This product is isolated and purified from the herbs of Inula japonica Thunb.
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
669.3ºC at 760 mmHg
>320 ºC (ethanol )
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For Reference Standard and R&D, Not for Human Use Directly.
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Increased sugar consumption, especially fructose, is strongly related to the development of type 2 diabetes (T2D) and metabolic syndrome. The aim of this study was to evaluate long term effects of fructose supplementation on Wistar rats. Three-week-old male rats were randomly divided into 2 groups: control (C; n = 14) and fructose fed (FF; n = 18), with a fructose enriched drink (20-25% w/v fructose in water) for 21 weeks. Systolic blood pressure, fasting glycemia, and bodyweight were regularly measured. Glucose tolerance was evaluated three times using an oral glucose tolerance test. Insulin levels were measured concomitantly and insulin resistance markers were evaluated (HOMA 2-IR, Insulin Sensitivity Index for glycemia (ISI-gly)). Lipids profile was evaluated on plasma. This fructose supplementation resulted in the early induction of hypertension without renal failure (stable theoretical creatinine clearance) and in the progressive development of fasting hyperglycemia and insulin resistance (higher HOMA 2-IR, lower ISI-gly) without modification of glucose tolerance. FF rats presented dyslipidemia (higher plasma triglycerides) and early sign of liver malfunction (higher liver weight). Although abdominal fat weight was increased in FF rats, no significant overweight was found. In Wistar rats, 21 weeks of fructose supplementation induced a metabolic syndrome (hypertension, insulin resistance, and dyslipidemia) but not T2D.
Metabolic Syndrome and Hypertension Resulting from Fructose Enriched Diet in Wistar Rats
Julie Dupas, 1 Annie Feray, 1 , 2 Christelle Goanvec, 1 , 3 , * Anthony Guernec, 1 , 2 Nolwenn Samson, 4 Pauline Bougaran, 1 Francois Guerrero, 1 , 2 and Jacques Mansourati 1 , 5
The intron sequences of the human L-type pyruvate kinase gene (PKLR) were determined by using primers selected from the known cDNA sequence. Oligonucleotide primers for these determined intron sequences were used to sequence the exons. When this technique was applied to the DNA of 10 unrelated patients with pyruvate kinase deficiency, the following eight different mutations in the coding region were detected: del391-393, A401, C464, G721, A1076, T1456, T1484, A1529. The A1529 mutation was found repeatedly in unrelated individuals, even in the homozygous state. The context with respect to a polymorphism at nt 1705 was compatible with a single origin for this mutation, and it may represent a balanced polymorphism. In normal subjects, five differences from the published cDNA sequence were documented.
Analysis of pyruvate kinase-deficiency mutations that produce nonspherocytic hemolytic anemia.
L Baronciani and E Beutler
1993 May 1
Recent evidence suggests that DNA sequences from the region lying 5′ of the human epsilon-globin gene are important for erythroid-specific expression of human beta-like globin genes. This region, as well as a region 20 kilobases (kb) downstream from the beta-globin gene, contains a set of developmentally stable, DNase I-superhypersensitive sites that are thought to reflect a chromatin structure supporting active globin gene expression. We have analyzed the chromatin structure in these two regions in a wide variety of nonerythroid and erythroid cells. The study included analysis of chromatin structure changes occurring during globin gene activation in mouse erythroleukemia-human nonerythroid cell hybrids. The results identified a hypersensitive site (III) 14.8 kb upstream of the epsilon-globin gene that was strictly correlated with active globin gene transcription. Interestingly, a multipotent human embryonal carcinoma cell line exhibited a hypersensitive site (IV) 18.4 kb upstream of epsilon-globin that was absent in all other nonerythroid cells examined, suggesting that chromatin structure changes at specific hypersensitive sites during embryonic development may also be important in globin gene repression.
Erythroid-specific nuclease-hypersensitive sites flanking the human beta-globin domain.
V Dhar, A Nandi, C L Schildkraut, A I Skoultchi