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  • Green tea extract protects leptin-deficient, spontaneously obese mice from hepatic steatosis and injury. 18203899

    The incidence of nonalcoholic fatty liver disease (NAFLD) has risen along with the ongoing obesity epidemic. Green tea extract (GTE) inhibits intestinal lipid absorption and may regulate hepatic lipid accumulation. The objective of this study was to determine whether GTE protects against hepatic lipid accumulation during the development of NAFLD in an obese mouse model. Five-wk-old ob/ob (obese) mice and their lean littermates (8 mice x genotype(-1) x dietary treatment(-1)) were fed GTE at 0, 1, or 2% (wt:wt) for 6 wk. The body weights of obese mice and lean littermates fed diets containing GTE were 23-25% and 11-20% lower (P 0.05) than their respective controls fed no GTE. Histologic evaluation showed a significant reduction in hepatic steatosis in GTE-fed obese mice only and histologic scores were correlated with hepatic lipid concentration (r = 0.84; P 0.05), which was reduced dose dependently by GTE. GTE protected against hepatic injury as suggested by 30-41% and 22-33% lower serum alanine aminotransferase and aspartate aminotransferase activities, respectively. Hepatic alpha-tocopherol was 36% higher in obese mice than lean mice. GTE tended (P = 0.06) to lower hepatic alpha-tocopherol, which was not fully explained by the GTE-mediated reduction in hepatic lipid. Hepatic ascorbic acid was lower in obese mice than in lean mice (P 0.05) and was unaltered by GTE. Obese mice had lower serum adiponectin than lean mice and this was not affected by GTE. The results suggest that GTE protects against NAFLD by limiting hepatic lipid accumulation and injury without affecting hepatic antioxidant status and adiponectin-mediated lipid metabolism. Further study is underway to define the events by which GTE protects against obesity-triggered NAFLD.
    Tipo de documento:
    Referencia
    Referencia del producto:
    EZMADP-60K
    Nombre del producto:
    Mouse Adiponectin ELISA
  • Atherogenecity of LDL and unfavorable adipokine profile in metabolically obese, normal-weight woman. 18239579

    OBJECTIVE: The relationship of visceral adiposity with adipocytokines and low-density lipoprotein (LDL) particle distribution and oxidation in Asian metabolically obese, normal-weight (MONW) individuals has not been evaluated. We aimed to investigate the association between visceral adiposity and adipocytokines and cardiovascular disease (CVD) risk factors in MONW Korean women with normal glucose tolerance. METHODS AND PROCEDURES: We examined the metabolic characteristics of 135 non-obese (BMI 25 kg/m(2)) women aged 25-64 years. Twenty-five women (BMI 25 kg/m(2) and visceral fat adiposity (VFA) > or =100 cm(2)) were classified as MONW and 25 women (BMI 25 kg/m(2) and VFA 100 cm(2)), pair-matched for age, weight, height, and menopausal status, as control group. Plasma lipid profiles and adipocytokines were evaluated in these two groups. RESULTS: MONW subjects had higher systolic (P 0.05) and diastolic blood pressure (P 0.005) and higher concentrations of triacylglycerol (TG) (P 0.005), insulin (P 0.01), and free fatty acid (FFA) (P 0.05) than control subjects. There was no significant difference between two groups in LDL-cholesterol (LDL-C) concentrations; however, MONW subjects had smaller LDL particles (P 0.01) and higher concentrations of oxidized LDL (ox-LDL) (P 0.05) compared with controls. Moreover, MONW subjects had higher concentrations of tumor necrosis factor-alpha (TNF-alpha) (P 0.05), interleukin-6 (IL-6) (P 0.05) and leptin (P 0.05), and lower plasma adiponectin concentrations (P 0.05). Higher intake of saturated fat with lower ratio of polyunsaturated fatty acids (PUFAs) to saturated fatty acids (SFA) and lower fiber intake than normal subjects were found in MONW women. DISCUSSION: We found an unfavorable inflammatory profile and a more atherogenic LDL profile in MONW female subjects even in the absence of a known CVD risk factors. Moreover, MONW consumed more saturated fat and less fiber than the control group.
    Tipo de documento:
    Referencia
    Referencia del producto:
    5005
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