Microfluidic Production of Monodisperse Biopolymer Microcapsules for Latent Heat Storage

Microencapsulation of phase change materials in a polymer shell is a promising technology to prevent them from leakage and to use them as a handleable powder state. However, the microencapsulation process is a time-consuming process because the typical shell-forming step requires polymerization or evaporation of the solvent. In this study, we report a simple and rapid flow process to prepare monodisperse biocompatible cellulose acetate (CA) microcapsules encapsulating n-hexadecane (HD) for latent heat storage applications. The microcapsules were prepared by combining microfluidic droplet formation and subsequent rapid solvent removal from the droplets by solvent diffusion. The diameter and shell thickness of the microcapsules could be controlled by adjusting the flow rate and the HD-to-CA weight ratio in the dispersed phase. We found that 1-hexadecanol added to the microcapsules played the role of a nucleation agent and mitigated the supercooling phenomenon during crystallization. Furthermore, cross-linking of the CA shell with poly(propylene glycol), tolylene 2,4-diisocyanate terminated, resulted in the formation of a thin and dense shell. The microcapsules exhibited a 66 wt % encapsulation efficiency and a 176 J g–1 latent heat storage capacity, with negligible supercooling. We believe that this microflow process can contribute to the preparation of environmentally friendly microcapsules for heat storage applications

Distinct Time Course of the Decrease in Hepatic AMP-Activated Protein Kinase and Akt Phosphorylation in Mice Fed a High Fat Diet

<div><p>AMP-activated protein kinase (AMPK) plays an important role in insulin resistance, which is characterized by the impairment of the insulin-Akt signaling pathway. However, the time course of the decrease in AMPK and Akt phosphorylation in the liver during the development of obesity and insulin resistance caused by feeding a high fat diet (HFD) remains controversial. Moreover, it is unclear whether the impairment of AMPK and Akt signaling pathways is reversible when changing from a HFD to a standard diet (SD). Male ddY mice were fed the SD or HFD for 3 to 28 days, or fed the HFD for 14 days, followed by the SD for 14 days. We examined the time course of the expression and phosphorylation levels of AMPK and Akt in the liver by immunoblotting. After 3 days of feeding on the HFD, mice gained body weight, resulting in an increased oil red O staining, indicative of hepatic lipid accumulation, and significantly decreased AMPK phosphorylation, in comparison with mice fed the SD. After 14 days on the HFD, systemic insulin resistance occurred and Akt phosphorylation significantly decreased. Subsequently, a change from the HFD to SD for 3 days, after 14 days on the HFD, ameliorated the impairment of AMPK and Akt phosphorylation and systemic insulin resistance. Our findings indicate that AMPK phosphorylation decreases early upon feeding a HFD and emphasizes the importance of prompt lifestyle modification for decreasing the risk of developing diabetes.</p></div

Dietary change improves weight gain, liver steatosis, glucose tolerance, and insulin resistance.

<p>The diet was changed on day 14 (black diamonds) or continued as a SD (white circles). (A) Body weight. Results are means ± standard deviation. n = 5 per group. *<i>P</i> < 0.05. (B) Oil Red O-stained liver sections from SD-fed mice or those subjected to a dietary change. Scale bar, 100 μm. (C and D) Intraperitoneal glucose tolerance test (GTT) in SD-fed mice or those subjected to a dietary change on day 3 (C) or day 14 (D). (E and F) Insulin tolerance test (ITT) in SD-fed mice or those subjected to a dietary change on day 3 (E) or day 14 (F). Results are means ± standard deviation. n = 4‒5 per group. *<i>P</i> < 0.05.</p

Hepatic AMPK and Akt phosphorylation levels in mice subjected to dietary change or SD.

<p>(A and B) Representative western blot quantification of AMPK phosphorylation (relative to total AMPK protein). n = 4‒5 per group. (C and D) Representative western blot quantification of insulin-stimulated Akt phosphorylation (relative to total Akt protein). n = 4‒5 per group.</p

Hepatic AMPK and Akt phosphorylation levels in SD- or HFD-fed mice.

<p>(A and B). Representative western blots and quantification of AMPK phosphorylation (relative to total AMPK protein). n = 4 per group. *<i>P</i> < 0.05. (C) and (D). Representative western blots and quantification of insulin-stimulated Akt phosphorylation (relative to total Akt protein). n = 4 per group. *<i>P</i> < 0.05.</p