Reinforcement and Controlling the Stability of Poly(ε-caprolactone)-Based Polymeric Materials via Reversible and Movable Cross-Links Employing Cyclic Polyphenylene Sulfide.

Due to its biodegradation ability, poly(ε-caprolactone) (PCL) is a suitable alternative for packaging materials; however, its biodegradation can also lead to instability in its usage. Cyclic polyphenylene sulfide (7U) has been shown to form rotaxane structures with PCL by simple blending to generate the π-π stacking effect and movable cross-link. A 2-fold increase in toughness and no decrease in Young's modulus for the PCL-based polyurethane with 7U are observed. The rotaxane structures mainly exist in the amorphous regions and have no impact on the crystallinity of PCL. Under the catalysis of lipase in aqueous solution, the stability of PCL is improved due to the 7U's suppression of the attack from the enzymes on PCL. After dissolution of the PCL films in the organic solvent, the dispersion of 7U and the breakage of the cross-links lead to little suppression on degradation during the catalysis of lipase. Thus, the controlled stability of PCL using 7U can prolong the life span of the biodegraded PCL materials.

Impaired Fat Absorption from Intestinal Tract in High-Fat Diet Fed Male Mice Deficient in Proglucagon-Derived Peptides.

(1) Background: Proglucagon-derived peptides (PDGPs) including glucagon (Gcg), GLP-1, and GLP-2 regulate lipid metabolism in the liver, adipocytes, and intestine. However, the mechanism by which PGDPs participate in alterations in lipid metabolism induced by high-fat diet (HFD) feeding has not been elucidated. (2) Methods: Mice deficient in PGDP (GCGKO) and control mice were fed HFD for 7 days and analyzed, and differences in lipid metabolism in the liver, adipose tissue, and duodenum were investigated. (3) Results: GCGKO mice under HFD showed lower expression levels of the genes involved in free fatty acid (FFA) oxidation such as Hsl, Atgl, Cpt1a, Acox1 (p < 0.05), and Pparα (p = 0.05) mRNA in the liver than in control mice, and both FFA and triglycerides content in liver and adipose tissue weight were lower in the GCGKO mice. On the other hand, phosphorylation of hormone-sensitive lipase (HSL) in white adipose tissue did not differ between the two groups. GCGKO mice under HFD exhibited lower expression levels of Pparα and Cd36 mRNA in the duodenum as well as increased fecal cholesterol contents compared to HFD-controls. (4) Conclusions: GCGKO mice fed HFD exhibit a lesser increase in hepatic FFA and triglyceride contents and adipose tissue weight, despite reduced ß-oxidation in the liver, than in control mice. Thus, the absence of PGDP prevents dietary-induced fatty liver development due to decreased lipid uptake in the intestinal tract.