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  • Preoperative serum leptin levels in patients with breast cancer. 19412673

    Leptin is an adipocyte-derived protein and plays an important role in the control of body weight by acting as a neurohormone regulating energy balance and food intake in the hypothalamus. The high serum leptin levels and the overexpression of leptin receptors have been documented in breast cancer patients, but the levels never checked preoperatively. In the present study, the relationship between preoperative serum leptin levels of the breast cancer patients and the healthy controls were evaluated. The serum leptin levels in 30 breast cancer patients were compared to 30 healthy female volunteers. In addition, the association of serum leptin levels and the various well-known risk factors were studied. Serum leptin levels of patients with breast cancer (28.55 + 19.7 ng/ml) were tended to be higher than those of controls (26.43 + 19.4 ng/ml), but it did not reach statistical difference (P = 0.712). There was significant correlation between the expression of ER, PR, and serum leptin levels (P = 0.018 and 0.037, respectively), but not with the HER-2/neu receptor expression (P = 0.067). Also association was not found between the tumor size, lymph node involvement, and the levels of serum leptin (P = 0.235, 0.34, and 0.86, respectively). The serum leptin level was also found to be similar in premenopausal (24.85 +/- 18.14 ng/ml) and postmenopausal (30.49 +/- 17.19 ng/ml) patients (P = 0.235). The preoperative serum leptin levels in breast cancer patients were similar to healthy controls. In subset analysis, the significant correlation between the leptin level and hormonal status was noted, but association with HER-2/neu was not detected. These findings should be confirmed with larger studies.
    Document Type:
    Reference
    Product Catalog Number:
    EZHL-80SK
    Product Catalog Name:
    Human Leptin "Dual Range" 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.
    Document Type:
    Reference
    Product Catalog Number:
    5005

  • 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.
    Document Type:
    Reference
    Product Catalog Number:
    EZMADP-60K
    Product Catalog Name:
    Mouse Adiponectin ELISA

  • Effect of short-term fasting on urinary excretion of primary lipid peroxidation products and on markers of oxidative DNA damage in healthy women. 16401636

    The goal of this study was to determine whether short-term fasting changes in urinary biomarkers related to oxidative stress: malondialdehyde (MDA), 8-isoprostaglandin F2alpha (8-isoPGF), 8-hydroxydeoxy-guanosine (8-OHdG) and 1,N6-ethenodeoxyadenosine (epsilondA) among female volunteers participating in the short-term fasting program in South Korea. The study subjects were 52 healthy women (mean age 28, range 15-48 years old) who provided urine samples both before and after the fasting program (average 7.2, range: 3-11 days). Urinary MDA was measured by HPLC-UV and epsilondA levels were measured by immuno-affinity purification followed by HPLC-fluorescence detection. Urinary 8-OHdG and 8-isoPGF concentrations were determined by ELISA. Plasma leptin levels were also measured by radioimmunoassay. Information on demographic characteristics, personal habits (smoking and alcohol consumption) and previous medical history were collected by a self-administered questionnaire. Percent loss of body weight (average 6.3%, 4.28 +/- 0.25 kg) was significantly correlated with fasting duration (r = 0.70, n = 52, P 0.01). The plasma leptin levels after fasting (5.89 +/- 1.10 ng/ml) were significantly lower than before fasting (6.91 +/- 1.13 ng/ml) (n = 27, P = 0.05). Urinary MDA levels after fasting (0.18 +/- 1.10 mg/g creatinine) were significantly lower than before fasting (0.37 +/- 1.11) (n = 51, P 0.01). Urinary 8-isoPGF also were significantly reduced after fasting (n = 47, P 0.01). However, there was no significant difference in 8-OHdG or epsilondA. There was a statistically significant correlation between % change of urinary MDA level with % change of 8-isoPGF level (partial correlation coefficient r = 0.57, n = 46, P = 0.01). The correlations between % change of 8-OHdG and plasma leptin was also significant (partial correlation coefficient r = 0.51, n = 27, P = 0.02). Our results demonstrate that the short-term fasting reduces lipid peroxidation products but does not affect oxidative stress-induced DNA damage.
    Document Type:
    Reference
    Product Catalog Number:
    HL-81K
    Product Catalog Name:
    Human Leptin RIA

  • Is sprint exercise a leptin signaling mimetic in human skeletal muscle? 21659488

    This study was designed to determine whether sprint exercise activates signaling cascades linked to leptin actions in human skeletal muscle and how this pattern of activation may be interfered by glucose ingestion. Muscle biopsies were obtained in 15 young healthy men in response to a 30-s sprint exercise (Wingate test) randomly distributed into two groups: the fasting (n = 7, C) and the glucose group (n = 8, G), who ingested 75 g of glucose 1 h before the Wingate test. Exercise elicited different patterns of JAK2, STAT3, STAT5, ERK1/2, p38 MAPK phosphorylation, and SOCS3 protein expression during the recovery period after glucose ingestion. Thirty minutes after the control sprint, STAT3 and ERK1/2 phosphorylation levels were augmented (both, P < 0.05). SOCS3 protein expression was increased 120 min after the control sprint but PTP1B protein expression was unaffected. Thirty and 120 min after the control sprint, STAT5 phosphorylation was augmented (P < 0.05). Glucose abolished the 30 min STAT3 and ERK1/2 phosphorylation and the 120 min SOCS3 protein expression increase while retarding the STAT5 phosphorylation response to sprint. Activation of these signaling cascades occurred despite a reduction of circulating leptin concentration after the sprint. Basal JAK2 and p38 MAPK phosphorylation levels were reduced and increased (both P < 0.05), respectively, by glucose ingestion prior to exercise. During recovery, JAK2 phosphorylation was unchanged and p38 MAPK phosphorylation was transiently reduced when the exercise was preceded by glucose ingestion. In conclusion, sprint exercise performed under fasting conditions is a leptin signaling mimetic in human skeletal muscle.
    Document Type:
    Reference
    Product Catalog Number:
    EZHL-80SK
    Product Catalog Name:
    Human Leptin "Dual Range" ELISA