OBJECTIVE: Metabolic disease is a multifaceted condition characterized by the disruption of numerous metabolic parameters within the host. Its prevalence has surged significantly in recent years and it has become a prominent non-communicable disease worldwide. The effect of gut microbiota on various beige fat induction is well studied, while the mechanisms behind the link remain unclear. Given that gut microbiota-derived metabolites (meta-metabolites) secreted in the gut serve as a key mode of communication with their host through direct circulation or indirect host physiology modification, understanding the effect of meta-metabolites on adipose tissue is essential.
METHODS: In our previous in-vivo studies, we observed a correlation between gut microbiota and the formation of beige fat. In this study, we further aimed to validate this correlation by treating the adipocyte cell line (3T3-L1) with meta-metabolites collected from the cecum of mice exhibiting beige adipose tissue formation. Additionally, we treated the adipocyte cell line with known beige fat inducers (L-Rhamnose and Ginsenoside) to assess meta-metabolites\' efficacy on beige fat formation.
RESULTS: Upon treatment with the meta-metabolites from the antibiotic-treated mice, we observed a significant increase in lipid metabolism and beige-specific gene expression. Analyzing the metabolites in these cells revealed that a set of metabolites potentially govern adipocytes, contributing to a metabolically active state. These effects were at par or even better than those of cells treated with L-Rhamnose or Ginsenoside.
CONCLUSIONS: This research sheds light on the intricate interplay between microbial metabolites and adipose tissue, offering valuable clues for understanding and potentially manipulating these processes for therapeutic purposes.

暂无摘要。

UNASSIGNED: Sleep complaints were reported to be associated with stroke, however, the evidence on the association between healthy sleep pattern and stroke risk in Chinese is limited.
UNASSIGNED: The aim of this study was to investigate the association between healthy sleep pattern and stroke in Chinese, and the influence of metabolic diseases on the association.
UNASSIGNED: A total of 11,851 participants from the Kailuan study in China without stroke at baseline were included. We calculated a healthy sleep score according to four sleep factors, and defined the low-risk groups as follows: no insomnia, no excessive daytime sleepiness, no frequent snoring, and sleep 7-8h/d. Each low-risk sleep factor was assigned a score of 1. Cox proportional hazard models were used to assess the association between healthy sleep score and stroke. Mediation analysis was used to estimate the role of metabolic diseases (obesity, diabetes, and hypertension) in the healthy sleep score-stroke association.
UNASSIGNED: During a mean follow-up period of 7.7 years, 504 cases of stroke were identified. A higher healthy sleep score was associated with a lower risk of stroke in a dose-response manner (P-trend=0.03). The adjusted hazard ratio (HR) for participants with a healthy sleep score of 4 versus ≤2 was 0.75 (95% confidence interval [CI]: 0.56, 0.96). In addition, obesity, diabetes, and hypertension collectively explained 21.9% (95% CI: 17.2, 26.5) of the association between healthy sleep score and stroke.
UNASSIGNED: Adherence to healthy sleep pattern was associated with a lower risk of stroke, and the favorable association was partially mediated by metabolic diseases.

The gut-liver axis plays a pivotal role in maintaining body homeostasis. Disruption of the gut-liver axis is linked to a multitude of diseases, including metabolic dysfunction-associated steatotic liver disease (MASLD). Probiotic strains from the Lactobacillaceae family are commonly used to mitigate experimental MASLD. Over the years, numerous studies have demonstrated the efficacy of these probiotics, often focusing on the outcome of liver disease. This review aims to further understand MASLD as a systemic metabolic dysfunction and to highlight the effects of probiotics on multi-organ axis, including organs such as the gastrointestinal tract, pancreas, muscle, adipose tissue, and the immune system. We specifically discuss evidence on how supplementation with Lactobacillaceae strains may alleviate MASLD by not only restoring liver health but also by modulating the physiology of other organ systems.

Everyone knows that an infection can make you feel sick. Although we perceive infection-induced changes in metabolism as a pathology, they are a part of a carefully regulated process that depends on tissue-specific interactions between the immune system and organs involved in the regulation of systemic homeostasis. Immune-mediated changes in homeostatic parameters lead to altered production and uptake of nutrients in circulation, which modifies the metabolic rate of key organs. This is what we experience as being sick. The purpose of sickness metabolism is to generate a metabolic environment in which the body is optimally able to fight infection while denying vital nutrients for the replication of pathogens. Sickness metabolism depends on tissue-specific immune cells, which mediate responses tailored to the nature and magnitude of the threat. As an infection increases in severity, so do the number and type of immune cells involved and the level to which organs are affected, which dictates the degree to which we feel sick. Interestingly, many alterations associated with metabolic disease appear to overlap with immune-mediated changes observed following infection. Targeting processes involving tissue-specific interactions between activated immune cells and metabolic organs therefore holds great potential for treating both people with severe infection and those with metabolic disease. In this review, we will discuss how the immune system communicates in situ with organs involved in the regulation of homeostasis and how this communication is impacted by infection.

UNASSIGNED: Light at night disrupts circadian rhythms, and circadian disruption is a risk factor for type 2 diabetes. Whether personal light exposure predicts diabetes risk has not been demonstrated in a large prospective cohort. We therefore assessed whether personal light exposure patterns predicted risk of incident type 2 diabetes in UK Biobank participants, using ∼13 million hours of light sensor data.
UNASSIGNED: Participants (N = 84,790, age (M ± SD) = 62.3 ± 7.9 years, 58% female) wore light sensors for one week, recording day and night light exposure. Circadian amplitude and phase were modeled from weekly light data. Incident type 2 diabetes was recorded (1997 cases; 7.9 ± 1.2 years follow-up; excluding diabetes cases prior to light-tracking). Risk of incident type 2 diabetes was assessed as a function of day and night light, circadian phase, and circadian amplitude, adjusting for age, sex, ethnicity, socioeconomic and lifestyle factors, and polygenic risk.
UNASSIGNED: Compared to people with dark nights (0-50th percentiles), diabetes risk was incrementally higher across brighter night light exposure percentiles (50-70th: multivariable-adjusted HR = 1.29 [1.14-1.46]; 70-90th: 1.39 [1.24-1.57]; and 90-100th: 1.53 [1.32-1.77]). Diabetes risk was higher in people with lower modeled circadian amplitude (aHR = 1.07 [1.03-1.10] per SD), and with early or late circadian phase (aHR range: 1.06-1.26). Night light and polygenic risk independently predicted higher diabetes risk. The difference in diabetes risk between people with bright and dark nights was similar to the difference between people with low and moderate genetic risk.
UNASSIGNED: Type 2 diabetes risk was higher in people exposed to brighter night light, and in people exposed to light patterns that may disrupt circadian rhythms. Avoidance of light at night could be a simple and cost-effective recommendation that mitigates risk of diabetes, even in those with high genetic risk.
UNASSIGNED: Australian Government Research Training Program.

NLRP3 plays a role in the development of autoinflammatory diseases. NLRP3, ASC, and Caspases 1 or 8 make up the NLRP3 inflammasome, which is an important part of innate immune system. The NLRP3 inflammasome-mediated inflammatory cytokines may also participate in metabolic disorders, such as diabetes, hyperlipidemia, atherosclerosis, non-alcoholic fatty liver disease, and gout. Hence, an overview of the NLRP3 regulation in these metabolic diseases and the potential drugs targeting NLRP3 is the focus of this review.

The human microbiome functions as a separate organ in a symbiotic relationship with the host. Disruption of this host-microbe symbiosis can lead to serious health problems. Modifications to the composition and function of the microbiome have been linked to changes in host metabolic outcomes. Industrial lifestyles with high consumption of processed foods, alcoholic beverages and antibiotic use have significantly altered the gut microbiome in unfavorable ways. Therefore, understanding the causal relationship between the human microbiome and host metabolism will provide important insights into how we can better intervene in metabolic health. In this review, I will discuss the potential use of the human microbiome as a therapeutic target to improve host metabolism.

Background and Objectives: Phenylketonuria (PKU) is a rare genetic disorder characterized by the inability to convert the essential amino acid phenylalanine into tyrosine. Early dietary treatment can successfully prevent complications, but controversies still exist regarding the attainment of normal growth in these patients. Materials and Methods: Eighteen patients with PKU from two Romanian reference centers were compared to eighteen non-PKU controls, matched for age and gender. The comparisons used weight-for-height, weight-for-age, height/length-for-age, and body mass index-for-age z-scores from birth to three years of age. Results: The PKU study group consisted of nine boys and nine girls, with a median follow-up period of thirty-six months (interquartile range = 9.75). While median values of all four growth metrics remained within the normal range across the entire study period, weight-for-age z-scores were significantly lower in PKU patients throughout most of the study (p < 0.001). Conclusions: The persistent lower weight-for-age z-scores of the PKU patients compared to controls indicate that ongoing monitoring and potential adjustments in dietary therapy may be necessary to further optimize growth outcomes.

Elevations in fructose consumption have been reported to contribute significantly to an increased incidence of obesity and metabolic diseases in industrial countries. Mechanistically, a high fructose intake leads to the dysregulation of glucose, triglyceride, and cholesterol metabolism in the liver, and causes elevations in inflammation and drives the progression of nonalcoholic fatty liver disease (NAFLD). A high fructose consumption is considered to be toxic to the body, and there are ongoing measures to develop pharmaceutical therapies targeting fructose metabolism. Although a large amount of work has summarized the effects fructose exposure within the intestine, liver, and kidney, there remains a gap in our knowledge regarding how fructose both indirectly and directly influences immune cell recruitment, activation, and function in metabolic tissues, which are essential to tissue and systemic inflammation. The most recent literature demonstrates that direct fructose exposure regulates oxidative metabolism in macrophages, leading to inflammation. The present review highlights (1) the mechanisms by which fructose metabolism impacts crosstalk between tissues, nonparenchymal cells, microbes, and immune cells; (2) the direct impact of fructose on immune cell metabolism and function; and (3) therapeutic targets of fructose metabolism to treat NAFLD. In addition, the review highlights how fructose disrupts liver tissue homeostasis and identifies new therapeutic targets for treating NAFLD and obesity.