Among the genetic and environmental risk factors, nutrition plays a crucial role in determining the timing of puberty. Early menarche onset (EMO) is defined as when girls reach menarche onset at an age which is earlier than the mean/median age of menarche, between 12 and 13 years of age, according to individual ethnicity. The present study examined the association between nutrient intake in childhood and EMO risk in healthy girls by performing a systematic review and meta-analysis of prospective studies. We screened EMBASE, Cochrane Library, PubMed/MEDLINE, and Web of Science databases for 16 eligible studies with all medium-to-high quality scores ranging from 3 to 5 of 6 possible points with 10,884 subjects. Higher intakes of energy (risk ratio (RR) = 3.32, 95% confidence interval (CI) = 1.74–6.34, I² = 97%), and protein (RR = 3.15, 95% CI = 2.87–3.44, I² = 0%) were associated with EMO risk. For each additional 1 g/day animal protein intake in childhood, the age at menarche was approximately two months earlier (β = −0.13, I² = 55%), and high iron intake was associated with EMO (RR = 1.20, 95% CI = 1.03–1.40, I² = 0%). Polyunsaturated fatty acid (PUFAs) intake was associated with EMO risk with a dose-response effect (RR = 1.25, 95% CI = 1.05–1.49, I² = 44%). Girls with a high intake of fiber and monosaturated fatty acids (MUFAs) in childhood experienced later menarche onset (RR = 0.83, 95% CI = 0.69–1.00, I² = 31%; RR = 0.66, 95% CI = 0.50–0.86, I² = 0%, respectively). Thus, adherence to a high intake of animal proteins-, iron- and PUFA-rich food diet makes girls more likely to have EMO, while a high intake of fiber- and MUFA-rich foods may protect girls from EMO. Further studies are expected to investigate the role of specific types of PUFAs and MUFAs on EMO to promote healthy sexual maturity in girls.

With the increasing prevalence of sleep deprivation (SD)-related disorders, the effective treatment of sleep disorders has become a critical health research topic. Thus, we hypothesized and investigated the effectiveness of a 3-week melatonin intervention on neuropsychiatric behavioral responses mediated throughout melatonin receptors, gut microbiota, and lipid metabolites in rats with chronic SD. Eighteen 6-week-old Wistar rats were used and divided into the control grup (C, n = 6), SD group (n = 6), and melatonin-supplemented group (SDM, n = 6). During weeks 0 to 6, animals were provided with the AIN-93M diet and free access to water. Four-week chronic SD was conducted from weeks 7 to 10. Exogenous melatonin administration (10 mg/kg BW) was injected intraperitoneally 1 h before the daily administration of SD for 3 weeks in the SDM group. SD rats exhibited anxiety-like behavior, depression-like behavior, and cognitive impairment. Exogenous melatonin administration ameliorated neuropsychiatric behaviors induced by chronic SD. Analysis of fecal metabolites indicated that melatonin may influence brain messaging through the microbiota–gut–brain axis by increasing the production of short-chain fatty acids (SCFA) and decreasing the production of secondary bile acids (SBA). Four-week SD reduced the cerebral cortex expression of MT1, but not in the colon. Chronic SD led to anxiety and depression-like behaviors and cognitive decline, as well as the reduced intestinal level of SCFAs and the enhanced intestinal level of SBAs in rats. In this work, we confirmed our hypothesis that a 3-week melatonin intervention on neuropsychiatric behavioral response mediated throughout melatonin receptors, gut microbiota, and lipid metabolites in rats with chronic SD.

The prevalence of depression is increasing, and geriatric depression, in particular, is difficult to recognize and treat. Depression in older adults is often accompanied by neuroinflammation in the central nervous system (CNS). Neuroinflammation affects the brain's physiological and immune functions through several pathways and induces depressive symptoms. This study investigated the relationship among depression, neuroinflammation, and fish oil supplementation. Thirty-six male Sprague-Dawley rats were used in an aging-related depression animal model to simulate geriatric depression. Cognitive function, depressive-like symptoms, peripheral nervous system and CNS inflammation status, and the tryptophan-related metabolic pathway were analyzed. The geriatric depression animal model was associated with depressive-like behaviors and cognitive impairment. The integrity of the blood-brain barrier was compromised, resulting in increased expression of ionized calcium-binding adapter molecule 1 and the glial fibrillary acidic protein in the brain, indicating increased neuroinflammation. Tryptophan metabolism was also negatively affected. The geriatric-depressive-like rats had high levels of neurotoxic 5-hydroxyindoleacetic acid and kynurenine in their hippocampus. Fish oil intake improved depressive-like symptoms and cognitive impairment, reduced proinflammatory cytokine expression, activated the brain's glial cells, and increased the interleukin-10 level in the prefrontal cortex. Thus, fish oil intervention could ameliorate abnormal neurobehaviors and neuroinflammation and elevate the serotonin level in the hippocampus.

Eccentric contraction can easily cause muscle damage and an inflammatory response, which reduces the efficiency of muscle contraction. Resveratrol causes anti-inflammatory effects in muscles, accelerates muscle repair, and promotes exercise performance after contusion recovery. However, whether resveratrol provides the same benefits for sports injuries caused by eccentric contraction is unknown. Thus, we explored the effects of resveratrol on inflammation and energy metabolism. In this study, mice were divided into four groups: a control group, an exercise group (EX), an exercise with low-dose resveratrol group (EX + RES25), and an exercise with high-dose resveratrol group (EX + RES150). The results of an exhaustion test showed that the time before exhaustion of the EX + RES150 group was greater than that of the EX group. Tumour necrosis factor-α (Tnfα) mRNA expression was lower in the EX + RES150 group than in the EX group. The energy utilisation of the EX + RES150 group was greater than that of the EX + RES25 group in different muscles. High-dose resveratrol intervention decreased Tnfα mRNA expression and enhanced the mRNA expressions of sirtuin 1, glucose transporter 4, AMP-activated protein kinase α1, and AMP-activated protein kinase α2 in muscles. These results revealed that high-dose resveratrol supplementation can reduce inflammation and oxidation and improve energy utilisation during short-duration high-intensity exercise.

: Oligodendrocytes (OL) and myelin abnormalities have emerged as important contributors to the pathogenesis of Alzheimer’s Disease (AD). OL maintain neuronal health through myelin axon interactions and by supplying neurotrophic and metabolic support. To gain insight on how OL and myelin may improve neuronal deficits associated with AD, we have generated a novel mouse model (AD/cKO) by crossing the App ^NL-G-F mouse which carries three human AD mutations in the mouse App gene with the Fus ^OL cKO, which has thicker myelin associated with greater cholesterol biosynthesis. The spatial working memory deficits manifested by the aged AD mouse were fully rescued by the Fus ^OL cKO. This outcome was associated with reduced neuronal oxidative damage, preserved presynaptic structures at the plaque niches and a shift in microglia state at the niches in both hippocampus and cortex. In contrast, plaque burden and microglia density were decreased in the hippocampus but not in cortex, uncoupling the neuronal and microglia effects from the amyloid burden. Single cell transcriptomics of AD/cKO hippocampal OL revealed upregulation of energy metabolism and antioxidant genes, suggesting a role of OL enhanced energy metabolism in protecting neurons and affecting microglia state in AD pathology.