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A practical and efficient trans-diboration of propargyl alcohols was accomplished using sodium hydride (NaH) as a base in N,N-dimethylformamide at room temperature. The mild reaction conditions demonstrate general applicability, facilitating the successful conversion of both terminal and internal propargyl alcohols with diverse structures and functional groups into highly functionalized alkenediboronates [4-borylated 1,2-oxaborol-2(5H)-oles]. The resulting products, which incorporate two boron groups, can be selectively activated and subjected to stepwise transformations, thereby providing an effective platform for synthesizing a wide range of structurally diverse trisubstituted alkenes.

Background:Suppressor of cytokine signaling-1 and -3 (SOCS-1 and SOCS-3) are two important negative regulators in the insulin-signaling pathway, and their overexpression may aggravate insulin resistance. Subjects with insulin resistance are often obese and have increased expressions of SOCS-1 and SOCS-3. We speculated that SOCS-1 and SOCS-3 may be involved in abnormal deposition of adipose tissues during insulin resistance.Methods:A catch-up growth intrauterine growth retardation (CG-IUGR) rat model with insulin resistance was established; mRNA and protein expression of SOCS-1, SOCS-3, the CCAAT/enhancer binding protein (C/EBPa), and peroxisome proliferator-activated receptor (PPAR?) in adipose tissue were measured by real-time PCR and western blot; plasmids carrying small hairpin RNAs (shRNAs) targeting the SOCS-1 and SOCS-3 genes were constructed and transfected into preadipocytes, which were then induced to mature. At 72?h after differentiation was induced, the expressions of C/EBPa and PPAR?, two important molecules promoting the differentiation of preadipocytes, were detected.Results:Expressions of SOCS-1, SOCS-3, C/EBPa, and PPAR? were markedly increased in adipose tissues of CG-IUGR rats, whereas the expressions of C/EBPa and PPAR? were significantly reduced after gene silencing of SOCS-1 or SOCS-3 in adipocytes.Conclusion:Overexpression of SOCS-1 and SOCS-3 may enhance the expression of C/EBPa and PPAR?, resulting in abnormal deposition of adipose tissues during insulin resistance.