Search Results (46)

Hypsizygus marmoreus (Peck) H.E. Bigelow is a commercial edible mushroom includes two primary commercial varieties: brown and white. To reveal the genetic and metabolic differences between these two varieties, genomic and metabolomic comparisons of the white strain F4 and the brown strain B5-15 were performed. The assembled genome sizes were 40,851,948 bp for F4 and 41,902,673 bp for B5-15. Molecular clock analysis estimated that H. marmoreus diverged from Termitomyces sp. approximately 59.4 million years ago during the Paleocene based on the genomic information. The two genomes showed little difference in the gene compositions related to β-Glucosidase and certain lignin degrading auxiliary enzymes. In contrast, the structures of the mating-type loci, including gene copy numbers and the transcriptional orientation of open reading frames, differed between the varieties, and it exhibited higher mating-type locus diversity. Comparative genomic analysis further indicated that the brown strain can biosynthesize melanin-like compounds using chorismate as the starting molecule, with tyrosinase acting as a key enzyme. Moreover, metabolomic profiling based on principal component analysis (PCA) and orthogonal partial least squares-discriminant analysis (OPLS-DA) revealed distinct metabolic profiles between the two varieties. Collectively, these findings improve our understanding of the genetic basis underlying the phenotypic differences between the two H. marmoreus varieties. Full article

In the study of eggplant (Solanum melongena L.), a cross between the green peel line 19143 and the white peel line 19147 produced E4957 F₁ hybrids with a purple–brown peel. Self-fertilization of the F₁ hybrids yielded E4957 F₂ offspring with a segregation ratio of 27:9:21:7 among individuals with purple–brown, purple–red, green, and white peel colors, respectively, which was consistent with a genetic model controlled by reciprocal recessive epistasis between D and P, and Gv1 likely acting as a modifying factor. The green peel line 19143 exhibited higher chlorophyll but lower anthocyanin levels than the white peel line 19147, which contained low levels of both pigments, while the E4957 F₁ hybrids had elevated levels of both pigments. Two epistatic genes, D and P, associated with anthocyanin synthesis, were mapped on chromosomes 10 and 8, respectively. The putative modifying locus Gf, involved in chlorophyll accumulation in the flesh, was mapped on chromosome 8, and the localization interval was close to the previously reported Gv1 locus associated with chlorophyll synthesis in the peel. DNA markers (InDel22522, InDel5531, InDel-APRR2) were developed to genotype 237 F₂ individuals and correlate genotypes with phenotypes. Sequence analysis revealed a 6 bp deletion in the SmMYB1 (D) gene and a large deletion in the SmAPRR2-Like (Gv1) gene in the white peel line 19147, as well as a T to A mutation in the SmANS (P) gene in the green line 19143. This study provided evidence for inheritance between loci involved in anthocyanin and chlorophyll pathways contributing to eggplant peel color variation and provides molecular markers that may facilitate the breeding of eggplant varieties with diverse peel colors. Full article

Obesity treatments increasingly target multiple pathways beyond appetite suppression. We evaluated KBN2202, a salicylate-derived small molecule, in a high-fat diet (60% kcal from fat) mouse model using female and male C57BL/6J mice treated for 8 weeks with oral KBN2202 (20 mg/kg/day) or a matched-volume vehicle (1% DMSO/PBS). Body weight was recorded weekly, and food intake was measured daily; serum hormones and cytokines, adipose tissue histology, and open-field behavior were assessed at the end of the study. Under our experimental conditions, HFD increased body weight and gonadal white adipose tissue (gWAT)/brown adipose tissue (BAT) mass in females, whereas males showed only modest HFD-associated weight gain and did not develop a clear obesity phenotype. KBN2202 significantly reduced peri-ovarian gWAT mass and adipocyte size without altering overall body weight. In females, circulating glucagon-like peptide-1 (GLP-1) increased, uncoupling protein 1 (UCP1) in gWAT showed a non-significant upward trend, and serum TNF-α was selectively decreased, while MCP-1 and IL-1β were unchanged. Locomotor activity was unaltered, and anxiety-like behavior was reduced. Male mice did not show comparable adipose effects. These findings indicate depot-specific, peripheral modulation of adipose remodeling, hormonal balance, and inflammatory tone by KBN2202, supporting its further investigation as an adipose-targeted metabolic modulator complementary to incretin-based therapies. Full article

Atherosclerosis is now recognized as a chronic inflammatory disease of the arterial wall, in which perivascular adipose tissue (PVAT) has evolved from a passive structural component to a key player in regulating vascular homeostasis and the pathophysiology of atherosclerosis, playing an active, not just structural, role. PVAT surrounds blood vessels and influences them metabolically, immunologically, and vascularly by secreting adipokines, cytokines, and other bioactive mediators. Under physiological conditions, PVAT has protective roles, as it produces adiponectin, nitric oxide (NO), and other vasodilatory factors that help maintain vascular tone and reduce inflammation. In particular, brown-like PVAT (rich in Uncoupling Protein-1 (UCP1) and mitochondria) offers significant vasoprotective effects. Under pathological conditions (obesity, dyslipidemia, insulin resistance), PVAT undergoes a phenotypic transition towards a pro-inflammatory profile by increasing leptin, tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) secretion and decreasing adiponectin, contributing to endothelial dysfunction, vascular smooth muscle cell (VSMC) proliferation, local immune cell recruitment, extracellular matrix (ECM) remodeling, and fibrosis. PVAT plays a complex role in vascular health and disease, interacting with systemic metabolism through the secretion of bioactive molecules. Metabolic imbalances can promote PVAT inflammation. Epigenetic alterations and micro ribonucleic acid (miRNAs) can influence PVAT inflammation, and modern imaging methods for PVAT assessment, such as the fat attenuation index (FAI) and artificial intelligence-assisted radiomic profiling, may become predictive biomarkers of cardiac risk. Future directions aim to identify biomarkers and develop targeted therapies that modulate PVAT inflammation and dysfunction in the context of cardiovascular diseases. Full article

Adipose tissue enlargement in obesity leads to hypoxia, which may promote premature aging. This study aimed to understand the hypoxic response in 3D cultures of SGBS cells, a model for brown-like adipose tissue expressing uncoupling protein 1 (UCP1). Single-nucleus RNA sequencing of SGBS organoids revealed a heterogeneous composition and sub-population-specific responses to hypoxia. The analysis identified a cluster of transcriptional repression, indicating dying cells, and implied a role of ferroptosis in this model. Further experiments with SGBS cells and white adipose tissue-derived stem/progenitor cells showed that Acyl-CoA synthetase long-chain family member 4 (ACSL4), a key enzyme in ferroptosis, is expressed only in the presence of browning factors. Hypoxia downregulated ACSL4 protein in SGBS organoids but induced an inflammaging phenotype. Analysis of brown-like epicardial adipose tissue from cardiac surgery patients revealed a significant positive correlation of ACSL4 mRNA with UCP1 and hypoxia-inducible pro-inflammatory markers, while ACSL4 protein appeared to be inversely correlated. In conclusion, this study demonstrates that adipocytes’ capability to undergo ACSL4-mediated ferroptosis is linked to brown-like adipogenesis, suggesting an opportunity to modulate ferroptotic signaling in adipose tissue. The dual role of hypoxia by inhibiting ACSL4 but promoting inflammaging indicates a relationship between ferroptosis and aging that warrants further investigation. Full article

The antimicrobial and antibiofilm efficacy of two Ocimum basilicum L., essential oils sourced from Colombia (BEOC) and Italy (BEOI), was evaluated against multidrug-resistant fish isolates of Salmonella enterica subsp. salamae, Bacillus thuringiensis, and Bacillus oceanisediminis—species for which such activity has not been previously reported. Using a fish-based model system (FBMS), we found that BEOI, rich in linalool (69.86%), exhibited stronger antimicrobial activity than camphor-dominated BEOC (24.61%). The antimicrobial effects of both EOs were strain- and concentration-dependent, with minimum bactericidal concentration (MBC) 3.75–15.0 µL/mL for BEOI and 15.0–30.0 µL/mL for BEOC. Pure linalool showed even greater potency (MBC: 0.0125 to 0.025 µL/mL). Confocal laser scanning microscopy revealed that BEOI induced severe membrane damage (27% of the cells within 1 h), ultimately leading to the death of 96% of the cells after 24 h. Biofilm formation, assessed in both FBMS and tryptone soy broth (TSB), was strain-dependent, with FBMS promoting higher biofilm production than TSB. Moreover, significant differences in biofilm morphotypes were observed, with the morphotype PDAR (pink dry and rough), characterized by only cellulose, being the most frequently exhibited by the strains (7/15), while BDAR (brown dry and rough), characterized by only curli, was the least expressed (7/15); the remaining strains presented morphotype RDAR. In addition, the strains in polystyrene surfaces accumulated more biomass than stainless steel 304. Notably, BEOI and linaool significantly reduced biofilm formation across all strains, with a reduction of 90% in S. enterica subsp. salamae strains (TJC19 and TJC21. These strains with the RDAR phenotype likely contribute to their strong biofilm-forming capacity. Our findings highlight BEOI’s potential as a natural anti-biofilm agent in food processing environments, offering a promising strategy to combat multidrug-resistant bacteria biofilm-related challenges in the food industry. Full article

Obesity has emerged as a global epidemic, creating an increased burden of weight-related diseases and straining healthcare systems worldwide. While the fundamental principle of energy balance—caloric intake versus expenditure—remains central to weight regulation, real-world outcomes often deviate from simplistic predictions due to a multitude of physiological and environmental factors. Genetic predispositions, variations in basal metabolic rates, adaptive thermogenesis, physical activity, and nutrient losses via fecal and urinary excretion contribute to interindividual differences in energy homeostasis. Additionally, factors such as meal timing, macronutrient composition, gut microbiota dynamics, and diet-induced thermogenesis (DIT) further modulate energy utilization and metabolic efficiency. This Perspective explores key physiological determinants of the energy balance, while also highlighting the clinical significance of thrifty versus spendthrifty metabolic phenotypes. Key strategies for individualized weight management include precision calorimetry, circadian-aligned meal timing, the use of protein- and whole food diets to enhance DIT, and increases in non-exercise activity, as well as mild cold exposure and the use of thermogenic agents (e.g., capsaicin-like compounds) to stimulate brown adipose tissue activity. A comprehensive, personalized approach to obesity management that moves beyond restrictive caloric models is essential to achieving sustainable weight control and improving long-term metabolic health. Integrating these multifactorial insights into clinical practice will enhance obesity treatment strategies, fostering more effective and enduring interventions. Full article

Background/Objectives: Tic disorders are neurodevelopmental conditions often associated with comorbidities like attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Our aims were: (a) in a sample of youth with tic disorders to explore the clinical and psychopathological characteristics of different phenotypes based on the presence of comorbid ADHD and/or ASD and gender; (b) in a subgroup of patients treated with Aripiprazole, to evaluate symptoms variation over time and to identify potential predictors of response. Methods: A total of 95 subjects with tic disorders (age range 6 to 17.9 years, mean 11.1 ± 2.11 years, 80 males) were naturalistically recruited. Questionnaires and semi-structured interviews were administered to assess the symptomatology and investigate the presence of psychiatric comorbidities (Clinic Global Impression-Severity (CGI-S), Children’s Global Assessment Scale (C-GAS), Yale Global Tic Severity Scale (YGTSS), Premonitory Urge for Tics Scale (PUTS), Child Yale–Brown Obsessive Compulsive Scale for Children (CYBOCS), Child Behavior Checklist 6–18 (CBCL 6–18), Conners’ Parent Rating Scale-Revised—short form (CRSR-S), Reactivity Intensity Polarity Stability Questionnaire—youth version (RIPoSt-Y), and Social Communication Questionnaire—lifetime version (SCQ); Autism Diagnostic Observation Scale—second version (ADOS-2) and Autism Diagnostic Interview—revised version (ADI-R) were administered where ASD was suspected). A total of 22 subjects treated with Aripiprazole were reassessed through the use of some of the clinical measures used at baseline. Results: The presence of ADHD was associated with higher externalizing problem scores on the CBCL 6–18, while ASD was linked to higher internalizing problem scores. A positive correlation was found between the ADHD–ASD interaction and increased internalizing symptoms on CBCL 6–18 and higher ADOS-2 scores. Patients treated with Aripiprazole showed significant improvement across all scales during follow-up. ADHD was identified as a negative predictor of reduced tic severity on the YGTSS. Conclusions: Comorbid neurodevelopmental disorders, such as ADHD or ASD, result in worse emotional and behavioral functioning in patients with tic disorders. ADHD–ASD interaction may be linked to more internalizing symptoms and autistic behaviors. Aripiprazole improves overall clinical outcomes, although comorbid ADHD may hinder the reduction of tic symptoms. Full article

Obesity is characterized by low-grade inflammation that originates predominantly from the expanding visceral adipose tissue, in which adipocytes respond to lipid overload with hypertrophy, and consequently die by apoptosis. Recruited adipose tissue macrophages (ATMs) take up the excess lipids and remove the dead cells; however, long-term exposure to high concentrations of lipids alters their phenotype to M1-like ATMs that produce pro-inflammatory cytokines and resistin leading to insulin resistance and other obesity-related pathologies. Mer tyrosine kinase is expressed by macrophages and by being an efferocytosis receptor, and by suppressing inflammation, we hypothesized that it might play a protective role against obesity. To our surprise, however, the loss of Mer protected mice against high-fat diet (HFD)-induced obesity. We report in this paper that Mer is also expressed by adipocytes of both white and brown adipose tissues, and while its activity facilitates adipocyte lipid storage both in vitro and in vivo in mice exposed to HFD, it simultaneously attenuates thermogenesis in the brown adipose tissue contributing to its ‘whitening’. Our data indicate that Mer is one of the adipocyte tyrosine kinase receptors, the activity of which contributes to the metabolic decision about the fate of excess lipids favoring their storage within the body. Full article

This study sought to evaluate the genetic variations of the ovocalyxin-32 gene and its association with egg quality traits in indigenous chicken populations, focusing on exons 1 and 6. Genotype frequencies of SNPs (G/T and A/G) within these exons were assessed for their conformity to the Hardy–Weinberg equilibrium (HWE) across several strains. While most strains exhibited close adherence to HWE expectations, some like light-brown and gray strains indicated substantial discrepancies, particularly for the TT genotype, which points towards the possible effects of genetic drift as well as selection pressures. This study also analyzed the influence of such SNPs on egg quality parameters. A thinner eggshell, reduced shell weight, and decreased breaking strength were associated with the G/T SNP in exon 1, suggesting a likely negative effect on egg quality in T allele carriers. Conversely, the AG genotype displayed better performance in shell thickness, weight and egg weight in the A/G SNP in exon 1, whilst yolk height was best improved by the AA genotype compared to breaking strength. For instance, in exon 6, the A/G SNP enhanced the shell and yolk quality among AG genotypes, while the CC genotype resulted in better eggshell characteristics with enlarged yolks because the C/T SNP was linked. Nonetheless, there were no significant deviations from the HWE despite these associations, which suggested that most breeds had a stable genetic background. Further, considering SNPs’ additive and dominant effects in this research, it was indicated that additive effects account for phenotypic expressions given by the G/T SNP located at exon 1. In contrast, significant additive and dominant effects were observed under the A/G SNP situated at the exon. Generally, it therefore could be concluded from this study that specific SNPs within the ovocalyxin-32 gene may act as good markers for marker-assisted selection (MAS) that can improve desired characteristics—such as those of egg quality—in indigenous chicken breeds. This study demonstrated that both additive and dominance effects must be taken into account when performing genetic analyses, thereby emphasizing the complexity of phenotypic variation caused by genetic mechanisms in native chicken races. Full article

Adipose tissue plays a crucial role in regulating metabolic homeostasis, and its dysfunction in obesity leads to insulin resistance and type 2 diabetes (T2D). White adipose tissue (WAT) primarily stores energy as lipids, while brown adipose tissue (BAT) regulates thermogenesis by dissipating energy as heat. The process of browning involves the transdifferentiation of WAT into brown-like or beige adipocytes, which exhibit a similar phenotype as BAT. The browning of WAT is an attractive approach against obesity and T2D, and the activation of the energy sensor AMP-activated protein kinase (AMPK) has been shown to play a role in browning. Carnosic acid (CA), a polyphenolic diterpene, found in many plants including rosemary, is reported to possess potent antioxidant, anti-inflammatory, and anti-hyperglycemic properties. The limited evidence available indicates that CA activates AMPK and may have anti-obesity and antidiabetic potential; however, the effects in adipocyte browning remain largely unexplored. This study aimed to examine the effects of CA on the markers of adipocyte browning. The treatment of 3T3L1 adipocytes with CA activated AMPK, reduced lipid accumulation, and increased the expression of browning protein markers (UCP-1, PGC-1α, PRDM16, and TFAM) and mitochondrial biogenesis. The use of compound C, an AMPK inhibitor, significantly attenuated the effects of CA, indicating AMPK involvement. These studies demonstrate that CA can activate AMPK and stimulate the browning of white adipocytes. Future animal and human studies are required to examine the effects of CA in vivo. Full article

Changes in the number, structure, and function of mitochondria during the early life stages of animals can play an important role for an organism’s metabolic rate, growth, and health. Previous studies have shown that juvenile brown trout (Salmo trutta) subjected to elevated temperatures during the embryonic stage respond phenotypically with a reduced metabolic rate. The aim of this study was to explore if embryonic temperature affects the mitochondria content of young brown trout and as such explains the previously found differences in metabolic rates. Here, we optimize a quantitative PCR (qPCR) method for the mitochondria cytochrome c oxidase subunit I gene, and then use the method as a proxy for mitochondrial DNA content. We hypothesize that young trout subjected to elevated temperatures during the embryonic stage respond phenotypically with a reduced mitochondrial DNA content. To test this hypothesis, we subjected brown trout to either control ambient (4.4 ± 1.5 °C) or elevated temperatures (7.1 ± 0.6 °C) during embryogenesis. Subsequently, we extracted DNA from liver and white muscle tissue of juvenile brown trout from the two different incubation temperature treatments and successively optimized qPCR for mitochondrial DNA. We found that the amount of mitochondria DNA in liver tissue was 18 times higher than in white muscle tissue, but there was no significant difference in mitochondria content in liver or muscle tissue between brown trout exposed to elevated and ambient control temperatures during embryogenesis. We conclude that reduced metabolic rate is not likely associated with mitochondria DNA content. We also suggest that qPCR is a simple and cost-effective method to quantify mitochondria DNA in frozen and partly degraded tissue from different treatment groups and a useful proxy for identification of differences in mitochondria number. Full article

Conferring crops with resistance to multiple diseases is crucial for stable food production. Genetic engineering is an effective means of achieving this. The rice receptor-like cytoplasmic kinase BSR1 mediates microbe-associated molecular pattern-induced immunity. In our previous study, we demonstrated that rice lines overexpressing BSR1 under the control of the maize ubiquitin promoter exhibited broad-spectrum resistance to rice blast, brown spot, leaf blight, and bacterial seedling rot. However, unfavorable phenotypes were observed, such as a decreased seed germination rate and a partial darkening of husked rice. Herein, we present a strategy to address these unfavorable phenotypes using an OsUbi7 constitutive promoter with moderate expression levels and a pathogen-inducible PR1b promoter. Rice lines expressing BSR1 under the influence of both promoters maintained broad-spectrum disease resistance. The seed germination rate and coloration of husked rice were similar to those of the wild-type rice. Full article

Intermittent cold exposure (ICE) has garnered increased attention in popular culture, largely for its proposed effects on mood and immune function, but there are also suggestions that the energy-wasting mechanisms associated with thermogenesis may decrease body weight and fat mass. Considering the continued and worsening prevalence of obesity and type II diabetes, any protocol that can reduce body weight and/or improve metabolic health would be a substantial boon. Here, we present a narrative review exploring the research related to ICE and adipose tissue. Any publicly available original research examining the effects of repeated bouts of ICE on adipose-related outcomes was included. While ICE does not consistently lower body weight or fat mass, there does seem to be evidence for ICE as a positive modulator of the metabolic consequences of obesity, such as glucose tolerance and insulin signaling. Further, ICE consistently increases the activity of brown adipose tissue (BAT) and transitions white adipose tissue to a phenotype more in line with BAT. Lastly, the combined effects of ICE and exercise do not seem to provide any additional benefit, at least when exercising during ICE bouts. The majority of the current literature on ICE is based on rodent models where animals are housed in cold rooms, which does not reflect protocols likely to be implemented in humans such as cold water immersion. Future research could specifically characterize ICE via cold water immersion in combination with controlled calorie intake to clearly determine the effects of ICE as it would be implemented in humans looking to lower their body weight via reductions in fat mass. Full article

Interleukin 18 (IL18) was originally identified as an inflammation-induced cytokine that is secreted by immune cells. An increasing number of studies have focused on its non-immunological functions, with demonstrated functions for IL18 in energy homeostasis and neural stability. IL18 is reportedly required for lipid metabolism in the liver and brown adipose tissue. Furthermore, IL18 (Il18) deficiency in mice leads to mitochondrial dysfunction in hippocampal cells, resulting in depressive-like symptoms and cognitive impairment. Microarray analyses of Il18^−/− mice have revealed a set of genes with differential expression in liver, brown adipose tissue, and brain; however, the impact of IL18 deficiency in these tissues remains uncertain. In this review article, we discuss these genes, with a focus on their relationships with the phenotypic disease traits of Il18^−/− mice. Full article