Involvement of SIK3 in Glucose and Lipid Homeostasis in Mice

Salt-inducible kinase 3 (SIK3), an AMP-activated protein kinase-related kinase, is induced in the murine liver after the consumption of a diet rich in fat, sucrose, and cholesterol. To examine whether SIK3 can modulate glucose and lipid metabolism in the liver, we analyzed phenotypes of SIK3-deficent mice. Sik3−/− mice have a malnourished the phenotype (i.e., lipodystrophy, hypolipidemia, hypoglycemia, and hyper-insulin sensitivity) accompanied by cholestasis and cholelithiasis. The hypoglycemic and hyper-insulin-sensitive phenotypes may be due to reduced energy storage, which is represented by the low expression levels of mRNA for components of the fatty acid synthesis pathways in the liver. The biliary disorders in Sik3−/− mice are associated with the dysregulation of gene expression programs that respond to nutritional stresses and are probably regulated by nuclear receptors. Retinoic acid plays a role in cholesterol and bile acid homeostasis, wheras ALDH1a which produces retinoic acid, is expressed at low levels in Sik3−/− mice. Lipid metabolism disorders in Sik3−/− mice are ameliorated by the treatment with 9-cis-retinoic acid. In conclusion, SIK3 is a novel energy regulator that modulates cholesterol and bile acid metabolism by coupling with retinoid metabolism, and may alter the size of energy storage in mice

Reactions of (polypyrazolylborato)(benzonitrile)rutheniums with terminal alkynes: Reactivity changeover by triethylamine toward arylalkyne polymerization or formation of (arylmethyl)(carbonyl) complexes

Reactions of (κ 3-polypyrazolylborato)(benzonitrile) rutheniums [RuCl{B(4-Ypz) 4}(PhCN) 2] {4-Ypz; 4-bromo-1-pyrazolyl (Y = Br) and 1-pyrazolyl (Y = H) groups} with terminal alkynes were studied. For the reactions with arylalkynes HC≡C(aryl) in the presence of NEt 3, (arylmethyl)(carbonyl)rutheniums [Ru{CH 2(aryl)}{B(4-Ypz) 4}(CO)(PhCN)] were yielded, indicating alkyne C≡C bond cleavage, whereas in the absence of NEt 3, arylalkyne polymerization proceeded instead of the (arylmethyl)ruthenium formation. Reasonably attributed reaction mechanism shows significant role of the vinylidene intermediates "Ru=C=CH(aryl)"

Association of night eating habits with metabolic syndrome and its components: a longitudinal study

Abstract Background Night time eating is a risk factor for metabolic syndrome and obesity. The aim of this study was to investigate whether dinner immediately before bed, snacks after dinner, or combinations of both were associated with metabolic syndrome and its components in a large Japanese cohort. Methods We enrolled 8153 adults aged 40–54 years who participated in specific medical checkups in an Okayama facility from 2009 to 2010 and from 2013 to 2014. Age-adjusted and multivariable-adjusted odds ratios of metabolic syndrome and its components in participants with both night eating habits for an average of 3.9 years were evaluated. The relative excess risk due to interaction (RERI) was utilized to determine the supra-additive interaction of both eating habits on metabolic syndrome and its components. Results The multivariable-adjusted odds ratio for obesity for those with both eating habits compared to those with neither habit was 2.11 (95% confidence interval [CI], 1.42–3.15) for men and 3.02 (95%CI, 1.72–5.29) for women. Both habits had a supra-additive interaction effect on obesity development in women (RERI, 1.67; RERI%, 85.0; p = 0.058), although this result was not significant. In women, there was an association between eating habits at night and metabolic syndrome, but in men it was unrelated. Both night eating habits were associated with dyslipidemia in men and women. Conclusions These findings suggest the need for intervention and awareness among individuals with night eating habits to mitigate further complications

Nitrogen supply rate regulates microbial resource allocation for synthesis of nitrogen-acquiring enzymes.

Although microorganisms will preferentially allocate resources to synthesis of nitrogen (N)-acquiring enzymes when soil N availability is low according to the resource allocation model for extracellular enzyme synthesis, a robust link between microbial N-acquiring enzyme activity and soil N concentration has not been reported. To verify this link, we measured several indices of soil N availability and enzyme activity of four N-acquiring enzymes [N-acetyl-β-glucosaminidase (NAG), protease (PR), urease (UR), and L-asparaginase (LA)] and a carbon (C)-acquiring enzyme [β-D-glucosidase (BG)] in arable and forest soils. Although the ratios of NAG/BG and PR/BG were not significantly related with indices of soil N availability, ratios of LA/BG and UR/BG were strongly and negatively related with potentially mineralizable N estimated by aerobic incubation but not with pools of labile inorganic N and organic N. These results suggest that microorganisms might allocate their resources to LA and UR synthesis in response to N supply rate rather than the size of the easily available N pools. It was also suggested that the underlying mechanism for synthesis was different between these N-acquiring enzymes in soil microorganisms: microbial LA and UR were primarily synthesized to acquire N, whereas NAG and PR syntheses were regulated not only by N availability but also by other factors