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Treatment of obesity and metabolic-associated fatty liver disease with a diet or orlistat: A randomized controlled trial.
Feng, X, Lin, Y, Zhuo, S, Dong, Z, Shao, C, Ye, J, Zhong, B
The American journal of clinical nutrition. 2023;117(4):691-700
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Metabolic-associated fatty liver disease (MAFLD) is characterised by excessive lipid accumulation in hepatocytes. Weight management by the treatment to target strategy through lifestyle intervention remains the primary approach for MAFLD treatment. The aim of this study was to compare the efficacy of a conventional energy-restricted diet (the control group), orlistat, and an experimental diet in the Asian population with obesity and MAFLD. This study was a prospective, open-label, monocentric randomised controlled study. Participants (n = 118) were randomly assigned to the control (n = 39), orlistat (n = 40), or experimental diet (n = 39) groups at a 1:1:1 allocation. Results showed that: - orlistat and the experimental diet were superior to lifestyle intervention in ameliorating liver steatosis [fatty liver]. - the experimental diet had an advantage over lifestyle intervention when patients adhered to the diet. - orlistat was superior to the experimental diet and lifestyle modifications in decreasing liver fat content. Authors conclude that more multicentre, large-scale, prospective studies are needed to verify the long-term efficacy and safety of the experimental diet and orlistat treatment in subjects with MAFLD.
Abstract
BACKGROUND Losing weight by lifestyle interventions is the first-line treatment for metabolic-associated fatty liver disease (MAFLD) but is limited by low compliance. OBJECTIVES This study aimed to compare the effects of orlistat or an experimental high-protein/lower-carbohydrate diet with a control diet in Asian patients with obesity and MAFLD. METHODS A total of 118 Asian patients with obesity and MAFLD confirmed with MRI-based proton density fat fraction with Dixon sequence were enrolled and allocated to the control group, the orlistat group, or the experimental diet group for 24 wk. The primary endpoint was the relative change in liver fat content (LFC) assessed by MRI-based proton density fat fraction. RESULTS A total of 118 subjects with obesity and MAFLD were randomly assigned to the control group (n = 39), the orlistat group (n = 40), or the experimental diet group (n = 39). All 3 groups demonstrated improvement in liver steatosis at wk 24. The absolute decrease in LFC in the orlistat group was 9.1% and 5.4% in the experimental diet group, both significantly higher than that in the control group (P < 0.05). The relative reduction in LFC was 30.2% in the experimental diet group, which was significantly higher than the 12.2% observed in the control group (P = 0.01). CONCLUSIONS Orlistat and the experimental diet group reduced liver steatosis compared to the control group. This trial was registered at Chinese Clinical Trial Registry (ChiCTR-1900027172). http://www.chictr.org.cn.
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Mycotoxin-Linked Mutations and Cancer Risk: A Global Health Issue.
Ekwomadu, T, Mwanza, M, Musekiwa, A
International journal of environmental research and public health. 2022;19(13)
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Mycotoxins are toxic substances produced by fungi, which can be found in common foods like maize, wheat, nuts, and foods containing them. Mycotoxins such as aflatoxins, ochratoxin, fumonisins, zearalenone, and some Penicillium toxins can alter genetic material. According to previous studies, they can damage genetic material and affect cell growth. Usage of chemicals such as fertilizers and fungicides is a common practice in the agricultural industry to protect plants from fungus and to feed them. However, fungicides can accelerate mycotoxin production. 16 studies were included in this Systematic Review and 11 in Meta-Analysis. This research looked at the harmful effects of mycotoxins such as aflatoxins, fumonisins, ochratoxin, T2, zearalenone, and some Penicillium toxins in causing cancers. The researchers evaluated the link between aflatoxin exposure and liver cancer, fumonisin B1 exposure and liver cancer, zearalenone exposure and breast cancer, zearalenone exposure and cervical cancer, citrinine and patulin exposure and colorectal cancer, and NEO, HT-2, and T-2 exposure and Oesophageal cancer. This research did not show significant associations between various mycotoxins and cancer risk. As currently, most studies are primarily focused on aflatoxin; more robust studies are needed to assess the cancer risk associated with different mycotoxin exposure. Using the results of this study, healthcare professionals can gain a better understanding of how mycotoxins affect our bodies.
Abstract
Humans continue to be constantly exposed to mycotoxins, mainly through oral exposure (dietary), inhalation, or dermal contact. Recently, it has been of increasing interest to investigate mycotoxin-linked carcinogenicity. This systematic review was conducted to synthesize evidence of the association between mycotoxin-linked mutations and the risk of cancer, to provide an overview of the data linking exposure to different mycotoxins with human cancer risk, and to provide an update on current research on the risk of cancer associated with human exposure to mycotoxins. PRISMA guidelines were used when conducting the systematic review. PubMed, MEDLINE, and CINAHL electronic databases were comprehensively searched to extract the relevant studies published from inception to May 2022. A total of sixteen relevant studies (4907 participants) were identified and included in this review. Of these, twelve studies were from Asia, while four of the studies were conducted in Africa. The overall meta-analysis result found no significant association, although some of the studies confirmed an association between mycotoxin-linked mutations and primary liver cancer risk. Mainly, the experimental studies have shown associations between mycotoxin-linked mutations and cancer risk, and there is a need for researchers to confirm these links in epidemiological studies in order to guide public health policies and interventions.
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Moderate alcohol consumption and lipoprotein subfractions: a systematic review of intervention and observational studies.
Wilkens, TL, Tranæs, K, Eriksen, JN, Dragsted, LO
Nutrition reviews. 2022;80(5):1311-1339
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Moderate consumption of alcohol has been considered as cardioprotective as it may reduce the risk of cardiovascular diseases by improving the lipid profile. This systematic review investigated the effects of regular moderate alcohol consumption of up to 60 g/day on lipoprotein subfraction changes and underlying mechanisms. A total of one hundred and fourteen studies were included in this review. The results showed that up to 60 g/day of alcohol intake increased the high-density lipoprotein (HDL) subfractions. Alcohol also increased the cardioprotective effect by increasing the cholesterol efflux capacity and paraoxonase activity in moderate drinkers. Moderate intake may also positively affect the low-density lipoprotein size. Further robust studies are required to investigate the effects of alcohol consumption on LDL subfractions and apoB lipoproteins in people with chronic diseases. Healthcare professionals can use the results of this research to understand the impact of moderate alcohol intake on HDL subfractions and its association with cardiovascular disease.
Abstract
CONTEXT Moderate alcohol consumption is associated with decreased risk of cardiovascular disease (CVD) and improvement in cardiovascular risk markers, including lipoproteins and lipoprotein subfractions. OBJECTIVE To systematically review the relationship between moderate alcohol intake, lipoprotein subfractions, and related mechanisms. DATA SOURCES Following PRISMA, all human and ex vivo studies with an alcohol intake up to 60 g/d were included from 8 databases. DATA EXTRACTION A total of 17 478 studies were screened, and data were extracted from 37 intervention and 77 observational studies. RESULTS Alcohol intake was positively associated with all HDL subfractions. A few studies found lower levels of small LDLs, increased average LDL particle size, and nonlinear relationships to apolipoprotein B-containing lipoproteins. Cholesterol efflux capacity and paraoxonase activity were consistently increased. Several studies had unclear or high risk of bias, and heterogeneous laboratory methods restricted comparability between studies. CONCLUSIONS Up to 60 g/d alcohol can cause changes in lipoprotein subfractions and related mechanisms that could influence cardiovascular health. SYSTEMATIC REVIEW REGISTRATION PROSPERO registration no. 98955.
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Prenatal exposure to phthalate and decreased body mass index of children: a systematic review and meta-analysis.
Lee, DW, Lim, HM, Lee, JY, Min, KB, Shin, CH, Lee, YA, Hong, YC
Scientific reports. 2022;12(1):8961
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Phthalates are widely used chemicals to improve the utility of plastics and personal care products. Phthalates can be classified as high-molecular-weight phthalates and low-molecular-weight phthalates. The aim of this study was to clarify whether prenatal and postnatal exposures to phthalates are associated with physical growth as measured by body composition indices in children. This study is a systematic literature review and meta-analysis of 39 studies about the association of phthalates with body composition indices among children. Results showed that prenatal exposure to phthalates is significantly associated with low body mass index in children, but not with body fat mass. In addition, prenatal phthalate exposure may affect the disturbance of normal growth of children rather than act as an obesogen. Authors conclude that it is necessary to administer stricter and broader regulations on phthalates in living environments.
Abstract
Phthalates are well-known endocrine-disrupting chemicals. Many detrimental health effects of phthalates were investigated, but studies on the association of phthalates with obesity in children showed inconsistent results. Thus, this systematic review and meta-analysis were performed to clarify whether prenatal and postnatal exposures to phthalates are associated with physical growth disturbances in children. We performed the systematic review and meta-analysis following the PRISMA 2020 statement guidelines, and found 39 studies that met our inclusion criteria, including 22 longitudinal and 17 cross-sectional studies. We observed a significant negative association between the prenatal exposure to DEHP and the body mass index (BMI) z-score of the offspring (β = - 0.05; 95% CI: - 0.10, - 0.001) in the meta-analysis, while no significant association between the prenatal exposure to DEHP and the body fat percentage of the offspring was observed (β = 0.01; 95% CI: - 0.41, 0.44). In the systematic review, studies on the association between phthalates exposure in childhood and obesity were inconsistent. Prenatal exposure to phthalates was found to be associated with decreased BMI z-score in children, but not associated with body fat percentage. Our findings suggest that phthalates disturb the normal muscle growth of children, rather than induce obesity, as previous studies have hypothesized.
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Cigarette Smoke Extract Disturbs Mitochondria-Regulated Airway Epithelial Cell Responses to Pneumococci.
Aghapour, M, Tulen, CBM, Abdi Sarabi, M, Weinert, S, Müsken, M, Relja, B, van Schooten, FJ, Jeron, A, Braun-Dullaeus, R, Remels, AH, et al
Cells. 2022;11(11)
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Cigarette smoking can affect airway epithelial cells, causing overproduction of mucus, damage, and inflammation, which may result in the progression of airway diseases. Airway epithelial cells (AEC) rely on mitochondria for energy, and mitochondrial dysfunction may affect innate immunity and the integrity of the airway epithelium. Cigarette smoking is found to accelerate mitochondrial damage within AEC. Maintaining a normal microbial composition within the respiratory tract is essential for maintaining immunity. There is evidence that smoking cigarettes disrupts the microbial composition and increases the spread of pathogenic bacteria such as Streptococcus pneumoniae (Sp) which causes inflammation. By exposing 16HBE cells to Sp and cigarette smoke extract (CSE), this study investigated the effect of cigarette smoking on mitochondrial dysfunction in ACE in an in vitro model. Additionally, the study examined the direct and indirect pathways involved in cigarette smoking-induced mitochondrial dysfunction and altered innate immune response to Sp infection. CSE exposure decreases mitochondrial complex protein levels and mitochondrial membrane potential, which affects energy production. It also increases mitochondrial oxidative stress and mitochondrial degradation. All these factors lead to mitochondrial dysfunction in ACE. CSE exposure to ACE was associated with altered gene expression in the tight and adherence junctions that serve as a protective barrier against pathogens and pollutants and reduced type I interferon immune responses to Sp. Using the results of this study, healthcare professionals can gain a better understanding of the impact of cigarette smoking on mitochondrial dysfunction and how it increases susceptibility to Sp-related immune responses. It is necessary to conduct further studies to evaluate the effects of cigarette smoking on mitochondrial dysfunction, microbial composition disruption, and the interaction between AECs and elevated immune responses.
Abstract
Mitochondrial functionality is crucial for the execution of physiologic functions of metabolically active cells in the respiratory tract including airway epithelial cells (AECs). Cigarette smoke is known to impair mitochondrial function in AECs. However, the potential contribution of mitochondrial dysfunction in AECs to airway infection and airway epithelial barrier dysfunction is unknown. In this study, we used an in vitro model based on AECs exposed to cigarette smoke extract (CSE) followed by an infection with Streptococcus pneumoniae (Sp). The levels of oxidative stress as an indicator of mitochondrial stress were quantified upon CSE and Sp treatment. In addition, expression of proteins associated with mitophagy, mitochondrial content, and biogenesis as well as mitochondrial fission and fusion was quantified. Transcriptional AEC profiling was performed to identify the potential changes in innate immune pathways and correlate them with indices of mitochondrial function. We observed that CSE exposure substantially altered mitochondrial function in AECs by suppressing mitochondrial complex protein levels, reducing mitochondrial membrane potential and increasing mitochondrial stress and mitophagy. Moreover, CSE-induced mitochondrial dysfunction correlated with reduced enrichment of genes involved in apical junctions and innate immune responses to Sp, particularly type I interferon responses. Together, our results demonstrated that CSE-induced mitochondrial dysfunction may contribute to impaired innate immune responses to Sp.
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Relationship between Prenatal or Postnatal Exposure to Pesticides and Obesity: A Systematic Review.
Pinos, H, Carrillo, B, Merchán, A, Biosca-Brull, J, Pérez-Fernández, C, Colomina, MT, Sánchez-Santed, F, Martín-Sánchez, F, Collado, P, Arias, JL, et al
International journal of environmental research and public health. 2021;18(13)
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Obesity is a multifactorial disease with biological, psychosocial, and behavioural factors that include genetic, socioeconomic, and cultural influences. Exposure to pesticides can result in weight gain through different pathways. The aim of this study was to assess a possible association between prenatal and postnatal exposure to pesticides and obesity in offspring from human and animal studies. This study is a systematic review of 9 animal studies and 25 human studies (23 cohorts and 2 crossover experimental designs). Results show that there is still scarce evidence to support a clear relationship between exposure to pesticides and obesity in humans and experimental animals. In fact, the effects of pesticide exposure on body weight change are mostly inconclusive and report conflicting results. Authors conclude that further research is required to improve understanding of whether repeated exposures over time or just short-term exposures to pesticides during critical windows of development are related to obesity.
Abstract
In recent years, the worldwide prevalence of overweight and obesity among adults and children has dramatically increased. The conventional model regarding the onset of obesity is based on an imbalance between energy intake and expenditure. However, other possible environmental factors involved, such as the exposure to chemicals like pesticides, cannot be discarded. These compounds could act as endocrine-disrupting chemicals (EDC) that may interfere with hormone activity related to several mechanisms involved in body weight control. The main objective of this study was to systematically review the data provided in the scientific literature for a possible association between prenatal and postnatal exposure to pesticides and obesity in offspring. A total of 25 human and 9 animal studies were analyzed. The prenatal, perinatal, and postnatal exposure to organophosphate, organochlorine, pyrethroid, neonicotinoid, and carbamate, as well as a combined pesticide exposure was reviewed. This systematic review reveals that the effects of pesticide exposure on body weight are mostly inconclusive, finding conflicting results in both humans and experimental animals. The outcomes reviewed are dependent on many factors, including dosage and route of administration, species, sex, and treatment duration. More research is needed to effectively evaluate the impact of the combined effects of different pesticides on human health.