased in the WT mice fed on the HFHS diet compared to WT mice on the chow diet. The ablation of miR-21 reversed all these changes in the mice treated with HFHS, suggesting miR-21 deficiency ameliorated CMD in metabolic syndrome. Moreover, we used endothelial-specific miR-21 knockout to study the endothelial miR-21 function. Interestingly, the endothelial mi-R21 KO phenocopied the global knockouts, suggesting the benefit of miR-21 deficiency to coronary microvascular function in metabolic syndrome is from endothelial cells. The study provides the potential therapeutic strategy to target vascular endothelial cells with miR-21 antagomir for CMD in metabolic syndromes. AHA 970663,1R56HL165207,1 R01 HL165207-01A1 to LY and 1 F31 HL156726-01A1 to CJ. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Altered Autonomic Function in Metabolic Syndrome: Interactive Effects of Multiple Components

Metabolic syndrome (MetS) describes a set of disorders that collectively influence cardiovascular health, and includes hypertension, obesity, insulin resistance, diabetes, and dyslipidemia. All these components (hypertension, obesity, dyslipidemia, and prediabetes/diabetes) have been shown to modify autonomic function. The major autonomic dysfunction that has been documented with each of these components is in the control of sympathetic outflow to the heart and periphery at rest and during exercise through modulation of the arterial baroreflex and the muscle metaboreflex. Many studies have described MetS components in singularity or in combination with the other major components of metabolic syndrome. However, many studies lack the capability to study all the factors of metabolic syndrome in one model or have not focused on studying the effects of how each component as it arises influences overall autonomic function. The goal of this review is to describe the current understanding of major aspects of metabolic syndrome that most likely contribute to the consequent/associated autonomic alterations during exercise and discuss their effects, as well as bring light to alternative mechanisms of study.

Assessment of left atrial function in patients with metabolic syndrome by four-dimensional automatic left atrial quantification

ObjectiveThis study aimed at assessing the changes of left atrial (LA) volume and strain function in metabolic syndrome (MS) patients using four-dimensional automatic left atrial quantification (4D-LAQ) and exploring independent correlative factors for LA function. MethodsA total of 110 MS patients and 70 normal controls were selected and assigned into the MS group and the control group, respectively. Echocardiogram parameters were routinely examined and the thickness of epicardial adipose tissue (EAT) were measured with a parasternal long axis of left ventricle(LV). The LA volume and strain parameters were determined using 4D-LAQ. The independent correlation factors for LA strain parameters in MS patients were investigated through linear regression analysis. ResultsCompared with the control group, LA volume parameters were increased in the MS group, LA strain parameters and LA emptying fraction (LAEF) were decreased (all P < 0.05). EAT thickness is associated with LA reservoir longitudinal strain (LASr), conduit longitudinal strain (LAScd), reservoir circumferential strain (LASr-c), and conduit circumferential strain (LAScd-c) (all P < 0.05). LA contraction longitudinal (LASct) and circumferential strain (LASct-c) were not statistically significant. Regression analysis results show that systolic blood pressure (SBP) and triglyceride (TG) are independent correlative factors. Intra-observer and inter-observer repeatability test showed that the LA parameters examined by 4D-LAQ had good agreement. Conclusions4D-LAQ is capable of effectively assessing the LA function in MS patients and providing a useful reference for clinical diagnosis. SBP and TG serve as the independent correlative factors for LA function.

Kiosk 11R-TA-08 - The Breathing-induced Myocardial Oxygenation Reserve as a Marker for Vascular Function in Metabolic Syndrome

Kiosk 11R-TA-08 - The Breathing-induced Myocardial Oxygenation Reserve as a Marker for Vascular Function in Metabolic Syndrome

Effect of hyperbaric oxygen (HBO) therapy on kidney function in metabolic syndrome (MetS) patients

Background: Hyperbaric Oxygen (HBO) therapy is the therapy of inhaling 100% pure oxygen in a hyperbaric chamber of more than 1 absolute atmosphere. Currently, the use of hyperbaric oxygen therapy is increasingly widespread, not only for decompression sickness and diving problems. But it has been used for clinical therapy, cosmetics, and geriatric care. The American Food and Drug Administration (FDA) has also confirmed various clinical indications, especially those related to metabolic syndromes such as Diabetes Mellitus (DM) and Diabetic Foot Ulcers (DFU). But the use of Hyperbaric Oxygen Therapy for kidney disease has not been fully study yet. Purpose: Here we summarized the scientific reason to use this therapy as adjuvant for patients with chronic kidney disease due to metabolic syndrome. Opinion: Several benefits of HBO has been reported such as reducing oxidative stress, alleviate vascular dysfunction and amyloid burden, ischemia and reperfusion injury, Increased NO production, and suggested to be useful as an adjuvant therapy in T2DM suspected with chronic kidney disease (CKD), as HBO therapy decrease the proteinuria by 50%. Renal hypoxia is the underlying causes of CK progression and associated hypertension. In hypoxic conditions, cells lack of oxygen, so that the cells carry out anaerobic metabolism or fermentation or Warburg effect. HBO therapy can assist in supplying oxygen more quickly at the cellular level (internal respiration), so that metabolism can re-process aerobically. Conclusion: HBO Therapy improves the patient's general condition in CKD with MetS, thereby preventing kidney disease complications. The effectiveness of HBOT for kidney disease still requires further research with a more frequent and longer treatment.

Abstract 13047: The Modulatory Effects of Perivascular Adipose Tissue on the Renal Arterial Vasorelaxation and Its Relationship With Kidney Function in Metabolic Syndrome

Metabolic syndrome (MetS) is a cluster condition that increases the risk of cardiovascular diseases and type 2 diabetes. Perivascular adipose tissue (PVAT) regulates the arterial tone. We have demonstrated that the renal arterial PVAT enhances the vasorelaxation response in MetS model strains, SHRSP.Z- Lepr fa /IzmDmcr rats (SPZF) and SHR/NDmcr-cp rats (CP). Furthermore, we have found that overactivation of angiotensin II type 1 receptor (AT1R) signaling and a decrease in apelin levels in PVAT leads to a decline in compensatory PVAT effects. MetS is associated with chronic kidney disease, and the dysfunction of the PVAT favoring the vasorelaxation response could be a reason for kidney disease development. Therefore, we investigated the relationship between PVAT function and kidney function using MetS model rats.Renal arteries were isolated from the male and female SPZF and CP at 23 weeks of age. Vasorelaxation and mRNA transcript levels in PVAT were examined using organ bath methods and quantitative real-time polymerase chain reaction, respectively. Systolic blood pressure (sBP) was measured using a tail-cuff method. Insulin, glucose, and creatinine in the serum and protein in the urine were measured using commercial kits and eGFR, and the HOMA-IR were calculated.sBP was higher in SPZF than CP, but lower in females than males. HOMA-IR and urine protein levels were the lowest, while eGFR and enhancing effects of PVAT on acetylcholine-induced relaxations were the highest in female CP among the groups. eGFR was negatively correlated with sBP, HOMA-IR, and urinary protein levels. The enhancements of relaxations by PVAT were negatively correlated with sBP, HOMA-IR, and AT1R activity in PVAT.This study suggests that the insulin resistance and high blood pressure are associated with PVAT dysfunction, resulting from AT1 activation in PVAT, while it does not support the hypothesis that the disappearance of the effects of PVAT directly leads to kidney dysfunction.

Mechanisms of Oxidative Stress in Metabolic Syndrome.

Metabolic syndrome is a cluster of conditions associated with the risk of diabetes mellitus type 2 and cardiovascular diseases (CVDs). Metabolic syndrome is closely related to obesity. Increased adiposity promotes inflammation and oxidative stress, which are precursors of various complications involving metabolic syndrome components, namely insulin resistance, hypertension, and hyperlipidemia. An increasing number of studies confirm the importance of oxidative stress and chronic inflammation in the etiology of metabolic syndrome. However, few studies have reviewed the mechanisms underlying the role of oxidative stress in contributing to metabolic syndrome. In this review, we highlight mechanisms by which reactive oxygen species (ROS) increase mitochondrial dysfunction, protein damage, lipid peroxidation, and impair antioxidant function in metabolic syndrome. Biomarkers of oxidative stress can be used in disease diagnosis and evaluation of severity.

Effect of Metabolic Dysfunction-Associated Fatty Liver Disease on Left Ventricular Deformation and Atrioventricular Coupling in Patients With Metabolic Syndrome Assessed by MRI.

Metabolic dysfunction-associated fatty liver disease (MAFLD) was recently recognized as an important risk factor for cardiovascular diseases. To examine the effect of MAFLD on cardiac function in metabolic syndrome by MRI. Retrospective. One hundred seventy-nine patients with metabolic syndrome (MetS), 101 with MAFLD (MAFLD [+]) and 78 without (MAFLD [-]). Eighty-one adults without any of the components of MetS or cardiac abnormalities were included as control group. 3.0 T; balanced steady-state free precession sequence. Left atrial (LA) strain was assessed during three phases: reservoir strain (LA-RS), conduit strain (LA-CS), and booster strain (LA-BS). Left ventricular (LV) global longitudinal (LV-GLS) strain was also derived. The left atrioventricular coupling index (LACI) was calculated as the ratio of LA end-diastolic volume (LA-EDV) and LV-EDV. Student's t test or Mann-Whitney U test; One-way analysis of variance. A P value <0.05 was considered statistically significant. Among MetS patients, individuals with MAFLD had significantly lower magnitude LV-GLS (-11.6% ± 3.3% vs. -13.8% ± 2.7%) than those without MAFLD. For LA strains, LA-RS (36.9% ± 13.7% vs. 42.9% ± 13.5%) and LA-CS (20.0% ± 10.6% vs. 24.1% ± 9.2%) were also significantly reduced in MAFLD (+) compared to MAFLD (-). The LACIs (17.2% [12.9-21.2] % vs. 15.8% [12.2-19.7] %) were significantly higher in patients with MAFLD compared to those without MAFLD. After adjustment for other clinical factors, MAFLD was found to be independently correlated with LV-GLS (β=-0.270) and LACI (β=0.260). MAFLD had an unfavorable effect on LV myocardial strain in MetS. Moreover, LA strain and atrioventricular coupling were further impaired in patients with concomitant MAFLD compared to those without MAFLD. Last, MAFLD was independently associated with subclinical LV dysfunction and atrioventricular coupling after adjustment for other clinical factors. 3 TECHNICAL EFFICACY: 3.

Involvements of apelin derived from perivascular adipose tissue on modulation of vasorelaxation and kidney function in metabolic syndrome

Involvements of apelin derived from perivascular adipose tissue on modulation of vasorelaxation and kidney function in metabolic syndrome

PS-B11-10: IRON DEFICIENCY AFFECTS CARDIAC FUNCTION BUT HAS NO EFFECT ON BLOOD PRESSURE IN MICE WITH METABOLIC SYNDROME

Objective: Metabolic syndrome is a serious problem concerning public health, increasing the risk of cardiovascular diseases. Some epidemiological studies have reported that iron overload is associated with metabolic syndrome; however, it remains unknown whether iron deficiency affects the pathogenesis of metabolic syndrome. Therefore, in this study, we investigated the impact of dietary iron deficiency in genetically obese KKAy mice, a model of human metabolic syndrome. Methods: Four-week-old male KKAy mice and control C57BL/6J mice (wild-type mice, WT) were fed a normal or an iron-restricted diet, and the impact of dietary iron deficiency was investigated 12 weeks after diet initiation. Results: Compared with WT mice, systolic blood pressure presented an increasing trend in KKAy mice; however, the difference was not statistically significant between the two groups, and this trend did not change after iron restriction. Notably, some KKAy mice died following iron restriction, while no deaths were recorded in WT mice. Of interest, obese KKAy mice exhibited cardiac hypertrophy and cardiac dysfunction, thereby developing heart failure with pulmonary congestion after iron restriction. Conclusions: These results indicate that iron deficiency affects cardiac function in metabolic syndrome.

Extracellular vesicles and insulin-mediated vascular function in metabolic syndrome.

Metabolic Syndrome (MetS) raises cardiovascular disease risk. Extracellular vesicles (EVs) have emerged as important mediators of insulin sensitivity, although few studies on vascular function exist in humans. We determined the effect of insulin on EVs in relation to vascular function. Adults with MetS (n=51, n=9M, 54.8 ± 1.0 years, 36.4 ± 0.7kg/m2 , ATPIII: 3.5 ± 0.1a.u., VO2 max: 22.1 ± 0.6ml/kg/min) were enrolled in this cross-sectional study. Peripheral insulin sensitivity (M-value) was determined during a euglycemic clamp (40 mU/m2 /min, 90 mg/dl), and blood was collected for EVs (CD105+, CD45+, CD41+, TX+, and CD31+; spectral flow cytometry), inflammation, insulin, and substrates. Central hemodynamics (applanation tonometry) was determined at 0 and 120 min via aortic waveforms. Pressure myography was used to assess insulin-induced arterial vasodilation from mouse 3rd order mesenteric arteries (100-200 μm in diameter) at 0.2, 2 and 20 nM of insulin with EVs from healthy and MetS adults. Adults with MetS had low peripheral insulin sensitivity (2.6 ± 0.2 mg/kg/min) and high HOMA-IR (4.7 ± 0.4 a.u.) plus Adipose-IR (13.0 ± 1.3 a.u.). Insulin decreased total/particle counts (p < 0.001), CD45+ EVs (p=0.002), AIx75 (p=0.005) and Pb (p=0.04), FFA (p < 0.001), total adiponectin (p=0.006), ICAM (p=0.002), and VCAM (p=0.03). Higher M-value related to lower fasted total EVs (r=-0.40, p=0.004) while higher Adipose-IR associated with higher fasted EVs (r=0.42, p=0.004) independent of VAT. Fasting CD105+ and CD45+ derived total EVs correlated with fasting AIx75 (r=0.29, p < 0.05) and Pb (r=0.30, p < 0.05). EVs from MetS participants blunted insulin-induced vasodilation in mesenteric arteries compared with increases from healthy controls across insulin doses (all p < 0.005). These data highlight EVs as potentially novel mediators of vascular insulin sensitivity and disease risk.

Inflammaging and Vascular Function in Metabolic Syndrome: The Role of Hyperuricemia.

Background and Objectives: Early vascular aging determines a more rapid course of age-related arterial changes. It may be induced by a proinflammatory state, caused by hyperuricemia and metabolic syndrome and their interrelationship. However, the impact of serum uric acid (SUA) on early arterial stiffening and vascular function remains uncertain. Materials and Methods: A total of 696 participants (439 women aged 50–65 and 257 men aged 40–55) from the Lithuanian High Cardiovascular Risk (LitHiR) primary prevention program were enrolled in the study. They underwent anthropometric measurements and laboratory testing along with arterial parameters’ evaluation. Quality carotid stiffness (QCS), carotid-radial pulse wave velocity (crPWV), carotid-femoral pulse wave velocity (cfPWV), flow-mediated dilatation (FMD), and carotid intima-media thickness (CIMT) were registered. Results: We found that hyperuricemia was significantly associated with inflammation, registered by high-sensitivity C-reactive protein in both sexes. A very weak but significant association was observed between cfPWV and SUA in men and in women, while, after adjusting for risk factors, it remained significant only in women. A positive, weak, but significant association was also observed for QCS, both right and left in women. No relationship was observed between crPWV, FMD, CIMT, and SUA.

Low THRB (thyroid hormone receptor beta) Promoter Methylation Levels in Peripheral Blood Leukocytes Induced By Systematic Inflammation Are Involved in Low Thyroid Hormone Function in Metabolic Syndrome.

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Bimodal Effects of P2Y12 Antagonism on Matrix Metalloproteinase–Associated Contractile Dysfunction in İnsulin-Resistant Mammalian Heart

The matrix metalloproteinases (MMPs) contribute to matrix remodeling in diabetes via tissue degradation; however, their contributions can be different depending on the pathology. For instance, MMPs are elevated in acute stress hyperglycemia, whereas they can be degraded in chronic hyperglycemia. Since studies emphasize the possible cardioprotective effect of ticagrelor (Tica) beyond its antiplatelet action, we aimed to examine whether Tica treatment can reverse the depressed heart function of metabolic syndrome (MetS) rats via affecting the expression levels of MMPs. Tica treatment of high-carbohydrate-induced MetS rats could not affect significantly the depressed contractile activity of Langendorff-perfused heart preparations. On the other hand, the Tica treatment provided a significant recovery in the reduced relaxation activity of the aortic preparations from the same animals. Histological examination of the hearts demonstrated marked damages in Mets rats, such as increases in the number of foamy cells and accumulation of collagen fiber and increases in the elastic lamellar irregularity of tunica media, while Tica treatment provided a slight improvement in the structure of left ventricle tissue. We also could not obtain a significant reverse in the high cytosolic labile Zn2+ ([Zn2+]i) with the treatment of cardiomyocytes with Tica. Furthermore, Tica treatment of MetS rats could not significantly reverse the degraded protein levels of MMP-2 and MMP-9 in the heart, as well. Overall, we demonstrated that Tica treatment of MetS rats has no significant benefits on the depressed heart function, although provide a significant beneficial impact on vascular relaxation. This action of Tica may be through its lack of action on both MMP degradation and high [Zn2+]i, which can further precipitate in cleavage of extracellular matrix in the heart.

Endothelial function in metabolic syndrome and its complications: the relationship of functional and structural changes in the cardiovascular system and mechanisms of vascular tone regulation

Endothelial dysfunction is a systemic pathological disorder characterized by weakening of endothelium-dependent vasodilation and vascular remodeling, which is an early manifestation of pathological processes in the cardiovascular system. Vascular endothelial abnormalities in a clinical setting can be diagnosed by biochemical and functional markers. However, there is still no unified optimal method for diagnosing endothelial dysfunction. The aim of the project was to evaluate endothelial dysfunction in patients with metabolic syndrome and to improve the diagnosis and monitoring of treatment effectiveness. Endothelial dysfunction was studied using the method of wavelet analysis of skin temperature fluctuations, and a thermal test was used to assess the properties dynamic state of the endothelium. The obtained data were compared with endothelial dysfunction biochemical markers at baseline and in dynamics after the therapy. The study showed that the wavelet analysis of skin temperature fluctuations technique can be used for diagnosing the endothelial dysfunction. This technique is simple, convenient, reproducible, it has been confirmed by laboratory determination of endothelial dysfunction markers.

Diabetic atherosclerosis: is there a role for the hypoxia-inducible factors?

Atherosclerosis is a major cause of mortality worldwide and is driven by multiple risk factors, including diabetes. Diabetes is associated with either an insulin deficiency in its juvenile form or with insulin resistance and obesity in Type 2 diabetes mellitus, and the latter is clustered with other comorbidities to define the metabolic syndrome. Diabetes and metabolic syndrome are complex pathologies and are associated with cardiovascular risk via vascular inflammation and other mechanisms. Several transcription factors are activated upon diabetes-driven endothelial dysfunction and drive the progression of atherosclerosis. In particular, the hypoxia-inducible factor (HIF) transcription factor family is a master regulator of endothelial biology and is raising interest in the field of atherosclerosis. In this review, we will present an overview of studies contributing to the understanding of diabetes-driven atherosclerosis, integrating the role of HIF in this disease with the knowledge of its functions in metabolic syndrome and diabetic scenario.

Dietary consumption and serum pattern of bioactive fatty acids in NAFLD patients

Introduction and objectivesNonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome. Some dietary fatty acids have showed different bioactive functions in metabolic syndrome. The aim of this study is to determine the dietary consumption patterns and serum percentage of bioactive fatty acids in NAFLD patients. Patients and methodsCross-sectional study with NAFLD patients and non-NAFLD patients. Dietary consumption of bioactive fatty acids was assessed by a food frequency questionnaire. NAFLD and liver fibrosis were diagnosed by transient elastography. The identification of serum bioactive fatty acids was achieved by gas chromatography–mass spectrometry (%). Bioactive fatty acids consumption was correlated with NAFLD clinical characteristics with the Spearman correlation analysis. ResultsA total of 299 patients were included, whose mean of age and body mass index were 44.2±9.9 years and 25.9±3.8kg/m2, respectively. The consumption of bioactive fatty acids was no different regarding the presence of NAFLD; however, the consumption of stearic and linoleic fatty acids was higher in relation with NAFLD severity (p≤0.05). The consumption of myristic acid was higher in patients with fibrosis (p=0.02). Serum percentage and dietary consumption did not show correlations. ConclusionDietary consumption of bioactive fatty acids is different according to NAFLD severity. Individualized diets according to NAFLD severity could be successful in order to prevent liver injury-related outcomes.

A study of endothelial function by flow-mediated vasodilatation in patients with metabolic syndrome

Background: Metabolic syndrome (MetS) is characterized by clustering of cardiovascular risk factors.Endothelial dysfunction is the key early event in atherogenesis that occurs long before structural atherosclerotic changes and promotes cardiovascular events. The assessment of endothelial function by flow-mediated dilation (FMD) of the brachial artery has been proposed as a non-invasive marker for cardiovascular risk. Aim: Assessment of flow mediated vasodilatation of brachial artery as a non invasive marker of endothelial function in metabolic syndrome and To assess the relationship of number of risk factors in metabolic syndrome with endothelial dysfunction. Methodology: A case control study in which 50 patients with Metabolic Syndrome as per new IDF criteria and 50 controls were studied. Detailed clinical history, examination and Blood investigations like Fasting blood glucose, fasting lipid profile and ECG was done for every patients. Endothelial function was assessed by brachial artery flow mediated vasodilatation. Results: In the present study 100 (50 cases and 50 controls) patients were studied, males (54%) and females (46%), majority in the age group between 40-60 years (mean age - 49.76 ± 13.76yrs in cases and 44.94 ± 16.09 years among controls). We identified a significant difference between cases and age- and sex-matched controls regarding brachial artery FMD% (7.24 ± 5.24 and 21.29 ± 9.29 respectively; P value-0.000). Negative corelations were found between FMD% and various variables and also between number of components and FMD% (r = -0.239). Conclusion: MetS is associated with endothelial dysfunction as evidenced by decreased FMD% compared to controls. There is a negative correlation between various components of MetS, number of components of MetS and FMD%.

Autonomic functions in metabolic syndrome in Indian subpopulation using heart rate variability - A pilot study

Background: The global industrialization and sedentary lifestyle has led to rise in obesity, hypertension, and diabetes which is associated with increased prevalence of metabolic syndrome (MS) all over the world, with rising trend among the younger population. Individuals with MS are at a higher risk of impaired cardiovascular autonomic function. Aim and Objective: Our study aims to understand the relationship between the MS and autonomic functions in order to improvise the wellbeing of the people who are at either risk of developing or are suffering from MS and promote healthy lifestyle. Materials and Methods: Heart rate variability (HRV) was recorded in 10 participants with MS. The HRV analysis included estimation of time domain parameters and frequency domain parameters, total power and low frequency/high frequency (LF/HF). Results: The HRV parameters showed a decrease in value along with a high LF/HF ratio in the study participants. Conclusion: The study shows that MS significantly leads to dysfunction of autonomic nervous system.

Pelargonidin 3-glucoside-enriched strawberry attenuates symptoms of DSS-induced inflammatory bowel disease and diet-induced metabolic syndrome in rats.

To determine whether the anthocyanin, pelargonidin 3-glucoside (P3G), attenuates symptoms of inflammatory bowel disease (IBD) and metabolic syndrome in rats. We tested P3G-enriched strawberry in two models of chronic inflammation in rats, chronic IBD induced by 0.5% dextran sodium sulphate in the drinking water for 12weeks (D) and metabolic syndrome induced by a high-carbohydrate, high-fat diet (H) for 16weeks. P3G-enriched strawberry was added to the diet for the final 6weeks in IBD rats (DP) or 8weeks in H rats (HP) to provide a dose of 8mg P3G/kg/day. D rats had marked diarrhoea, bloody stools, erosion of mucosal epithelium, crypt atrophy, loss of villi and goblet cells, and inflammatory cell infiltration. These symptoms were reversed by P3G with healthy stools and mucosal lining of ileum and colon including increased villi, crypts and goblet cells and reduced inflammation. H rats developed hypertension, dyslipidaemia, central obesity, increased ventricular stiffness, cardiac and liver inflammation, and steatosis. P3G treatment in H rats improved systolic blood pressure, ventricular stiffness, and cardiac and liver structure, and reduced abdominal fat, abdominal circumference and body weight gain. Our study indicates that dietary P3G decreased inflammation to decrease the symptoms of IBD, and to improve cardiovascular, liver and metabolic functions in metabolic syndrome.