Effect of a Proanthocyanidin-Rich Extract from Longan Flower on Markers of Metabolic Syndrome in Fructose-Fed Rats

Graduate Institute of Food Science and Technology, National Taiwan University, Taipei, Taiwan.
Journal of Agricultural and Food Chemistry (Impact Factor: 2.91). 11/2008; 56(22):11018-24. DOI: 10.1021/jf801966y
Source: PubMed


Recent evidence strongly suggests that oxidative stress due to redox imbalance is highly associated with metabolic syndrome. The objective of this study was to evaluate the effect of the supplementation of longan flower water extract (LFWE), which showed powerful antioxidative activity in vitro, on markers of metabolic syndrome in a fructose-fed rat model. Male Sprague-Dawley rats were randomly divided into four groups: group C, fed with standard Purina chow; group F, fed with high-fructose diet (HF) alone; group L, fed with HF plus LFWE 125 mg/kg bw per day by gavage; and group H, fed HF plus LFWE 250 mg/kg bw per day by gavage. The dietary manipulation lasted for 14 weeks. Results of our study showed that rats fed with HF resulted in oxidative stress and affected the antioxidant status including plasma thiobarbituric acid and liver antioxidant enzyme activity. Treatment with LFWE significantly augmented the antioxidant system. HF was able to cause insulin resistance and elevation of the blood pressure. The supplementation of LFWE ameliorated insulin resistance by enhancing the expression of insulin signaling pathway related proteins, including insulin receptor substrate-1 and glucose transporter 4. LFWE supplementation was also found to decrease systolic blood pressure. These findings indicate that longan flower water extract may improve the symptoms of metabolic syndrome in fructose-fed rats.

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    • "The fructose-fed rat is an interesting and well-validated animal model of diet-induced MS (predominantly acquired MS model) that is commonly used in MS research [15]. Different rat strains with distinct fructose ingestion protocols are reported in the literature and, in all cases, fructose has been observed to induce MS features such as moderate hypertension, glucose intolerance, hyperinsulinemia, insulin resistance, dyslipidemia (hypertriglyceridemia, hypercholesterolemia ), altered cytokine and adipokine status (altered tumor necrosis factor-alpha (TNF-í µí»¼) and leptin levels, e.g.), decreased melatonin production, and/or increased body fat and/or body weight [15] [16] [17] [18] [19] [20]. Both in humans and rats, a strong association has been found between MS and oxidative stress [21] and fructosefeeding associates with modification of the hepatic redox status [16, 22–24]. "
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    ABSTRACT: The Metabolic Syndrome increases the risk for atherosclerotic cardiovascular disease and type 2 Diabetes Mellitus. Increased fructose consumption and/or mineral deficiency have been associated with Metabolic Syndrome development. This study aimed to investigate the effects of 8 weeks consumption of a hypersaline sodium-rich naturally sparkling mineral water on 10% fructose-fed Sprague-Dawley rats (Metabolic Syndrome animal model). The ingestion of the mineral water (rich in sodium bicarbonate and with higher potassium, calcium, and magnesium content than the tap water used as control) reduced/prevented not only the fructose-induced increase of heart rate, plasma triacylglycerols, insulin and leptin levels, hepatic catalase activity, and organ weight to body weight ratios (for liver and both kidneys) but also the decrease of hepatic glutathione peroxidase activity and oxidized glutathione content. This mineral-rich water seems to have potential to prevent Metabolic Syndrome induction by fructose. We hypothesize that its regular intake in the context of modern diets, which have a general acidic character interfering with mineral homeostasis and are poor in micronutrients, namely potassium, calcium, and magnesium, could add surplus value and attenuate imbalances, thus contributing to metabolic and redox health and, consequently, decreasing the risk for atherosclerotic cardiovascular disease.
    International Journal of Endocrinology 02/2014; 2014(1):384583. DOI:10.1155/2014/384583 · 1.95 Impact Factor
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    • "Proanthocyanidin(PAC- ) rich extract from acacia bark was found to modulate the aforementioned kinases in addition to IKKβ in a dosedependent manner (unpublished). Others have also shown that PAC from a variety of botanicals improved symptoms of metabolic syndrome in vivo [14] [15]. "
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    ABSTRACT: The plant-based compounds rho-iso-alpha acids (RIAA) from Humulus lupulus (hops) and proanthocyanidins (PAC) from Acacia nilotica have been shown to modulate insulin signaling in vitro. We investigated their effects on triglyceride (TG) deposition in 3T3-L1 adipocytes, glucose and insulin in obese mouse models, and metabolic syndrome markers in adults with metabolic syndrome. The combination of RIAA and PAC synergistically increased TG content and adiponectin secretion in 3T3-L1 adipocytes under hyperinsulinemic conditions and reduced glucose or insulin in obese mice. In a clinical trial, tablets containing 100 mg RIAA and 500 mg PAC or placebo were administered to metabolic syndrome subjects (3 tablets/day, n = 35; 6 tablets/day, n = 34; or placebo, n = 35) for 12 weeks. Compared to placebo, subjects taking 3 tablets daily showed greater reductions in TG, TG : HDL, fasting insulin, and HOMA scores. The combination of RIAA : PAC at 1 : 5 (wt : wt) favorably modulates dysregulated lipids in insulin resistance and metabolic syndrome.
    Journal of nutrition and metabolism 05/2010; 2010. DOI:10.1155/2010/467316
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    • "Notably, determining what concentration would be comparable between humans and rats is difficult, given that a rat is expected to metabolize fructose at a different rate than a human (Truswell, 1994) and because rats typically require higher doses of drugs than humans to observe an effect. The 60 % fructose concentration, however, produces hippocampal insulin resistance in hamsters (Mielke et al., 2005) and is the amount that is used most extensively in current rodent studies (Behr-Roussel, Oudot, Compagnie, Gorny, Le Coz, Bernabe, Wayman, Alexandre, and Giuliano, 2008; de Moura et al., 2008; Tsai, Wu, and Hwang, 2008), which greatly facilitates comparison across studies. "
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    ABSTRACT: Over the past three decades there has been a substantial increase in the amount of fructose consumed by North Americans. Recent evidence from rodents indicates that hippocampal insulin signaling facilitates memory and excessive fructose consumption produces hippocampal insulin resistance. Based on this evidence, the present study tested the hypothesis that a high fructose diet would impair hippocampal-dependent memory. Adult male Sprague-Dawley rats (postnatal day 61) were fed either a control (0% fructose) or high fructose diet (60% of calories). Food intake and body mass were measured regularly. After 19 weeks, the rats were given 3 days of training (8 trials/day) in a spatial version of the water maze task, and retention performance was probed 48 h later. The high fructose diet did not affect acquisition of the task, but did impair performance on the retention test. Specifically, rats fed a high fructose diet displayed significantly longer latencies to reach the area where the platform had been located, made significantly fewer approaches to that area, and spent significantly less time in the target quadrant than did control diet rats. There was no difference in swim speed between the two groups. The retention deficits correlated significantly with fructose-induced elevations of plasma triglyceride concentrations. Consequently, the impaired spatial water maze retention performance seen with the high fructose diet may have been attributable, at least in part, to fructose-induced increases in plasma triglycerides.
    Neurobiology of Learning and Memory 07/2009; 92(3):410-6. DOI:10.1016/j.nlm.2009.05.007 · 3.65 Impact Factor
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