Recent advances in our understanding of adipose tissue biology have revealed that adipose tissue is not a simple organ for storing excess energy, as previously thought, but a more complex organ that regulates systemic metabolism through functions such as energy delivery and metabolism in response to changes in energy status as well as adipokine secretion. Since insulin plays a central role in many aspects of the regulation of adipose tissue function, insulin sensitivity in adipose tissue is considered an important factor in the control of systemic metabolism. In this article, we review new insights into the mechanisms of metabolic regulation by white adipocytes that have emerged from recent studies using mice with tissue-specific knockout mice of PDK1 and other insulin signaling molecules.

Sarcopenia is characterized by age-related loss of skeletal muscle mass and strength and is closely associated with lifestyle-related diseases such as diabetes, obesity, cardiovascular disease, chronic kidney disease (CKD), and chronic obstructive pulmonary disease (COPD). These diseases promote the development and progression of sarcopenia through insulin resistance, chronic inflammation, and hormonal abnormalities. In recent years, the pathophysiology of sarcopenia has been increasingly clarified, with a particular focus on its interaction with lifestyle-related diseases. This review outlines the relationship between sarcopenia and lifestyle-related diseases and presents evidence for the mechanism.

Historically, attempts to understand the pathogenesis of obesity have focused on hormonal perspectives, as exemplified by insulin. However, concurrent upregulation of hepatic gluconeogenesis and lipogenesis, one of the specific aspects of obesity-related pathogenesis, cannot be explained simply by insulin resistance, implying gaps in existing knowledge. C-terminal binding protein 2 (CtBP2) is a metabolite sensor that can be activated by NADH. We have demonstrated that CtBP2 is inactivated upon interaction with fatty acyl-CoAs, which are increased in tissues in obesity, thereby playing a critical role in this pathogenetic process. In the liver, CtBP2 suppresses gluconeogenesis and lipogenesis in healthy subjects but is dysregulated in obesity, leading to diabetes and steatosis. Inactivation of CtBP2 also contributes to the progressive decline of pancreatic β-cell function in obesity, suggesting possible involvement of CtBP2 in a variety of tissues. This article discusses the pathogenesis of obesity from metabolic perspectives by focusing on CtBP2.

Diet significantly affects the development and treatment of cardiovascular diseases. In recent years, attention has been paid to the setting of LDL-C targets for prevention of coronary artery disease, and it has been recommended that these should be even lower. According to the Japan Atherosclerosis Society guidelines, the LDL-C level for secondary prevention should be less than 100 mg/dL or less than 70 mg/dL, whereas in Western countries, less than 55 mg/dL is recommended. Diet is important, regardless of whether the LDL-C level it is hereditary or whether patients are medicated. In fact, even if the target level is reached under drug therapy, a 10‐20％ fluctuation in LDL-C occurs if the intake of cholesterol and fats (especially saturated and trans fats) increases. In the diet, it is important to pay attention to the proper total energy intake and fat-to-energy ratio, as well as the intake of saturated fatty acids and cholesterol. The low-sodium Japan diet improves lipid metabolism and is thought to be useful for prevention of arteriosclerotic disease.

An open crossover trial was conducted with 54 healthy adult males to investigate the effects of a rice-based Japanese-style breakfast (test meal) on cognitive function and brain hemodynamics in comparison with a bread-based breakfast (control meal). The test meal consisted of a bowl of rice, warm soup, salad, and meat or fish, providing 22‐28 g of protein, whereas the control diet included two pieces of bread, offering 11‐12 g of protein. The total caloric intake of both meals was adjusted to be nearly equal. Each participant consumed one type of meal for two weeks, followed by a two-week washout period, and then switched to the alternative meal for an additional two weeks. Cognitive performance was assessed using the Rapid Visual Information Processing (RVIP) and Digital Vigilance Test on the last day of each intervention, and dorsolateral prefrontal cortex hemodynamics were measured during the tests using fNIRS. Creativity was evaluated using the Alternative Uses Task. The results indicated that both meals significantly improved RVIP correct response rates but only in the test meal was associated with an increase of cerebral blood flow during the task, suggesting enhanced cognitive performance and brain activation. Heart rates were higher in the test group, indicating better whole-body blood flow. These findings suggest that a rice-based Japanese-style breakfast may improve cognitive and physiological functions.

We have previously reported that lipocalin-type prostaglandin D synthase (L-PGDS) in egg white reacts with IgE from patients with egg allergies. We subsequently developed an immune complex transfer enzyme immunoassay for L-PGDS and found that the amount of L-PGDS in hen eggs varies depending on the hen lineage and other factors. L-PGDS catalyzes the conversion of prostaglandin (PG) H₂ to PGD₂ in the arachidonic acid cascade. Although chicken L-PGDS has enzymatic activity, its pH stability, digestibility and the relationship between its digestibility and activity are unclear. Here, we examined the digestibility of L-PGDS by pepsin and trypsin and the effect of digestion on its activity. L-PGDS activity was maintained after 30 min of pepsin digestion. However, after a further 2 h of trypsin digestion, the activity was below the detection limit. Pepsin and trypsin digests of L-PGDS were analyzed using sodium dodecyl sulfate-polyacrylamide gel electrophoresis. After 30 min of pepsin digestion, most of the L-PGDS remained at its native molecular weight. However, after 30 min of pepsin digestion, followed by 2 h of trypsin digestion, most of it was degraded from approximately 23 kDa to 13.5 kDa. These results are consistent with the enzyme activity results.

In the present study, we investigated the effects of salt-free fermented soy paste on hypertension in spontaneously hypertensive rats (SHR). SHR/Izm were fed a diet containing 0％, 2.5％, 5％ or 10％ salt-free fermented soy paste for 10 weeks. A significant increase in blood pressure was observed in all groups during the experimental period. However, systolic blood pressure in SHR/Izm fed salt-free fermented soy paste was significantly lower than in the control group at 3 weeks after the start of the experiment. At 9 weeks, SHR/Izm fed the diet containing 2.5％, 5％ or 10％ salt-free fermented soy paste showed significantly lower diastolic blood pressure than the control group. No distinct dose-dependency was observed in the blood pressure-lowering effect of the salt-free fermented soy paste. Additionally, there were no remarkable differences in blood biochemistry parameters among the groups. Our findings indicate that a diet with at least 2.5％ salt-free fermented soy paste clearly attenuated the increase in blood pressure in SHR/Izm, suggesting that consumption of salt-free fermented soy paste can have a potentially beneficial effect on hypertension.