Catecholamines of the adrenal medula and their morphological changes during adaptation to repeated immobilization stress

Changes of the adrenal medulla of rats were studied in the course of adaptation to repeated immobilization stress. An increase in the number of cells in the adrenal medulla was found in the adapted animals; this increase was confirmed by weight indices of the medulla and by cell counts per surface unit. Simultaneous karyometric measurements of the nuclei of adrenal medulla cells and an analysis of the catecholamine contents in the adrenals explain the increased activity of the adrenal medulla in the course of adaptation

Fast Food: A Source of Exposure to Phthalates and Bisphenol A in a Nationally Representative Sample

Background: Certain phthalates and bisphenol A (BPA) are industrial chemicals widely used in consumer products that can adversely impact human health. Diet is hypothesized to be a major source of exposure but little is known about the impact of specific food sources. This study aims to investigate the association between fast food consumption with human exposure to high-molecular weight phthalates (di(2-ethylhexyl) phthalate (DEHP) and diisononyl phthalate (DINP)) and BPA, in 8876 participants, aged 6 to 85 years old, from the National Health and Nutrition Examination Survey (NHANES), 2003-2010. Methodology: During the NHANES mobile exam, participants: 1) provided a spot urine sample which was measured for metabolites of DEHP, DINP, and BPA; and 2) completed a 24-hour dietary recall survey. We calculated kilocalorie intake of fast food from the dietary survey, and modeled fast food consumption in the prior 24-hours dichotomously and categorically as the percent of total daily calories (0%, Results: The majority of study subjects had detectable levels of urinary phthalate and BPA metabolites in their urine. Those who had eaten fast food had significantly higher urinary metabolite levels of ΣDEHP [percent change (95%CI): 18.63% (10.38%, 27.50%)] and DINP [percent change (95%CI): 32.17% (20.04%, 45.52%)], but not BPA [percent change (95%CI): 2.36% (-2.59%, 7.56%)] compared to those who had not eaten fast food in adjusted models. For ΣDEHP and DINP, there was evidence of a positive dose-response effect (p for trend \u3c 0.0001). Meat and grain consumption were associated with ΣDEHP and DINP when adjusting for all food groups. Discussion: Findings suggest that fast food consumption may be an important exposure source for DEHP and DINP, but not BPA, among the general population. Consistent with other studies that report high phthalate residues in high fat foods, our findings suggest that meat-centric meals may in part be responsible for this association. Further research should investigate which components of the fast food industry (production and storage, cooking process, packaging, etc.) contribute to this association

Recent fast food consumption and bisphenol A and phthalates exposures among the U.S. population in NHANES, 2003-2010

Background: Phthalates and bisphenol A (BPA) are widely used industrial chemicals that may adversely impact human health. Human exposure is ubiquitous and can occur through diet, including consumption of processed or packaged food. Objective: To examine associations between recent fast food intake and BPA and urinary metabolites of di(2-ethylhexyl) phthalate (ΣDEHPm) and diisononyl phthalate (DiNPm) among the US population. Methods: We combined data on 8877 participants from the National Health and Nutrition Examination Survey (NHANES 2003-2010). Using 24-hour dietary recall data, we quantified: 1) fast food intake (percent of total energy intake (TEI) from fast food); 2) fast food-derived fat intake (percent of TEI from fat in fast food); and 3) fast food intake by food group (dairy, eggs, grains, meat, and other). We examined associations between dietary exposures and urinary chemical concentrations using multivariate linear regression. Results: We observed evidence of a positive, dose–response relationship between fast food intake and exposure to phthalates (p-trend \u3c 0.0001) but not BPA; participants with high consumption (≥ 34.9% TEI from fast food) had 23.8% (95% CI: 11.9%, 36.9%) and 39.0% (95% CI: 21.9%, 58.5%) higher levels of ΣDEHPm and DiNPm, respectively, than nonconsumers. Fast food-derived fat intake was also positively associated with ΣDEHPm and DiNPm (p-trend \u3c 0.0001). After adjusting for other food groups, ΣDEHPm was associated with grain and other intake, and DiNPm was associated with meat and grain intake. Conclusion: Fast food may be a source of exposure to DEHP and DiNP. These results, if confirmed, could inform individual and regulatory exposure reduction strategies

Vaginal douching and racial/ethnic disparities in phthalates exposures among reproductive-aged women: National Health and Nutrition Examination Survey 2001–2004

Background Diethyl phthalate (DEP) and di-n-butyl phthalate (DnBP) are industrial chemicals found in consumer products that may increase risk of adverse health effects. Although use of personal care/beauty products is known to contribute to phthalate exposure, no prior study has examined feminine hygiene products as a potential phthalate source. In this study, we evaluate whether vaginal douching and other feminine hygiene products increase exposure to phthalates among US reproductive-aged women. Methods We conducted a cross-sectional study on 739 women (aged 20–49) from the National Health and Nutrition Examination Survey 2001–2004 to examine the association between self-reported use of feminine hygiene products (tampons, sanitary napkins, vaginal douches, feminine spray, feminine powder, and feminine wipes/towelettes) with urinary concentrations of monoethyl phthalate (MEP) and mono-n-butyl phthalate (MnBP), metabolites of DEP and DnBP, respectively. Results A greater proportion of black women than white and Mexican American women reported use of vaginal douches, feminine spray, feminine powder, and wipes/towelettes in the past month whereas white women were more likely than other racial/ethnic groups to report use of tampons (p \u3c 0.05). Douching in the past month was associated with higher concentrations of MEP but not MnBP. No other feminine hygiene product was significantly associated with either MEP or MnBP. We observed a dose–response relationship between douching frequency and MEP concentrations (ptrend  \u3c 0.0001); frequent users (≥2 times/month) had 152.2 % (95 % confidence intervals (CI): (68.2 %, 278.3 %)) higher MEP concentrations than non-users. We also examined whether vaginal douching mediates the relationship between race/ethnicity and phthalates exposures. Black women had 48.4 % (95 % CI: 16.8 %, 88.6 %; p = 0.0002) higher MEP levels than white women. Adjustment for douching attenuated this difference to 26.4 % (95 % CI:−0.9 %, 61.2 %; p = 0.06). Mediation effects of douching were statistically significant for black-white differences (z = 3.71, p \u3c 0.001) but not for differences between Mexican Americans and whites (z = 1.80, p = 0.07). Conclusions Vaginal douching may increase exposure to DEP and contribute to racial/ethnic disparities in DEP exposure. The presence of environmental chemicals in vaginal douches warrants further examination

Reducing Chemical Exposures at Home: Opportunities For Action.

Indoor environments can influence human environmental chemical exposures and, ultimately, public health. Furniture, electronics, personal care and cleaning products, floor coverings and other consumer products contain chemicals that can end up in the indoor air and settled dust. Consumer product chemicals such as phthalates, phenols, flame retardants and per- and polyfluorinated alkyl substances are widely detected in the US general population, including vulnerable populations, and are associated with adverse health effects such as reproductive and endocrine toxicity. We discuss the implications of our recent meta-analysis describing the patterns of chemical exposures and the ubiquity of multiple chemicals in indoor environments. To reduce the likelihood of exposures to these toxic chemicals, we then discuss approaches for exposure mitigation: targeting individual behaviour change, household maintenance and purchasing decisions, consumer advocacy and corporate responsibility in consumer markets, and regulatory action via state/federal policies. There is a need to further develop evidence-based strategies for chemical exposure reduction in each of these areas, given the multi-factorial nature of the problem. Further identifying those at greatest risk; understanding the individual, household and community factors that influence indoor chemical exposures; and developing options for mitigation may substantially improve individuals’ exposures and health

Ketogenic Diet : a New Light Shining on Old but Gold Biochemistry

Diets low in carbohydrates and proteins and enriched in fat stimulate the hepatic synthesis of ketone bodies (KB). These molecules are used as alternative fuel for energy production in target tissues. The synthesis and utilization of KB are tightly regulated both at transcriptional and hormonal levels. The nuclear receptor peroxisome proliferator activated receptor \u3b1 (PPAR\u3b1), currently recognized as one of the master regulators of ketogenesis, integrates nutritional signals to the activation of transcriptional networks regulating fatty acid \u3b2-oxidation and ketogenesis. New factors, such as circadian rhythms and paracrine signals, are emerging as important aspects of this metabolic regulation. However, KB are currently considered not only as energy substrates but also as signaling molecules. \u3b2-hydroxybutyrate has been identified as class I histone deacetylase inhibitor, thus establishing a connection between products of hepatic lipid metabolism and epigenetics. Ketogenic diets (KD) are currently used to treat different forms of infantile epilepsy, also caused by genetic defects such as Glut1 and Pyruvate Dehydrogenase Deficiency Syndromes. However, several researchers are now focusing on the possibility to use KD in other diseases, such as cancer, neurological and metabolic disorders. Nonetheless, clear-cut evidence of the efficacy of KD in other disorders remains to be provided in order to suggest the adoption of such diets to metabolic-related pathologies

Cross-Sectional Associations between Exposure to Persistent Organic Pollutants and Leukocyte Telomere Length among U.S. Adults in NHANES, 2001-2002.

Background: Exposure to persistent organic pollutants (POPs) such as dioxins, furans, and polychlorinated biphenyls (PCBs) may influence leukocyte telomere length (LTL), a biomarker associated with chronic disease. In vitro research suggests dioxins may bind to the aryl hydrocarbon receptor (AhR) and induce telomerase activity, which elongates LTL. However, few epidemiologic studies have investigated associations between POPs and LTL. Objectives: We examined the association between 18 PCBs, 7 dioxins, and 9 furans and LTL among 1,330 U.S. adults from NHANES 2001-2002. Methods: We created three summed POP metrics based on toxic equivalency factor (TEF), a potency measure including affinity for the AhR: (a) non-dioxin-like PCBs (composed of 10 non-dioxin-like PCBs; no AhR affinity and no TEF); (b) non-ortho PCBs (composed of 2 non-ortho-substituted PCBs with high TEFs); and (c) toxic equivalency (TEQ) (composed of 7 dioxins, 9 furans, 2 non-ortho-substituted PCBs, and 6 mono-ortho-substituted PCBs; weighted by TEF). We tested the association between each metric and LTL using linear regression, adjusting for demographics, blood cell count and distribution, and another metric with a different TEF (i.e., non-ortho PCBs and TEQ adjusted for non-dioxin-like PCBs; non-dioxin-like PCBs adjusted for non-ortho PCBs). Results: In adjusted models, each doubling of serum concentrations of non-ortho PCBs and TEQ was associated with 3.74% (95% CI: 2.10, 5.40) and 5.29% (95% CI: 1.66, 9.05) longer LTLs, respectively. Compared with the lowest quartile, the highest quartile of exposure was associated with 9.16% (95% CI: 2.96, 15.73) and 7.84% (95% CI: -0.53, 16.92) longer LTLs, respectively. Non-dioxin-like PCBs were not associated with LTL. Conclusions: POPs with high TEFs and AhR affinity were associated with longer LTL. Because many dioxin-associated cancers are also associated with longer LTL, these results may provide insight into the mechanisms underlying PCB- and dioxin-related carcinogenesis

HDAC3 is a molecular brake of the metabolic switch supporting white adipose tissue browning.

White adipose tissue (WAT) can undergo a phenotypic switch, known as browning, in response to environmental stimuli such as cold. Post-translational modifications of histones have been shown to regulate cellular energy metabolism, but their role in white adipose tissue physiology remains incompletely understood. Here we show that histone deacetylase 3 (HDAC3) regulates WAT metabolism and function. Selective ablation of Hdac3 in fat switches the metabolic signature of WAT by activating a futile cycle of de novo fatty acid synthesis and β-oxidation that potentiates WAT oxidative capacity and ultimately supports browning. Specific ablation of Hdac3 in adipose tissue increases acetylation of enhancers in Pparg and Ucp1 genes, and of putative regulatory regions of the Ppara gene. Our results unveil HDAC3 as a regulator of WAT physiology, which acts as a molecular brake that inhibits fatty acid metabolism and WAT browning.Histone deacetylases, such as HDAC3, have been shown to alter cellular metabolism in various tissues. Here the authors show that HDAC3 regulates WAT metabolism by activating a futile cycle of fatty acid synthesis and oxidation, which supports WAT browning

Butyrate prevents visceral adipose tissue inflammation and metabolic alterations in a Friedreich's ataxia mouse model

Friedreich's ataxia (FA) is a neurodegenerative disease resulting from a mutation in the FXN gene, leading to mitochondrial frataxin deficiency. FA patients exhibit increased visceral adiposity, inflammation, and heightened diabetes risk, negatively affecting prognosis. We investigated visceral white adipose tissue (vWAT) in a murine model (KIKO) to understand its role in FA-related metabolic complications. RNAseq analysis revealed altered expression of inflammation, angiogenesis, and fibrosis genes. Diabetes like traits, including larger adipocytes, immune cell infiltration, and increased lactate production, were observed in vWAT. FXN downregulation in cultured adipocytes mirrored vWAT diabetes-like features, showing metabolic shifts toward glycolysis and lactate production. Metagenomic analysis indicated a reduction in fecal butyrate-producing bacteria, known to exert antidiabetic effects. A butyrate-enriched diet restrained vWAT abnormalities and mitigated diabetes features in KIKO mice. Our work emphasizes the role of vWAT in FA-related metabolic issues and suggests butyrate as a safe and promising adjunct for FA management