Hokkaido University · 의학
아키노부 나카무라 교수의 연구실은 간지방증과 제2형 당뇨병의 발달 기전을 밝히는 데 초점을 맞추고 있으며, 특히 갈락토키나제(Glucokinase)의 조절 기전과 그 기능 이상이 대사질환에 미치는 영향을 중심으로 연구를 진행하고 있습니다. 당화혈색소 수치 조절과 인슐린 분비 기능 향상을 위한 약물 타겟으로서의 갈락토키나제 활성화제의 임상적 적용 가능성을 탐색하고 있으며, β세포의 생존과 증식 메커니즘에 대한 분자생물학적 분석도 함께 수행하고 있습니다. 특히 비알코올성 간지방증(NASH)과 당뇨병의 연관성, 그리고 혈중 고분자량 어드포넥틴과 같은 대사조절 호르몬의 역할에 대해서도 심층적인 메타분석을 수행하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Nonalcoholic fatty liver disease (NAFLD) encompasses a clinicopathologic spectrum of diseases ranging from isolated hepatic steatosis to nonalcoholic steatohepatitis (NASH), the more aggressive form of fatty liver disease that may progress to cirrhosis and cirrhosis-related complications, including hepatocellular carcinoma. The prevalence of NAFLD, including NASH, is also increasing in parallel with the growing epidemics of obesity and diabetes. However, the causal relationships between obesity
Glucokinase is one of four members of the hexokinase family of enzymes. Its expression is limited to the major organs (such as the pancreas, liver, brain and the gastrointestinal tract) that are thought to have an integrated role in glucose sensing. In the liver, phosphorylation of glucose by glucokinase promotes glycogen synthesis, whereas in the β-cells, it results in insulin release. Studies of glucokinase-linked genetically-modified mice and mutations in humans have illustrated the important
We investigated the effect of glucokinase activator (GKA) on glucose metabolism and beta-cell mass. We analyzed four mouse groups: wild-type mice and beta-cell-specific haploinsufficiency of glucokinase gene (Gck(+/-)) mice on a high-fat (HF) diet. Each genotype was also treated with GKA mixed in the HF diet. Rodent insulinoma cells and isolated islets were used to evaluate beta-cell proliferation by GKA. After 20 wk on the above diets, there were no differences in body weight, lipid profiles, a
Glucokinase, which phosphorylates glucose to form glucose-6-phosphate, plays a critical role in regulating blood glucose levels. On the basis of data of glucokinase-knockout and transgenic mice and humans with glucokinase mutations, glucokinase was targeted for drug development aiming to augment its activity, and thereby reduce hyperglycaemia in patients with diabetes. In fact, various small molecule compounds have been developed and clinically tested as glucokinase activators. However, some hav
We investigated the association between serum high molecular weight (HMW) adiponectin and insulin secretion in a population-based study, with or without adjustment for insulin sensitivity. A total of 488 participants (263 women) were included in the present study. Insulin secretion was estimated using the homeostasis model assessment of β-cell function ± adjustment for insulin resistance using the disposition index. Multivariate analysis showed that HMW adiponectin was significantly and inversel
Efficacy of glucokinase activation on glycemic control is limited to a short-term period. One reason might be related to excess glucose signaling by glucokinase activation toward β-cells. In this study, we investigated the effect of glucokinase haploinsufficiency on glucose tolerance as well as β-cell function and mass using a mouse model of type 2 diabetes. Our results showed that in <i>db/db</i> mice with glucokinase haploinsufficiency, glucose tolerance was ameliorated by augmented insulin se
Two of the five patients diagnosed with Gitelman's syndrome were normomagnesaemic, which is uncommon in this syndrome. Our study indicates that renal clearance tests and mutation analysis can play an important role in diagnosing Gitelman's syndrome more precisely.
The presence of lung cavities was found to be a more important determinant of the treatment outcomes than that of diabetes per se in patients with pulmonary tuberculosis.
