Since ancient times green tea has been considered a health-promoting beverage. In recent years, scientists throughout the world have investigated the potential benefits of green tea and its most abundant catechin, epigallocatechin gallate (EGCG). The anti-cancer effects of green tea and EGCG were the focus of early research, and encouraging data from in vitro, animal model, and human studies have emerged. Due to the dominant role of cardiovascular disease and the dramatic rise of obesity and type 2 diabetes mellitus as major and interlinked healthcare problems, green tea and EGCG are increasingly being investigated in these areas. Dose-response relationships observed in several epidemiological studies have indicated that pronounced cardiovascular and metabolic health benefits can be obtained by regular consumption of 5-6 or more cups of green tea per day. Furthermore, intervention studies using similar amounts of green tea, containing 200-300 mg of EGCG, have demonstrated its usefulness for maintaining cardiovascular and metabolic health. Additionally, there are numerous in vivo studies demonstrating that green tea and EGCG exert cardiovascular and metabolic benefits in these model systems. Therefore, green tea and EGCG can be regarded as food components useful for the maintenance of cardiovascular and metabolic health. To prove the effectiveness for disease prevention or treatment, several multi-center, long-term clinical studies investigating the effects of one precisely-defined green tea product on cardiovascular and metabolic endpoints would be necessary. The aim of this manuscript is to provide an overview of the research investigating the effects of green tea and green tea catechins on cardiovascular and metabolic health.
Rose hip powder (RHP) alleviates osteoarthritis (OA) due to its anti-inflammatory and cartilage-protective properties. Substances contained in RHP might contribute to its clinical efficacy. The activity of two RHP (i.e., RH-A, from the whole fruit, RH-B, from fruits without seeds) was investigated in human peripheral blood leukocytes (PBL) and primary chondrocytes (NHAC-kn). RH-A and RH-B diminished the secretion of chemokines and cytokines in LPS/IFN-γ-activated PBL, including CCL5/RANTES, CXCL10/IP-10, interleukin- (IL-) 6, and IL-12. Most effects were transcriptional, since gene expression levels were significantly influenced by RH-A and RH-B. In IL-1βtreated normal chondrocytes (NHAC-kn), both RH preparations reduced the expression of matrix metalloproteinase- (MMP-) 1, MMP-3, and MMP-13 and ADAMTS-4. These changes are associated with diminished inflammatory damage or cartilage erosion. Principal component analysis revealed that (1) RH-A and RH-B modified a large pattern of biomarkers, and (2) RH-B outperformed RH-A. Furthermore, RH-B contained more chondroprotective and anti-inflammatory constituents than RH-A. Thus, RHP contributed to restore cellular homeostasis in PBL and chondrocytes. RH preparations from fruits without seeds are thus expected to have an improved OA-preventive or OA-therapeutic profile, as subsequently shown in a related clinical trial.
Objective— To assess the importance of genetic background for collateral artery development. Methods and Results— C57BL/6, BALB/c and 129S2/Sv mice were studied after femoral artery ligation by laser Doppler imaging, visible light oximetry, time-of-flight–magnetic resonance imaging, and treadmill testing; C57BL/6 and BALB/c also underwent electron paramagnetic resonance (EPR) oximetry, x-ray angiography, and histology. C57BL/6 had the least initial distal ischemia and most complete recovery. BALB/c had the most severe initial ischemia and poorest recovery. BALB/c had some vasodilatory reserve in their ligated limbs not seen in the other strains at 3 weeks. By in vivo TOF-magnetic resonance angiography, C57BL/6 had larger preexistent and developed collaterals. By x-ray angiography, C57BL/6 had a higher collateral-dependent filling score and number of visible collaterals immediately after femoral ligation and a higher number of visible collaterals at 1 week but not at 4 weeks. EPR oximetry and histology revealed hypoxia and tissue damage in regions of collateral growth of BALB/c but not C57BL/6 mice. In C57BL/6 BrdUrd uptake in the thigh was limited to larger vessels and isolated perivascular cells. Proliferative activity in collateral arterioles was similar in both strains. Conclusions— Genetic differences in preexistent collateral vasculature can profoundly affect outcome and milieu for compensatory collateral artery growth after femoral artery occlusion.
Fibroblast growth factor (FGF)-1 plays important roles during myocardial and coronary morphogenesis. FGF-1 is also involved in the physiological response of the adult heart against ischemia, which includes cardiomyocyte protection and vascular growth. In the present study, we have generated transgenic mice with specific myocardial overexpression of the gene. Transgene expression was verified by Northern blot, and increased FGF-1 protein content was assessed by Western blot and immunoconfocal microscopy. Anatomic, histomorphological, and ultrastructural analyses revealed no major morphological or developmental abnormalities of transgenic hearts. Capillary density was unaltered, whereas the density of coronary arteries, especially arterioles, was significantly increased, as was the number of branches of the main coronary arteries. In addition, the coronary flow was significantly enhanced in transgenic mice ex vivo. These differences in the anatomic pattern of the coronary vasculature are established during the second month of postnatal life. The present findings demonstrate an important role of FGF-1 in the differentiation and growth of the coronary system and suggest that it is a key regulatory molecule of the differentiation of the arterial system.
Abstract During the last decade, the traditional notion that green tea consumption benefits health has received significant scientific attention and, particularly, the areas of cardiovascular disease and cancer were subject to numerous studies. Due to the ever‐growing obesity pandemic, the anti‐obesity effects of green tea are being increasingly investigated in cell, animal, and human studies. Green tea, green tea catechins, and epigallocatechin gallate (EGCG) have been demonstrated in cell culture and animal models of obesity to reduce adipocyte differentiation and proliferation, lipogenesis, fat mass, body weight, fat absorption, plasma levels of triglycerides, free fatty acids, cholesterol, glucose, insulin and leptin, as well as to increase beta‐oxidation and thermogenesis. Adipose tissue, liver, intestine, and skeletal muscle are target organs of green tea, mediating its anti‐obesity effects. Studies conducted with human subjects report reduced body weight and body fat, as well as increased fat oxidation and thermogenesis and thereby confirm findings in cell culture systems and animal models of obesity. There is still a need for well‐designed and controlled clinical studies to validate the existing and encouraging human studies. Since EGCG is regarded as the most active component of green tea, its specific effects on obesity should also be investigated in human trials.
Green tea was suggested as a therapeutic agent for the treatment of diabetes more than 70 years ago, but the mechanisms behind its antidiabetic effect remains elusive. In this work, we address this issue by feeding a green tea extract (TEAVIGO™) with a high content of epigallocatechin gallate (EGCG) or the thiazolidinedione PPAR-γ agonist rosiglitazone, as positive control, to db/db mice, an animal model for diabetes.Young (7 week-old) db/db mice were randomized and assigned to receive diets supplemented with or without EGCG or rosiglitazone for 10 weeks. Fasting blood glucose, body weight and food intake was measured along the treatment. Glucose and insulin levels were determined during an oral glucose tolerance test after 10 weeks of treatment. Pancreata were sampled at the end of the study for blinded histomorphometric analysis. Islets were isolated and their mRNA expression analyzed by quantitative RT-PCR.The results show that, in db/db mice, EGCG improves glucose tolerance and increases glucose-stimulated insulin secretion. EGCG supplementation reduces the number of pathologically changed islets of Langerhans, increases the number and the size of islets, and heightens pancreatic endocrine area. These effects occurred in parallel with a reduction in islet endoplasmic reticulum stress markers, possibly linked to the antioxidative capacity of EGCG.This study shows that the green tea extract EGCG markedly preserves islet structure and enhances glucose tolerance in genetically diabetic mice. Dietary supplementation with EGCG could potentially contribute to nutritional strategies for the prevention and treatment of type 2 diabetes.
Background: Mice overexpressing peroxisome proliferator-activated receptorδ (PPARδ) in skeletal muscle are characterized by reduced adiposity, enhanced skeletal muscle lipid oxidation, increased numbers of type I fibers and markedly prolonged running time on the treadmill. It was hypothesized that treatment with PPARδ agonists could increase exercise capacity. Methods: Male C57BL/6J mice on a high-fat diet were randomized to receive GW501516 at 3, 10, or 30 mg/kg/day or placebo for 2 months. Two additional groups receiving GW501516 at 10 mg/kg/day or placebo were allowed to perform voluntary wheel running during the study. Body weight, body composition, glucose tolerance, voluntary wheel running activity and maximal exercise capacity on the treadmill were determined. Results: GW501516 decreased body weight and body fat and improved oral glucose tolerance in a dose-dependent manner. Voluntary wheel running activity significantly decreased over time in mice receiving GW501516 at 10 mg/kg/day. Maximal exercise capacity was not altered by GW501516 in sedentary mice. In voluntarily running mice, GW501516 modestly decreased maximal exercise capacity on the treadmill compared to placebo, which could be a direct consequence of the reduced voluntary running activity. Conclusion: Treatment with the synthetic PPARδ agonist GW501516 for 2 months does not improve maximal exercise capacity in sedentary mice. Furthermore, voluntary wheel running activity was reduced in mice receiving GW501516, which may have resulted in the observed decrease in treadmill exercise capacity.
