Hiroshi Inoue

A vagal sensory--hypothalamic oxytocin--brown adipose tissue pathway mediates cholecystokinin-induced thermogenesis

This study identifies a vagal sensory-hypothalamic oxytocin-brown adipose tissue pathway that mediates CCK-induced thermogenesis.

Global loss of responsiveness in key regulator metabolites and elevated enzyme proteins as metabolic dysregulation in skeletal muscle and liver of obese mice during starvation

The paper examines metabolic adaptations during starvation in obese mice, finding impaired responsiveness and elevated enzyme expression in skeletal muscle and liver.

Structural robustness and temporal vulnerability of the starvation-responsive metabolic network in liver of healthy and obese mice

The paper examines how obesity disrupts the temporally ordered metabolic network in the liver during starvation, revealing structural robustness but temporal vulnerability.

Trans-omic analysis reveals opposite metabolic dysregulation between feeding and fasting in liver associated with obesity

The paper compares metabolic dysregulation in obese mice during feeding and fasting using multi-omics data, revealing opposite metabolic shifts linked to obesity.

In vivo transomic analyses of glucose-responsive metabolism in skeletal muscle reveal core differences between the healthy and obese states

This study uses multiomic analysis of skeletal muscle in obese and healthy mice to reveal differences in metabolic regulation by metabolites and genes after glucose administration.

Logical design of oral glucose ingestion pattern minimizing blood glucose in humans

The paper develops a mathematical model to predict an optimal glucose ingestion pattern that minimizes peak blood glucose levels in humans, validated through experimental testing.

Trans-omic analysis reveals allosteric and gene regulation-axes for altered glucose-responsive liver metabolism associated with obesity

The paper analyzes trans-omic data from healthy and obese mice to reveal that glucose-responsive liver metabolism is regulated by rapid changes in metabolites and gene expression in the healthy state, and by slow transcriptional regulation in the obese state.