Severe maternal stress alters placental function, resulting in adipose tissue and liver dysfunction in offspring of mice.

The developmental origins of health and disease (DOHaD) hypothesis is that future lifestyle diseases in offspring are associated with intrauterine origins in the mother; stress during pregnancy is a risk factor for these diseases in offspring. This study aimed to clarify association of maternal stress with placental dysfunction and offspring development in mice. We applied water stress for 24 h during late pregnancy to explore the metabolic response of offspring to a normal diet (ND) and high-fat diet (HFD). Placental functions were altered by maternal stress, reducing the birth weight of the offspring. In the later life of offspring fed with ND, maternal stress impaired systemic glucose tolerance and altered adipokine secretion in adipose tissue and/or liver. The female offspring of stress-induced dams were light in body weight with lower adipose tissue and smaller adipocytes in both the ND and HFD groups. Abnormal situations, such as dysregulation of plasma glucose levels and fatty liver despite and lower increases in body weight, were observed in the female offspring of stress-induced dams, especially in the HFD-treated group. These findings suggest that long-lasting abnormal conditions and responses to metabolic challenges in maternal stress-induced offspring are linked to placental dysregulation and fetal programming.

Association between self-reported night sleep duration and cognitive function among older adults with intact global cognition.

OBJECTIVES: The purpose of this study was to clarify the association between self-reported night sleep duration and cognitive functions such as word memory, story memory, attention, executive function, and processing speed of older adults with normal global cognitive function. METHODS: A total of 241 functionally independent older adults (mean age, 75.5 ± 6.4 years) participated in this study. No participants had a history of dementia diagnosis, and each had a Mini-Mental State Examination (MMSE) score ≥ 24. Participants were evaluated for self-reported sleep duration and cognitive function using the National Center for Geriatrics and Gerontology-Functional Assessment Tool (NCGG-FAT). RESULTS: The longest sleep duration group (≥9 h) had lower MMSE scores (p = 0.010), Z-score of word list memory II (delayed recall; p = 0.001), and Z-score of story memory II (delayed recognition; p = 0.002) than the medium sleep duration group (7-8 h). Longest and long sleep duration (8-9 h) was significantly associated with impairment of story memory II (longest sleep duration: adjusted odds ratio [OR] = 3.58, 95% confidence interval [CI] = 1.13-11.37, long sleep duration: adjusted OR = 4.30, 95% CI = 1.34-13.82) with reference to medium sleep duration, but no impairment of MMSE according to multiple logistic regression analysis. Furthermore, short sleep duration (<7 h) was not associated with cognitive impairment. CONCLUSIONS: This study suggests that long sleep duration is associated with cognitive impairment, especially of story memory (delayed recognition) in older adults with normal global cognitive function.

Prostaglandin F2α receptor antagonist attenuates LPS-induced systemic inflammatory response in mice.

Although it is known that prostaglandin (PG) F2α level is elevated in the plasma of patients with sepsis, the roles of PGF2α is still unknown. We aimed to clarify the roles of PGF2α in the regulation of lipopolysaccharide (LPS)-induced systemic inflammation. At 24 hours after LPS administration, neutrophil infiltration in peritoneal cavity, the mRNA expression of pro-inflammatory cytokines such as tumor necrosis factor-α, interleukin (IL)-1ß, IL-6, and macrophage inflammatory protein-2, and tissue damages in lung, liver, and kidney were all increased. Inhibition of FP receptors significantly decreased LPS-induced neutrophil infiltration and lowered the mRNA expression of the pro-inflammatory cytokines. At 6 hour after LPS administration, the level of anti-inflammatory cytokine, IL-10 in peritoneal lavage fluid was higher than that in naïve mice. Inhibition of FP receptors in these mice increased IL-10 level further. Stimulation of isolated peritoneal neutrophils by LPS increased the gene expression of IL-10, which was further increased by AL8810 treatment. Administration of an anti-IL-10 antibody antagonized the AL8810-decreased mRNA expression of pro-inflammatory cytokines and tissue damages. These results indicate that inhibition of FP receptors by AL8810 attenuated LPS-induced systemic inflammation in mice via enhanced IL-10 production.