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The vanadium(V) alkylidene complex (ArN)V-(dCHSiMe 3 )(NdC t Bu 2 )(PMe 3 ) (6; Ar ) 2,6-Me 2 C 6 H 3 ) has been isolated from (ArN)V(CH 2 SiMe 3 ) 2 (NdC t Bu 2 ) ( 5) by R-hydrogen elimination in benzene-d 6 at 80 °C. The complex 6 initiated ring-opening metathesis polymerization (ROMP) of norbornene, yielding a high-molecularweight polymer with unimodal molecular weight distribution (M w ) 1.15 × 10 6 , M w /M n ) 1.6) in high yield (98%), and the activity increased at higher temperatures (80 °C).

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Over the past few decades, the prevalence of overweight and obesity has increased markedly worldwide, along with the adoption of westernized lifestyles characterized by excessive energy intake and a lack of physical activity. Consequently, obesity and a cluster of obesity-related comorbidities often referred to as the metabolic syndrome have become a serious public health problem and a major risk factor for the development of severe diseases such as cardiovascular disease. 1) Obesity is strongly associated with insulin resistance, in which elevation of circulating fatty acids results in increased fatty acid availability that exceeds the fat disposal capacity of cells, which decreases insulin-stimulated glucose oxidation in muscles and subsequently leads to contractile dysfunction of the heart. 2) The precise mechanisms underlying these "lipotoxic" consequences remain incompletely defined, but it is currently accepted that excessive fatty acid uptake into cells leads to the accumulation of proinflammatory lipid metabolites such as fatty acyl-CoA, diacylglycerol and ceramide. These metabolites stimulate stress-activated kinases, which interfere with insulin signaling. 2,3) It is also becoming clear that fatty acid beta-oxidation is increased in the insulin-resistant heart and oxidative skeletal muscle, and that mitochondrial overload and incomplete oxidation of fatty acids contribute to the impairment of insulin sensitivity. 2,4) Under these conditions, enhanced beta-oxidation, which is not accompanied by appropriate upregulation of the tricarboxylic acid (TCA) cycle or electron transport chain (ETC) activity, fails to oxidize fatty acids completely to CO 2 and deposits incomplete fat catabolites along with diminished levels of TCA cycle intermediates. These stressful environments created within mitochondria are thought to exacerbate cellular insulin resistance by enhanced oxidative stress, for example. 4) However, acyl-CoA thioesterase (ACOT) exists within the mitochondrial matrix of mammalian cells 5) and its expression is expected to be upregulated in response to fatty acid overload, as demonstrated in diabetic and fasted animals. 6,7) ACOT comprises a group of enzymes that are localized in multiple compartments in cells and catalyze the hydrolysis of long-chain acyl-CoA thioesters to free fatty acids and CoA-SH. For example, ACOT1 (formerly known as CTE-I or ACH2) and ACOT7a (CTE-II, BACH or ACT) are localized in the cytosol while ACOT2 (MTE-I or ARTISt) and ACOT7b (MTE-II or LACH1) are present in mitochondria. [8][9][10] These catalytic properties of ACOT mean that it is capable of lowering the increased levels of acyl-CoA imported by carnitine palmitoyltransferase (CPT) across the mitochondrial membranes from the cytosol. Accordingly, ACOT could counteract the enhanced beta-oxidation and reduce the mitochondrial stress caused by the imbalance between beta-oxidation and TCA cycle/ETC activity during fatty acid overload. Moreover, the ACOT isoforms present in the cytosol could scavenge surplus acyl-CoA to prev...

Treatment of V(NAr)(CH2SiMe3)3 (1, Ar = 2,6-Me2C6H3) with 1.0 equiv of various alcohols in n-hexane at 25 °C cleanly afforded the corresponding dialkyl complexes of the type V(NAr)(CH2SMe3)2(OR) [R = 2,6-Me2C6H3 (2a), 2,6- i Pr2C6H3 (2b), C6F5 (2c), t Bu (2d), CMe(CF3)2 (2e), yield 90−93%]. In contrast, the reactions with R′N(H)Me (R′ = Ph, cyclohexyl) or 2,6-Me2C6H3SH did not take place even if the reactions were attempted in C2D2Cl4 at 50 °C. Complexes 2a and 2b showed high catalytic activities for the ring-opening metathesis polymerization (ROMP) of norbornene in the presence of PMe3, and the activity increased at high temperature (80 °C). A vanadium(V)−alkylidene complex, V(CHSiMe3)(NAr)(O-2,6- i Pr2C6H3)(PMe3)x (3, x = 0.89), has been isolated when the C6D6 solution containing 2b was heated at 80 °C in the presence of PMe3 (5.0 equiv). Complex 3 showed remarkable catalytic activity for the ROMP of norbornene, and the polymerization at 25 °C proceeded in a living manner.