You will be shown an abstract from a biomedical research paper. Given this abstract, your task is to extract all unique entities of the following types: ["Protein", "Chemical"].

Please return the output as a JSON object of the format: {"Chemical" : ["Dexamethasone", ...], "Protein" : ["BRCA-1", ...]}. The keys should be entity types and values should be lists of extracted entities belonging to the corresponding type. If you cannot find entities belonging to a specific type, the value should be [].

Only output the JSON object and do not include any additional text.

Abstract:

Resistin knockout mice exhibit impaired adipocyte glucose-dependent insulinotropic polypeptide receptor (GIPR) expression.
Glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone that also plays a regulatory role in fat metabolism. In 3T3-L1 cells, resistin was demonstrated to be a key mediator of GIP stimulation of lipoprotein lipase (LPL) activity, involving activation of protein kinase B (PKB) and reduced phosphorylation of liver kinase B1 (LKB1) and AMP-activated protein kinase (AMPK). The current study was initiated to determine whether resistin has additional roles in GIP-regulated adipocyte functions. Analysis of primary adipocytes isolated from Retn(-/-), Retn(+/-), and Retn(+/+) mice found that GIP stimulated the PKB/LKB1/AMPK/LPL pathway and fatty acid uptake only in Retn(+/+) adipocytes, suggesting that GIP signaling and/or GIP responsiveness were compromised in Retn(+/-) and Retn(-/-) adipocytes. GIP receptor (GIPR) protein and mRNA were decreased in Retn(+/-) and Retn(-/-) adipocytes, but resistin treatment rescued LPL responsiveness to GIP. In addition, genes encoding tumor necrosis factor (TNF), TNF receptor 2 (TNFR2), and the signaling proteins stress-activated protein kinase (SAPK)/Jun NH(2)-terminal kinase (JNK), were downregulated, and phosphorylated levels of SAPK/JNK/c-Jun were decreased in Retn(-/-) mice. Chromatin immunoprecipitation assays were used to identify a 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element (TRE-III) responsible for c-Jun-mediated transcriptional activation of Gipr. Blunted GIP responsiveness in Retn(+/-) and Retn(-/-) adipocytes was therefore largely due to the greatly reduced GIPR expression associated with decreased c-Jun-mediated transcriptional activation of Gipr.
{"Chemical": ["glucose", "AMP", "TPA", "NH(2)", "Glucose", "fatty acid", "12-O-tetradecanoylphorbol-13-acetate"], "Protein": ["Glucose-dependent insulinotropic polypeptide", "PKB", "Resistin", "GIP receptor", "TRE-III", "TNF receptor 2", "Jun NH(2)-terminal kinase", "lipoprotein lipase", "GIPR", "LKB1", "AMPK", "glucose-dependent insulinotropic polypeptide receptor", "JNK", "protein kinase B", "LPL", "TNFR2", "12-O-tetradecanoylphorbol-13-acetate (TPA)-response element", "SAPK", "stress-activated protein kinase", "Retn", "AMP-activated protein kinase", "c-Jun", "liver kinase B1", "tumor necrosis factor", "Gipr", "TNF", "incretin hormone", "resistin", "GIP"]}