The aim of this study was to evaluate the antidiabetic activity of LH II purified from ethanolic seed extract of Eugenia jambolana in alloxan-induced mild diabetic (MD) and severely diabetic (SD) rabbits. Ethanolic extract upon chromatographic purification yielded partially purified hypoglycemic principle (SIII) which on further purification by sephadex LH 20 yielded pharmacological active compound LH II. Homogeneity of LH II was tested by HPLC. Phytochemical investigation of LH II by various structural spectra showed the presence of saturated fatty acid, Δ5 lipid and presence of sterol. LH II was administered orally at a dose of 10 mg kg−1 body weight to MD and SD. LH II resulted, significant fall in FBG at 90 min (21.2% MD: 28.6% SD), 7th day (35.6% MD) and 15th day (59.6% SD). Glycosylated hemoglobin was significantly decreased (50.5%) in SD after 15 days treatment (Tt). Plasma insulin levels were significantly increased (P < .001). In vitro studies with pancreatic islets showed 3-fold increase in insulin levels as compared to untreated animals. LH II also showed extrapancreatic effect by significantly increasing (P < .001) the activity of key enzymes of glycolysis and significantly decreasing (P < .001) the activity of key enzymes of gluconeogenesis. Liver and muscle glycogen content were increased by 36.6 and 30% for MD, and 52 and 47% for SD, respectively. Thus, the present study demonstrates that LH II possesses potent antidiabetic activity and it is effective in both MD and SD rabbits.
Background: Eotaxin (CCL11) is a small protein produced in the lungs of patients with asthma, and is a potent chemoattractant for eosinophils. Aim: To elucidate the role of eotaxin in asthma by an association study of functional and novel eotaxin polymorphisms in case-control and family-based study designs. Methods: Eotaxin +67G/A, -384A/G and -426C/T singlenucleotide polymorphisms and a hexanucleotide (GAAGGA) n repeat 10.9 kb upstream of the gene were genotyped in a cohort of age, sex and ethnically matched patients with asthma (n = 235) and healthy controls (n = 239), and also in a study population of 230 families with asthma recruited from north/ northwest India. Total serum IgE (TsIgE) and plasma eotaxin levels were measured using ELISA. Results: +67G/A polymorphism was found to be significantly associated with asthma in case-control (p = 0.009) and familybased studies (p = 0.006). Its functional role, as it was correlated with plasma eotaxin levels (p = 0.006), was also demonstrated. Further, -384C/T single-nucleotide polymorphism was found to be significantly associated with log 10 TsIgE (p = 0.016 in case-control and p = 0.018 in families) and eotaxin levels (p = 0.007). Most interestingly, for the first time, a highly significant association of the newly studied (GAAGGA) n hexanucleotide repeat with asthma (p = 3610 26 ), log 10 TsIgE (p = 0.006) and eotaxin levels (p = 0.004) was observed. G_A_C_8 was also identified as an important risk haplotype associated with high TsIgE and plasma eotaxin levels. Conclusions: This study provides further evidence that eotaxin polymorphisms are associated with the development of asthma by regulating eotaxin levels and reinforces towards the scanning of other chemokine genes present at 17q21 locus for their association with asthma and related phenotypes.
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