Mouse Pancreatic Derived Factor ELISA Kit (DEIA-BJ2555)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
Serum, plasma, cell culture supernatants, body fluid and tissue homogenate
Species Reactivity
Mouse
Intended Use
Mouse Pancreatic Derived Factor ELISA Kit kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of the Pancreatic Derived Factor. This ELISA kit is for research use only, not for therapeutic or diagnostic applications.
Contents of Kit
1. MICROTITER PLATE: 96 wells
2. ENZYME CONJUGATE: 6.0 mL or 10 ml
3. STANDARD A-F: 1 vial each
4. SUBSTRATE A: 6 mL
5. SUBSTRATE B: 6 mL
6. STOP SOLUTION: 6 mL
7. WASH SOLUTION (100 x): 10 mL
8. BALANCE SOLUTION: 3 mL
Storage
All components of this kit are stable at 2-8°C until the kit's expiration date.
Detection Range
1.0-25 ng/mL
Sensitivity
0.1 ng/mL

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References


FAM3B (PANDER) functions as a co-activator of FOXO1 to promote gluconeogenesis in hepatocytes

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE

Authors: Chi, Yujing; Meng, Yuhong; Wang, Junpei; Yang, Weili; Wu, Zhe; Li, Mei; Wang, Di; Gao, Fangfang; Geng, Bin; Tie, Lu; Zhang, Weiping; Yang, Jichun

FAM3B, also known as PANcreatic DERived factor (PANDER), promotes gluconeogenesis and lipogenesis in hepatocytes. However, the underlying mechanism(s) still remains largely unclear. This study determined the mechanism of PANDER-induced FOXO1 activation in hepatocytes. In mouse livers and cultured hepatocytes, PANDER protein is located in both the cytoplasm and nucleus. Nuclear PANDER distribution was increased in the livers of obese mice. In cultured mouse and human hepatocytes, PANDER was co-localized with FOXO1 in the nucleus. PANDER directly interacted with FOXO1 in mouse and human hepatocytes. PANDER overexpression enhanced PANDER-FOXO1 interaction, and detained FOXO1 in the nucleus upon insulin stimulation in hepatocytes. With the increase in PANDER-FOXO1 interaction, PANDER overexpression upregulated the expression of gluconeogenic genes and promoted gluconeogenesis in both human and mouse hepatocytes. Luciferase reporter assays further revealed that PANDER augmented the transcriptional activity of FOXO1 on gluconeogenic genes. Moreover, PANDER overexpression also interfered the binding of AS1842856, a specific FOXO1 inhibitor, with FOXO1, and impaired its inhibitory effects on gluconeogenic gene expression and gluconeogenesis in hepatocytes. siRNA mediated-silencing of FOXO1 inhibited PANDER-promoted gluconeogenic gene expression and glucose production in hepatocytes. In conclusion, PANDER protein is abundantly present in the nucleus, where it functions as a new co-activator of FOXO1 to induce gluconeogenic gene expression in hepatocytes.

Effects of circulating member B of the family with sequence similarity 3 on the risk of developing metabolic syndrome and its components: A 5-year prospective study

JOURNAL OF DIABETES INVESTIGATION

Authors: Wang, Haoyu; Yu, Fadong; Zhang, Zhuo; Hou, Yuanyuan; Teng, Weiping; Shan, Zhongyan; Lai, Yaxin

Aims/IntroductionMember B of the family with sequence similarity 3 (FAM3B), also known as pancreatic-derived factor, is mainly synthesized and secreted by islet -cells, and plays a role in abnormal metabolism of glucose and lipids. However, the prospective association of FAM3B with metabolic disorders remains unclear. The present study aimed to reveal the predictive relationship between pancreas-specific cytokine and metabolic syndrome (MetS). Materials and MethodsA total of 210 adults (88 men and 122 women) without MetS, aged between 40 and 65 years, were recruited and received a comprehensive health examination. Baseline serum FAM3B levels were determined by sandwich enzyme-linked immunosorbent assay. Subsequently, all participants underwent a follow-up examination after 5 years. MetS was identified in accordance with the International Diabetes Federation criteria. ResultsDuring follow up, 35.7% participants developed MetS. In comparison with the non-MetS group, participants with MetS had an increased serum FAM3B at baseline (21.85 ng/mL [19.38, 24.17 ng/mL] vs 28.56 ng/mL [25.32, 38.10 ng/mL], P < 0.001). Moreover, serum FAM3B was significantly associated with variations in fasting plasma insulin (r = -0.306, P < 0.001), homeostasis model assessment of -cell function (r = -0.328, P < 0.001) and homeostasis model assessment of insulin resistance (r = -0.191, P = 0.006). Furthermore, a positive correlation between baseline FAM3B and the incidence of MetS was observed, even after multivariable adjustment (relative risk 1.23 [1.15, 1.31], P < 0.001). Furthermore, the optimal cut-off values of FAM3B was 23.98 ng/mL for predicting MetS based on the Youden Index. ConclusionsElevated circulating FAM3B might be considered as a predictor of newly-onset MetS and its progression.

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