The ethylene adducts of copper(I) tris(pyrazolyl)borates, [HB(3,5-(CF 3 ) 2 Pz) 3 ]Cu(C 2 H 4 ), ),5-(C 6 H 5 )Pz) 3 ]Cu(C 2 H 4 ), and [HB(3-(CF 3 )Pz) 3 ]Cu(C 2 H 4 ), have been prepared by reacting the corresponding sodium derivative with CF 3 SO 3 Cu in the presence of ethylene. They were characterized both in the solid state and in solution using 1 H, 13 C, and 19 F NMR and IR spectroscopy and by X-ray crystallography. Solid samples of these nonionic copper complexes featuring fluorinated tris(pyrazolyl)borate ligands display notably high stability toward air oxidation and ethylene loss. The 1 H NMR chemical shifts of the copper(I)-bonded ethylene protons appear in the 4.8-5.2 ppm region. The 13 C signal of copper-coordinated ethylene shows an upfield shift of about 35 ppm, whereas the 1 J C-H shows a minor change (an increase of about 2-5 Hz) compared to the values for free ethylene. X-ray structural data show the presence of pseudo-tetrahedral copper ions and η 2 -bonded ethylene units and relatively unperturbed ethylene C-C distances. The copper adducts [HB(3,5-(CF 3 ) 2 Pz) 3 ]Cu-(C 2 H 4 ) and [HB(3-(CF 3 ),5-(C 6 H 5 )Pz) 3 ]Cu(C 2 H 4 ) are competent aziridination catalysts, readily converting a variety of olefins into the corresponding N-tosyl aziridines with N-tosyl phenyliodinane.

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That obesity is associated with insulin resistance and type II diabetes mellitus is well accepted. Overloading of white adipose tissue beyond its storage capacity leads to lipid disorders in non-adipose tissues, namely skeletal and cardiac muscles, pancreas, and liver, effects that are often mediated through increased non-esterified fatty acid fluxes. This in turn leads to a tissue-specific disordered insulin response and increased lipid deposition and lipotoxicity, coupled to abnormal plasma metabolic and (or) lipoprotein profiles. Thus, the importance of functional adipocytes is crucial, as highlighted by the disorders seen in both "too much" (obesity) and "too little" (lipodystrophy) white adipose tissue. However, beyond its capacity for fat storage, white adipose tissue is now well recognised as an endocrine tissue producing multiple hormones whose plasma levels are altered in obese, insulin-resistant, and diabetic subjects. The consequence of these hormonal alterations with respect to both glucose and lipid metabolism in insulin target tissues is just beginning to be understood. The present review will focus on a number of these hormones: acylation-stimulating protein, leptin, adiponectin, tumour necrosis factor alpha, interleukin-6, and resistin, defining their changes induced in obesity and diabetes mellitus and highlighting their functional properties that may protect or worsen lipid metabolism.

Background Brain metastasis (BM) is associated with poor prognosis, recurrence, and death in patients with non-small cell lung cancer (NSCLC). Lysophosphatidylcholine acyltransferase 1 (LPCAT1) has been reported to be involved in the progression, metastasis and recurrence of malignancies. However, the potential role of LPCAT1 in NSCLC remains poorly understood. This study was aimed to identify genes involved in lung adenocarcinoma (LUAD) brain metastasis, and look into the role of LPCAT1 in LUAD progression. Methods We used integrative genomic analysis to identify genes involved in lung adenocarcinomas. LPCAT1 expression was evaluated in tumor tissues from LUAD patients and LUAD cell lines. The role of LPCAT1 was subsequently investigated both in vitro and in vivo. The mechanism underlying the involvement of LPCAT1 in LUAD progression was explored with the activator of PI3K/AKT pathway. RNA sequencing was performed to confirm the involvement of LPCAT1 and associated pathway in LUAD brain metastasis. Results LPCAT1 was up-regulated in LUAD tissues and cell lines. shRNA-mediated depletion of LPCAT1 not only abrogated cell proliferation, migration and invasion in vitro, but also arrested tumor growth and brain metastases in vivo. Notably, LPCAT1 at least partially influenced LUAD progression through PI3K/AKT signal pathway by targeting MYC transcription. Moreover, expression of LPCAT1 was higher in tissues of LUAD patients with BM than those without BM as revealed by IHC staining, RNA-Sequencing and qPCR analysis. Finally, elevated LPCAT1 expression in patients with lung adenocarcinomas was associated with a poor clinical outcome. Conclusions This study showed that LPCAT1 works as a regulator of cell metastasis and may serve as a novel therapeutic target for BM in lung adenocarcinoma. Electronic supplementary material The online version of this article (10.1186/s13046-019-1092-4) contains supplementary material, which is available to authorized users.