Synthesizing nanoporous polymer from the block polymer template by selective removal of the sacrificial domain offers straightforward pore size control as a function of the degree of polymerization (N). Downscaling pore size into the microporous regime (<2 nm) has been thermodynamically challenging, because the low N drives the system to disorder and the small-sized pore is prone to collapse. Herein, we report that maximizing cross-linking density of a block polymer precursor with an increased interaction parameter (χ) can help successfully stabilize the structure bearing pore sizes of 1.1 nm. We adopt polymerization-induced microphase separation (PIMS) combined with hyper-cross-linking as a strategy for the preparation of the bicontinuous block polymer precursors with a densely cross-linked framework by copolymerization of vinylbenzyl chloride with divinylbenzene and also Friedel–Crafts alkylation. Incorporating 4-vinylbiphenyl as a higher-χ comonomer to the sacrificial polylactide (PLA) block and optimizing the segregation strength versus cross-linking density allow for further downscaling. Control of pore size by N of PLA is demonstrated in the range of 9.9–1.1 nm. Accessible surface area to fluorescein-tagged dextrans is regulated by the relative size of the pore to the guest, and pore size is controlled. These findings will be useful for designing microporous polymers with tailored pore size for advanced catalytic and separation applications.

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The aim of the current study was to elucidate the effect of seabuckthorn leaves (SL) extract and flavonoid glycosides extract from seabuckthorn leaves (SLG) on diet-induced obesity and related metabolic disturbances, and additionally, to identify whether flavonoid glycosides and other components in SL can exert a possible interaction for the prevention of metabolic diseases by comparing the effect of SL and SLG. C57BL/6J mice were fed a normal diet (ND, AIN-93G purified diet), high-fat diet (HFD, 60 kcal% fat), HFD + 1.8% (w/w) SL (SL), and HFD + 0.04% (w/w) SLG (SLG) for 12 weeks. In high fat-fed mice, SL and SLG decreased the adiposity by suppressing lipogenesis in adipose tissue, while increasing the energy expenditure. SL and SLG also improved hepatic steatosis by suppressing hepatic lipogenesis and lipid absorption, whilst also enhancing hepatic fatty acid oxidation, which may be linked to the improvement in dyslipidemia. Moreover, SL and SLG improved insulin sensitivity by suppressing the levels of plasma GIP that were modulated by secreted resistin and pro-inflammatory cytokine, and hepatic glucogenic enzyme activities. SL, especially its flavonoid glycosides (SLG), can protect against the deleterious effects of diet-induced obesity (DIO) and its metabolic complications such as adiposity, dyslipidemia, inflammation, hepatic steatosis, and insulin resistance.