Sentence examples for acid spillover from inspiring English sources

One important aspect of adipose tissue dysfunction is increased fatty acid spillover in the bloodstream [3], a condition that negatively impacts insulin-mediated glucose disposal in skeletal muscle [4].

In obese pregnant women, lower-body fat depots are replete and/or there is a preference to store fat centrally with the potential of fatty acid spillover and lipotoxicity.

Within 5 h of breakfast, dietary fatty acids (spillover fatty acids and chylomicron remnant TG) were incorporated into and represented 25% of VLDL-TG in lean and abdominally obese males, respectively.

In the postprandial state, precursors would include fatty acids arising from adipose tissue lipolysis and dietary spillover fatty acids.

The contribution of chylomicron-derived spillover fatty acids to VLDL-TG was not calculated during the overnight phase, as it is negligible during this period (40).

Although purely speculative at this stage, potential mechanisms may involve an increase in spillover fatty acids escaping from lipoprotein lipase action on chylomicron triacylglycerol or reduced insulin secretion/action, resulting in diminished suppression of adipocyte triacylglycerol lipolysis.

It was concluded that the strong Bronsted acid site of USY and spillover hydrogen formed on Pt-Pd bimetal particle in Pt-Pd/USY catalyst play an important role for the hydrodesulfurization of thiophene.

The superior catalytic performance of Ru/[Bmim]3PW12O40 has been characterized using the hydrogenolysis of cellobiose as a probe reaction and was attributed to the Brønsted acid sites generated from hydrogen spillover from the Ru sites to the O sites of the support.

The Brønsted acid site of HZSM-5 and spillover hydrogen formed on Pt particle in Pt/HZSM-5 catalyst play an important role for the hydrodesulfurization of thiophene.

The acid sites of FSM-16 and the spillover hydrogen formed on Pt particle in Pt/FSM-16 catalyst play an important role for the hydrodesulfurization of thiophene.

The authors propose that this elevation in hepatic glucose production creates a vicious cycle between the heart and the liver in which the spillover of VLDL triglyceride and oleic acid from the heart insults the liver via elevated protein kinase C signaling.