Takanori Kawano

To investigate whether supplementation of paramylon (PM)‐rich Euglena gracilis EOD‐1 powder (EOD‐1) reduces visceral fat obesity in moderately obese Japanese subjects. A randomized, double‐blind, placebo‐controlled intervention study was conducted involving 36 Japanese adults with a body mass index (BMI) ≥25 and 2. Subjects were randomly assigned into two groups to consume EOD‐1 capsules (EOD‐1 group, 2.6 g PM/day) or cellulose capsules (placebo group) for a 12‐week period. Anthropometric measurements including visceral fat area (VFA) and blood samples were measured at baseline and throughout the trial. There was no significant difference in VFA between the two groups, although subgroup analysis by gender showed a significant decrease in VFA in the male EOD‐1 group compared with the placebo group. Serum adiponectin levels in all subjects from the EOD‐1 group were significantly higher than in the placebo group. By comparison with the placebo group, the subjects in the EOD‐1 group showed a significant reduction in serum HbA1c levels. EOD‐1 intake led to a significant reduction in VFA in male subjects with moderate obesity (BMI 25–30 kg/m²). PM in EOD‐1 may contribute to preventing visceral fat obesity in male Japanese subjects. Moreover, PM may also contribute to improving glucose homeostasis in moderately obese Japanese adults.

Euglena gracilis, a type of microalgae, contains several nutrients and accumulates paramylon, a β-1,3-glucan. In recent studies, paramylon has shown to exhibit various activities including immunomoduratory and hepatoprotective effects. In the present study, using an in vitro cell culture system, we aimed to determine whether paramylon derived from the E. gracilis EOD-1 strain, which produces large amounts of paramylon, can augment SIRT1 expression in epidermal cells via activating gut–skin interactions. Results showed that paramylon augmented the expression of SIRT1 in Caco-2 cells, a human intestinal cell line. Furthermore, microarray analysis of Caco-2 cells treated with paramylon showed that paramylon activates epidermal cells through inducing the secretion of factors from intestinal cells. Then, we focused on skin cells as target cells of paramylon-activated intestinal cells. Results showed that secretory factors from Caco-2 cells treated with paramylon augmented the expression of SIRT1 in HaCaT cells, a human keratinocyte cell line, and that expression level of genes related to the growth and maintenance of epidermal cells were significantly changed in Caco-2 cells treated with paramylon as evidenced by microarray analysis. All these results suggest that paramylon can activate epidermal cells by inducing the production of secretory factors from intestinal cells.

Euglena gracilis EOD-1, a kind of microalgae, is known to contain a high proportion of paramylon, a type of β-1,3-glucan. Paramylon derived from E. gracilis EOD-1 is presumed to suppress cellular oxidative injury and expected to reduce fatigue and fatigue sensation. Therefore, we aimed to examine whether food containing paramylon derived from E. gracilis EOD-1 (EOD-1PM) ingestion reduced fatigue and fatigue sensation in healthy adults. We conducted a randomized, double-blind, placebo-controlled, parallel-group comparison study in 66 healthy men and women who ingested a placebo or EOD-1PM daily for 4 weeks (daily life fatigue). Furthermore, at the examination days of 0 and 4 weeks, tolerance to fatigue load was evaluated using mental tasks (task-induced fatigue). We evaluated fatigue sensation using the Visual Analogue Scale, the work efficiency of the advanced trail making test and measured serum antioxidant markers. The EOD-1PM group showed significantly lower levels of physical and mental fatigue sensations and higher levels of work efficiency as well as serum biological antioxidant potential levels than the placebo group. These results indicate that EOD-1PM ingestion reduced fatigue and fatigue sensation, which may be due to an increase in antioxidant potential and maintenance of selective attention during work.

Objective To determine whether ingesting a green tea beverage enriched with catechins with a galloyl moiety during a meal reduces body fat in moderately obese adults. Design Randomized double-blind placebo-controlled study. Subjects A total of 126 obese subjects (25 ≤ body mass index < 30 kg m⁻²) were randomly assigned to a group receiving green tea beverages without catechins (placebo), or a group receiving green tea beverages with a low or high content of catechins with a galloyl moiety. Each subject ingested 500 mL bottled green tea beverages containing 25, 180, or 279.5 mg green tea catechins (0, 149.5, or 246.5 mg catechins with a galloyl moiety, respectively), at mealtimes for 12 weeks; the subjects were instructed to ingest the beverage during the meal that had the highest fat content on that day. Methods Anthropometric measurements and blood chemistry analysis were performed during the run-in period; at weeks 0, 4, 8, and 12 of the intake period; and at the end of the withdrawal period. Abdominal fat area was measured by computed tomography at weeks 0, 8, and 12 of the intake period and at the end of the withdrawal period. Results Both the low- and high-dose groups exhibited significant reductions in visceral and subcutaneous fat areas compared to the control group at 12 weeks post-intervention. Conclusion Ingestion of a green tea beverage enriched with catechins with a galloyl moiety during a high-fat meal reduces body fat in moderately obese adults.

Kinesin‐1 anterogradely transports vesicles containing cargo proteins when a protein–protein interaction activates it from an inhibited state. The C‐terminal cytoplasmic region of kinesin‐1 cargo protein Alcadeinα (Alcα) interacts with the KLC1 subunit's tetratricopeptide repeat (TPR) region, activating kinesin‐1's association with vesicles and anterograde transport. We found that either of two 10‐amino‐acid WD motifs in Alcα cytoplasmic region was necessary and sufficient to initiate this activation. An artificial transmembrane protein containing either WD motif induced kinesin‐1's vesicular association and anterograde transport in a KLC‐dependent manner, even in the normally inhibiting presence of excess KLC1, thus allowing us to analyze the KLC1 TPR‐WD functional interaction in detail in vivo. A part of TPR region was dispensable for the WD motifs' activation of kinesin‐1 and transport, indicating that only part of the TPR structure is required for this function in vivo. For a different kinesin‐1 cargo protein, JIP1, an 11‐amino‐acid C‐terminal region was sufficient to recruit KLC1 to vesicles, but did not activate transport. These observations suggest that structurally different TPR‐interacting peptides may have different effects on kinesin‐1. This mechanism may partly explain how kinesin‐1 can organize the transport of a wide variety of cargo molecules.

Alcadeinα (Alcα) is an evolutionarily conserved type I membrane protein expressed in neurons. We show here that Alcα strongly associates with kinesin light chain ( K D≈4–8 × 10−9 M) through a novel tryptophan‐ and aspartic acid‐containing sequence. Alcα can induce kinesin‐1 association with vesicles and functions as a novel cargo in axonal anterograde transport. JNK‐interacting protein 1 (JIP1), an adaptor protein for kinesin‐1, perturbs the transport of Alcα, and the kinesin‐1 motor complex dissociates from Alcα‐containing vesicles in a JIP1 concentration‐dependent manner. Alcα‐containing vesicles were transported with a velocity different from that of amyloid β‐protein precursor (APP)‐containing vesicles, which are transported by the same kinesin‐1 motor. Alcα‐ and APP‐containing vesicles comprised mostly separate populations in axons in vivo . Interactions of Alcα with kinesin‐1 blocked transport of APP‐containing vesicles and increased β‐amyloid generation. Inappropriate interactions of Alc‐ and APP‐containing vesicles with kinesin‐1 may promote aberrant APP metabolism in Alzheimer's disease.