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Epidemiological studies have shown that abnormalities of glucose metabolism are involved in leucine‐rich repeat kinase 2 (LRRK2)‐associated Parkinson's disease (PD). However, the physiological significance of this association is unclear. In the present study, we investigated the effect of LRRK2 on high‐fat diet (HFD)‐induced glucose intolerance using Lrrk2‐knockout (KO) mice. We found for the first time that HFD‐fed KO mice display improved glucose tolerance compared with their wild‐type (WT) counterparts. In addition, high serum insulin and leptin, as well as low serum adiponectin resulting from HFD in WT mice were improved in KO mice. Using western blotting, we found that Lrrk2 is highly expressed in adipose tissues compared with other insulin‐related tissues that are thought to be important in glucose tolerance, including skeletal muscle, liver, and pancreas. Lrrk2 expression and phosphorylation of its kinase substrates Rab8a and Rab10 were significantly elevated after HFD treatment in WT mice. In cell culture experiments, treatment with a LRRK2 kinase inhibitor stimulated insulin‐dependent membrane translocation of glucose transporter 4 (Glut4) and glucose uptake in mouse 3T3‐L1 adipocytes. We conclude that increased LRRK2 kinase activity in adipose tissue exacerbates glucose tolerance by suppressing Rab8‐ and Rab10‐mediated GLUT4 membrane translocation.

We measured the thermal conductivity (λ) and thermal diffusivity (α) of tetragonal hen egg-white lysozyme (HEWL) crystals by the transient short-hot wire method. The crystals were grown by two different methods: Magnetically levitated crystals were realized with a superconducting magnet, the c-axis of which was perpendicularly orientated in the direction of the wire, and naturally grown crystals realized by the two-liquid method, grown randomly. We confirmed the temperature dependence in both the λ and α properties by measuring the variations in temperature and by statistical analysis. These properties differed slightly depending on the presence or absence of a magnetic field applied during the crystal growth. We hypothesize that the difference originated from the orientation of the crystals caused by the magnetic field. The statistical analyses demonstrated the possibility that asymmetric thermal conduction in the protein crystals provides anisotropic effects of the thermal properties.