Accumulation Of Adipose Tissue Research Articles

Efficacy of Probiotic Strains Lactobacillus sakei Probio65 and Lactobacillus plantarum Probio-093 in Management of Obesity: An In Vitro and In Vivo Analysis

The prevalence of obesity, characterized by an excessive accumulation of adipose tissue and adipocyte hypertrophy, presents a major public health challenge. This study investigates the therapeutic potential of two probiotic strains, Lactobacillus sakei Probio65 and Lactobacillus plantarum Probio-093, in the context of obesity. Utilizing 3T3-L1 cell-derived human adipocytes, we assessed Probio65’s and Probio-093’s capacity to mitigate triglyceride accumulation and influence adipocytokine production in vitro. Subsequently, an in vivo trial with male C57BL/6J mice examined the effects of both probiotic strains on adipose tissue characteristics, body weight, fat mass, and obesity-related gene expression. This study employed both live and ethanol-extracted bacterial cells. The results demonstrated significant reductions in the triglyceride deposition, body weight, and adipose tissue mass in the treated groups (p < 0.05). Furthermore, both strains modulated adipokine profiles by downregulating proinflammatory markers such as PAI-1, leptin, TNF-α, STAMP2, F4/80, resistin, and MCP-1, and upregulating the insulin-sensitive transporter GLUT4 and the anti-inflammatory adiponectin (p < 0.05). Our findings suggest that Lactobacillus sakei Probio65 and Lactobacillus plantarum Probio-093 are promising agents for microbiome-targeted anti-obesity therapies, offering the effective mitigation of obesity and improvement in adipocyte function in a murine model.

Effective treatment for fatty liver of liraglutide via inhibiting endoplasmic reticulum stress, oxidative stress and apoptosis pathways

IntroductionFatty liver disease (FLD) is a frequent medical condition marked by hepatic adipose tissue accumulation. It may cause liver damage in certain cases. This study examined liraglutide’s inhibition of FLD and its molecular mechanism.Material and methodsGSE63067 was downloaded from the Gene Expression Omnibus (GEO) database. The analysis of differentially expressed genes (DEGs) was performed using the Limma package. Enrichment analysis was performed. The Sprague-Dawley (SD) rats were fed a high-fat diet to develop FLD, then administered liraglutide. Serum lipid levels were tested by ELISA, and pathological sections were used for oil red O staining. In in vitro experiments, the hepatic cells were stimulated with free fatty acids (FFAs), liraglutide, and tunicamycin. Immunofluorescence double staining and western blot testing were carried out.ResultsEnrichment analysis showed that DEGs were enriched in endoplasmic reticulum (ER) stress, oxidative stress, and apoptosis pathways. Liraglutide treatment reduced the expression of p-PERK and CHOP resulting from FFAs. Western blot assessment revealed that liraglutide treatment reduced the expression of GRP78, GRP94, p-PERK, p-IRE1, ATF6, and CHOP resulting from FFAs but not the expression of these proteins resulting from FFAs and tunicamycin. Flow cytometry revealed that liraglutide treatment reduced SD rat liver cell apoptosis resulting from FFAs. Liraglutide treatment decreased the expression of cleaved caspase-3, caspase-9, caspase-12, and Bax resulting from FFAs.ConclusionsLiraglutide exerts a therapeutic effect in the context of FLD through its ability to suppress endoplasmic reticulum stress (ERS) and inhibit apoptosis of hepatic cells.

The combination of berberine and isoliquiritigenin synergistically improved adipose inflammation and obesity-induced insulin resistance.

White adipose tissue accumulation and inflammation contribute to obesity by inducing insulin resistance. Herein, we aimed to screen the synergistic components of the herbal pair Coptidis Rhizoma-Glycyrrhizae Radix et Rhizoma for the treatment of insulin resistance and explore the potential synergistic mechanisms. Enzyme-linked immunosorbent assay and quantitative PCR were used to detect expression levels of inflammatory genes in vitro and in vivo. Western blotting and immunohistochemistry were performed to detect protein levels of the insulin signaling pathway and macrophage markers. The effects on obesity-induced insulin resistance were verified using a diet-induced obesity (DIO) mouse model. Interactions between macrophage and adipocyte were assessed using a cellular supernatant transfer assay. Berberine (BBR) and isoliquiritigenin (ISL) alleviated mRNA levels and secretion of inflammatory genes in vitro and in vivo. Furthermore, BBR acted synergistically with ISL to ameliorate obesity and dyslipidemia in DIO mice. Meanwhile, the combination treatment significantly improved glucose intolerance and insulin resistance and decreased M1-macrophage accumulation and infiltration in the adipose tissue. Mechanistically, co-treatment with BBR and ISL upregulated the protein expression of the IRS1-PI3K-Akt insulin signaling pathway, enhanced glucose uptake in adipocyte, and suppressed the interaction between macrophage and adipocyte. BBR and ISL were identified as the synergistic components of the herbal pair Coptidis Rhizoma-Glycyrrhizae Radix et Rhizoma for treating insulin resistance. The synergistic combination of BBR with ISL can be a promising and effective strategy for improving obesity-induced adipose inflammation and insulin resistance.

Clinical and Ultrasound Efficacy of Topical Hypertonic Cream (Jovita Osmocell®) in the Treatment of Cellulite: A Prospective, Monocentric, Double-Blind, Placebo-Controlled Study.

Background and Objectives: Cellulite, or edemato-fibro-sclerotic panniculopathy (EFP), is characterized by dermal and hypodermal changes leading to adipose tissue accumulation and compromised venous circulation. This study investigates the efficacy of a hypertonic cream containing concentrated sodium chloride (Jovita Osmocell®) in addressing water retention and structural alterations in adipose tissue, aiming to interrupt the cellulite formation process. Materials and Methods: A 12-week, prospective, monocentric, double-blind, placebo-controlled study enrolled 30 female subjects with grade II or III cellulite. Patients were randomized to receive hypertonic cream or a placebo. Thigh circumference, ultrasound evaluations, and standardized photographs were collected at baseline, intermediate, and endpoint visits. Adverse events were monitored. Results: After 84 days, the hypertonic cream group exhibited a significant reduction in thigh circumference compared to the placebo group (p = 0.0037). B-mode ultrasound examinations revealed significant changes in the parameters studied, such as the thickness of the subcutaneous tissue. No statistically significant changes were noticed in the placebo group. Volunteers reported the investigational product's pleasantness and good anti-cellulite activity, with no reported adverse events. Conclusions: The hypertonic cream demonstrated efficacy in reducing thigh circumference, addressing water retention and structural alterations in adipose tissue. The proposed mechanism involves osmosis, releasing accumulated fluids between fat cells, supporting drainage, and reducing inflammation. This study supports the efficacy and safety of hypertonic sodium chloride emulsions in cellulite treatment and confirms safety and user satisfaction.

SLC25A28 Overexpression Promotes Adipogenesis by Reducing ATGL.

Adipose tissue dysfunction is seen among obese and type 2 diabetic individuals. Adipocyte proliferation and hypertrophy are the root causes of adipose tissue expansion. Solute carrier family 25 member 28 (SLC25A28) is an iron transporter in the inner mitochondrial membrane. This study is aimed at validating the involvement of SLC25A28 in adipose accumulation by tail vein injection of adenovirus (Ad)-SLC25A28 and Ad-green fluorescent protein viral particles into C57BL/6J mice. After 16 weeks, the body weight of the mice was measured. Subsequently, morphological analysis was performed to establish a high-fat diet (HFD)-induced model. SLC25A28 overexpression accelerated lipid accumulation in white and brown adipose tissue (BAT), enhanced body weight, reduced serum triglyceride (TG), and impaired serum glucose tolerance. The protein expression level of lipogenesis, lipolysis, and serum adipose secretion hormone was evaluated by western blotting. The results showed that adipose TG lipase (ATGL) protein expression was reduced significantly in white and BAT after overexpression SLC25A28 compared to the control group. Moreover, SLC25A28 overexpression inhibited the BAT formation by downregulating UCP-1 and the mitochondrial biosynthesis marker PGC-1α. Serum adiponectin protein expression was unregulated, which was consistent with the expression in inguinal white adipose tissue (iWAT). Remarkably, serum fibroblast growth factor (FGF21) protein expression was negatively related to the expansion of adipose tissue after administrated by Ad-SLC25A28. Data from the current study indicate that SLC25A28 overexpression promotes diet-induced obesity and accelerates lipid accumulation by regulating hormone secretion and inhibiting lipolysis in adipose tissue.

Aldo-keto reductase family 1 member A1 contributes to increase the glycolytic metabolism and to accelerate cellular senescence of bone derived mesenchymal stem cells

Skeletal aging characterizes the important event where bone loss is accompanied by accumulation of marrow adipose tissues. This event may be due to dysfunctional differentiation of bone derived mesenchymal stem cells (BMSCs) switched from osteoblasts (OBs) to adipocytes (ADs). Our accomplished work demonstrated that Aldo-keto reductase family 1 member A1 (Akr1A1) might serve as an important control to modify the NAD+-dependent SIRT signaling pathway for regulating the adipo-osteogenic lineage differentiation of BMSCs. In this study, we established a senescence cell model for examining whether increased Akr1A1 expression in BMSCs contributes to preferential lineage differentiation to ADs at the expense of osteogenesis by switching on the glycolytic metabolism in senescent cells with D-galactose induction or natural aging in MSCs. Our result suggests that increased expression of the glycolytic enzyme, Akr1A1 contributes to increase the glycolytic metabolism and to accelerate cellular senescence of MSCs. Such information might be useful to help develop the novel therapeutic strategy for treating age-related bone diseases with “perspective Akr1A1 inhibitors”. Grants supported by NSTC (112-2314-B-005 -004 -, NSC-111-2314-B-005-003-), iEGG and Animal Biotechnology Center from the Feature Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education (MOE-112-S-0023-A) in Taiwan, and partially by the grants of CYCH-NCHULS110003, CYCH-NCHULS111003, CYCH-NCHULS112002, TCVGH-NCHU 112-7616 to Y-ML. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Comparative proteomic analysis of pathological characterization of adipose tissue remodeling induced by high-fat diet and high-carbohydrate diet in grass carp (Ctenopharyngodon idellus)

Our previous research found that excessive accumulation of adipose tissue is an important factor that reduces fish tolerance and utilization of high-energy feeds and limits the development of high-energy feeds in the aquaculture industry. However, the pathological characteristics and molecular mechanisms of fish adipose tissue remodeling caused by high-energy diet were still unclear. In this study, using histopathological observation, we found that restricted adipocyte hyperplasia, adipocyte hypertrophy, inflammation, and fibrosis are the main characteristics of pathological remodeling of fish adipose tissue induced by high-fat diet (HFD) and high-carbohydrate diet (HCD). Besides, this study further analyzed the molecular mechanisms and key marker proteins invovled in pathological remodeling of adipose tissue induced by HFD and HCD through comparative proteomics. The results found: (1) Inhibition of the differentiation of preadipocytes may be the main pathway through which both HCD and HFD inhibited adipocyte hyperplasia in grass carp; (2) Although both HFD and HCD induce adipocyte hypertrophy by increasing the de novo lipogenesis (DNL) pathway and promoting triglycerides (TG) synthesis. But the difference is that HFD increases fatty acid transport, while HCD increases glycolysis; (3) The inhibitory effect of HCD on glucose transporter type 4 (Glut4) may be an important cause of carbohydrate intolerance in fish; (4) Both HFD and HCD increase lactate production by promoting the expression of lactate dehydrogenase (Ldh), which may be the molecular mechanism of high-energy diet-induced adipose tissue hypoxia; (5) Interleukin-8 (Il-8) can be used as a pro-inflammatory marker for identifying HFD and HCD induced adipose tissue inflammation. This study aims to incestigate the reasons why HFD and HCD have negative effects on fish from the perspective of pathological remodeling of adipose tissue, and provide new underlying regulatory targets for improving the tolerance and utilization of HCD or HFD in farmed fish.

Effects of 12 Weeks of Daily Melatonin Administration on Inflammatory Markers and Adipose Tissue Mass of Rats under Hypoestrogenism.

Background and Objectives: The hormonal state of hypoestrogenism is associated with the accumulation of white adipose tissue, which can induce an increase in pro-inflammatory markers, leading to progressive health complications. Melatonin can act on adipose tissue mass, promoting its reduction and influencing inflammation, reducing IL-6 and releasing IL-10, pro- and anti-inflammatory markers, respectively. However, the role of melatonin regarding such parameters under the context of hypoestrogenism remains unknown. The aim of this study was to determine the effect of 12 weeks of hypoestrogenism and melatonin on white adipose tissue mass and circulating levels of IL-6, IL-10, TGF-β-1, and leukotriene C4 (LTC4). Materials and Methods: The animals (Wistar rats with sixteen weeks of age at the beginning of the experiment) under hypoestrogenism were submitted to the surgical technique of bilateral ovariectomy. The animals received melatonin (10 mg·kg-1) or vehicles by orogastric gavage every day for 12 weeks and administration occurred systematically 1 h after the beginning of the dark period. White adipose tissue (perigonadal, peritoneal, and subcutaneous) was collected for mass recording, while blood was collected for the serum determination of IL-6, IL-10, TGF-β-1, and LTC4. Results: Hypoestrogenism increased the perigonadal and subcutaneous mass and IL-6 levels. Melatonin kept hypoestrogenic animals in physiological conditions similar to the control group and increased thymus tissue mass. Conclusions: Hypoestrogenism appears to have a negative impact on white adipose tissue mass and IL-6 and although melatonin commonly exerts a significant effect in preventing these changes, this study did not have a sufficiently negative impact caused by hypoestrogenism for melatonin to promote certain benefits.

Estimation of the Impact of Abdominal Adipose Tissue (Subcutaneous and Visceral) on the Occurrence of Carbohydrate and Lipid Metabolism Disorders in Patients with Obesity-A Pilot Study.

Obesity represents a significant global public health concern. The excessive accumulation of abdominal adipose tissue is often implicated in the development of metabolic complications associated with obesity. Our study aimed to investigate the impact of particular deposits of abdominal adipose tissue on the occurrence of carbohydrate and lipid metabolism complications. We established cut-off points for visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and the VAT/SAT ratio at which selected metabolic complications of obesity-related diseases (disorders of carbohydrate and/or lipid metabolism) occur. We conducted an observational study involving 91 subjects with first- and second-degree obesity, accounting for gender differences. Anthropometric measurements were taken, body composition analysis (BIA) was conducted, and biochemical determinations were made. Our findings suggest that commonly used parameters for assessing early metabolic risk, such as BMI or waist circumference, may overlook the significant factor of body fat distribution, as well as gender differences. Both visceral and subcutaneous adipose tissue were found to be important in estimating metabolic risk. We identified the cut-off points in women in terms of their elevated fasting glucose levels and the presence of insulin resistance (HOMA-IR: homeostasis model assessment of insulin resistance) based on SAT, VAT, and the VAT/SAT ratio. In men, cut-off points were determined for the presence of insulin resistance (HOMA-IR) based on VAT and the VAT/SAT ratio. However, the results regarding lipid disorders were inconclusive, necessitating further investigation of a larger population.

Immunoproteasomal Inhibition With ONX-0914 Attenuates Atherosclerosis and Reduces White Adipose Tissue Mass and Metabolic Syndrome in Mice.

Atherosclerosis is the major underlying pathology of cardiovascular disease and is driven by dyslipidemia and inflammation. Inhibition of the immunoproteasome, a proteasome variant that is predominantly expressed by immune cells and plays an important role in antigen presentation, has been shown to have immunosuppressive effects. We assessed the effect of ONX-0914, an inhibitor of the immunoproteasomal catalytic subunits LMP7 (proteasome subunit β5i/large multifunctional peptidase 7) and LMP2 (proteasome subunit β1i/large multifunctional peptidase 2), on atherosclerosis and metabolism in LDLr-/- and APOE*3-Leiden.CETP mice. ONX-0914 treatment significantly reduced atherosclerosis, reduced dendritic cell and macrophage levels and their activation, as well as the levels of antigen-experienced T cells during early plaque formation, and Th1 cells in advanced atherosclerosis in young and aged mice in various immune compartments. Additionally, ONX-0914 treatment led to a strong reduction in white adipose tissue mass and adipocyte progenitors, which coincided with neutrophil and macrophage accumulation in white adipose tissue. ONX-0914 reduced intestinal triglyceride uptake and gastric emptying, likely contributing to the reduction in white adipose tissue mass, as ONX-0914 did not increase energy expenditure or reduce total food intake. Concomitant with the reduction in white adipose tissue mass upon ONX-0914 treatment, we observed improvements in markers of metabolic syndrome, including lowered plasma triglyceride levels, insulin levels, and fasting blood glucose. We propose that immunoproteasomal inhibition reduces 3 major causes underlying cardiovascular disease, dyslipidemia, metabolic syndrome, and inflammation and is a new target in drug development for atherosclerosis treatment.

Anti-obesity effect of seaweed algae (Ascophyllum nodosum) extracts in the 3T3-L1 cell line and a high-fat diet-induced obesity rat model

Obesity can be induced by the accumulation of adipose tissue via overconsumption of high-energy intake, and unbalanced synthesis of various hormones. Recently, seaweed algae have attracted researchers’ attention due to their health-beneficial effects, however, the antiobesity effects of Ascophyllum nososum are still controversial. We conducted two experiments with 3T3-L1 cell line and obese mouse model to elucidate the exact mechanism of seaweed algae extract (AE).In the in vivo study, dietary AE supplementation decreased body weight without affecting feed consumption. AE reduced the total mass, fat mass, and gonadal fat of the mice without changing the lean mass weight. Additionally, dietary AE addition could restore serum markers related to lipid metabolism (triglycerides and total cholesterol) as much as those of control mice.Furthermore, the in vitro study with 3T3-L1 cells suggested that AE treatment significantly suppressed adipogenesis by decreasing expression levels of lipogenesis-related genes and lipid-utilization genes with increasing the ratio of phosphorylated AMPK to AMPK and phosphorylated ACC to ACC.Collectively, Ascophyllum nodosum extract could restore obesity induced by a high-fat diet, which might be due to the decrease in lipogenesis with the increase in lipid utilization through the AMPK-ACC signaling pathway.

Diverse effects of a Cyperus rotundus extract on glucose uptake in myotubes and adipocytes and its suppression on adipocyte maturation

Cyperus rotundus rhizomes have been used in longevity remedies in Thailand for nourishing good health, which led us to investigate the effect on energy homeostasis, especially glucose utilization in myotubes and adipocytes, and on inhibition of lipogenesis in adipocytes. The results showed that an ethyl acetate extract of C. rotundus rhizomes (ECR) containing 1.61%w/w piceatannol, with a half-maximal concentration of 17.76 ± 0.03 μg/mL in 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging assay, caused upregulation and cell-membrane translocation of glucose transporters GLUT4 and 1 in L6 myotubes but downregulation and cytoplasmic localization of GLUT4 expression in 3T3-L1 adipocytes and was related to the p-Akt/Akt ratio in both cells, especially at 100 μg/mL. Moreover, ECR (25–100 μg/mL) significantly inhibited lipid accumulation via Adenosine Monophosphate-Activated Protein Kinase (AMPK), Acetyl CoA Carboxylase (ACC), and Glycogen Synthase Kinase (GSK) pathways. Its immunoblot showed increased expression of p-AMPKα/AMPKα and p-ACC/ACC but decreased expression of p-Akt/Akt and p-GSK3β/GSK3β in 3T3-L1 adipocytes. Moreover, the decreased expression of the adipogenic effectors, perilipin1 and lipoprotein lipase, in ECR-incubated adipocytes (50 and 100 μg/mL) indicated reduced de novo lipogenesis. Our study elucidated mechanisms of C. rotundus that help attenuate glucose tolerance in skeletal muscle and inhibit lipid droplet accumulation in adipose tissue.

Mechanistic correlation of molecular pathways in obesity-mediated stroke pathogenesis.

Obesity, a prominent risk factor for the development of heart attacks and several cardiovascular ailments. Obesity ranks as the second most significant avoidable contributor to mortality, whereas stroke stands as the second leading cause of death on a global scale. While changes in lifestyle have been demonstrated to have significant impacts on weight management, the long-term weight loss remains challenging, and the global prevalence of obesity continues to rise. The pathophysiology of obesity has been extensively studied during the last few decades, and an increasing number of signal transduction pathways have been linked to obesity preclinically. This review is focused on signaling pathways, and their respective functions in regulating the consumption of fatty food as well as accumulation of adipose tissue, and the resulting morphological and cognitive changes in the brain of individuals with obesity. We have also emphasized the recent progress in the mechanisms behind the emergence of obesity, as elucidated by both experimental and clinical investigations. The mounting understanding of signaling transduction may shed light on the future course of obesity research as we move into a new era of precision medicine.

New Mechanisms to Prevent Heart Failure with Preserved Ejection Fraction Using Glucagon-like Peptide-1 Receptor Agonism (GLP-1 RA) in Metabolic Syndrome and in Type 2 Diabetes: A Review.

This review examines the impact of obesity on the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and focuses on novel mechanisms for HFpEF prevention using a glucagon-like peptide-1 receptor agonism (GLP-1 RA). Obesity can lead to HFpEF through various mechanisms, including low-grade systemic inflammation, adipocyte dysfunction, accumulation of visceral adipose tissue, and increased pericardial/epicardial adipose tissue (contributing to an increase in myocardial fat content and interstitial fibrosis). Glucagon-like peptide 1 (GLP-1) is an incretin hormone that is released from the enteroendocrine L-cells in the gut. GLP-1 reduces blood glucose levels by stimulating insulin synthesis, suppressing islet α-cell function, and promoting the proliferation and differentiation of β-cells. GLP-1 regulates gastric emptying and appetite, and GLP-1 RA is currently indicated for treating type 2 diabetes (T2D), obesity, and metabolic syndrome (MS). Recent evidence indicates that GLP-1 RA may play a significant role in preventing HFpEF in patients with obesity, MS, or obese T2D. This effect may be due to activating cardioprotective mechanisms (the endogenous counter-regulatory renin angiotensin system and the AMPK/mTOR pathway) and by inhibiting deleterious remodeling mechanisms (the PKA/RhoA/ROCK pathway, aldosterone levels, and microinflammation). However, there is still a need for further research to validate the impact of these mechanisms on humans.

Molecular mechanisms and potential therapeutic targets in the pathogenesis of hypertension in visceral adipose tissue induced by a high-fat diet.

Hypertension (HTN) presents a significant global public health challenge with diverse causative factors. The accumulation of visceral adipose tissue (VAT) due to a high-fat diet (HFD) is an independent risk factor for HTN. While various studies have explored pathogenic mechanisms, a comprehensive understanding of impact of VAT on blood pressure necessitates bioinformatics analysis. Datasets GSE214618 and GSE188336 were acquired from the Gene Expression Omnibus and analyzed to identify shared differentially expressed genes between HFD-VAT and HTN-VAT. Gene Ontology enrichment and protein-protein interaction analyses were conducted, leading to the identification of hub genes. We performed molecular validation of hub genes using RT-qPCR, Western-blotting and immunofluorescence staining. Furthermore, immune infiltration analysis using CIBERSORTx was performed. This study indicated that the predominant characteristic of VAT in HTN was related to energy metabolism. The red functional module was enriched in pathways associated with mitochondrial oxidative respiration and ATP metabolism processes. Spp1, Postn, and Gpnmb in VAT were identified as hub genes on the pathogenic mechanism of HTN. Proteins encoded by these hub genes were closely associated with the target organs-specifically, the resistance artery, aorta, and heart tissue. After treatment with empagliflozin, there was a tendency for Spp1, Postn, and Gpnmb to decrease in VAT. Immune infiltration analysis confirmed that inflammation and immune response may not be the main mechanisms by which visceral adiposity contributes to HTN. Our study pinpointed the crucial causative factor of HTN in VAT following HFD. Spp1, Postn, and Gpnmb in VAT acted as hub genes that promote elevated blood pressure and can be targets for HTN treatment. These findings contributed to therapeutic strategies and prognostic markers for HTN.

Plasticity of Adipose Tissues: Interconversion among White, Brown, and Beige Fat and Its Role in Energy Homeostasis.

Obesity, characterized by the excessive accumulation of adipose tissue, has emerged as a major public health concern worldwide. To develop effective strategies for treating obesity, it is essential to comprehend the biological properties of different adipose tissue types and their respective roles in maintaining energy balance. Adipose tissue serves as a crucial organ for energy storage and metabolism in the human body, with functions extending beyond simple fat storage to encompass the regulation of energy homeostasis and the secretion of endocrine factors. This review provides an overview of the key characteristics, functional differences, and interconversion processes among white adipose tissue (WAT), brown adipose tissue (BAT), and beige adipose tissue. Moreover, it delves into the molecular mechanisms and recent research advancements concerning the browning of WAT, activation of BAT, and whitening of BAT. Although targeting adipose tissue metabolism holds promise as a potential approach for obesity treatment, further investigations are necessary to unravel the intricate biological features of various adipose tissue types and elucidate the molecular pathways governing their interconversion. Such research endeavors will pave the way for the development of more efficient and targeted therapeutic interventions in the fight against obesity.

Retrospective investigation of the energy requirements for weight loss and weight maintenance after weight loss programme in obese dogs.

Obesity is a highly prevalent disease in dogs and is characterized by the excessive accumulation of adipose tissue that results in metabolic changes. Its treatment is based on a negative energy balance focusing on energy restriction. However, there are few studies in dogs that assessed the energy intake needed for adequate weight loss and to weight maintenance afterward. The aim of this study was to evaluate data about the treatment of canine obesity, with emphasis on energy restriction to induce weight loss and to maintain body weight (BW) and ideal body condition after weight loss. This was a retrospective study in which records of obese dogs from a veterinary teaching hospital were assessed between 2014 and 2020. Sixteen dogs were considered in the study according to inclusion and exclusion criteria and 10 of these participated in the maintenance phase after weight loss. The animals lost a mean of 23.2% their initial weight in a mean of 422 days. The mean weekly weight loss rate was 0.58% of BW, and the mean daily energy intake for weight loss was 59 kcal/kg current BW0.75. When the target BW was considered, which was defined as the current weight minus 10% for every point in the body condition score scale above 5, the mean energy for weight loss was 71 kcal/kg target BW0.75. In the maintenance phase, the animals were assessed for a mean of 134 days. The mean energy intake to maintenance BW was 70 kcal/kg BW0.75. The lower energy requirement of obese dogs during and after weight loss can work as an alert for the formulations of therapeutic weight loss diets to contain a high nutrient density focusing on the wellbeing, health, and quality of life of obese dogs, not just for the weight loss phase, but a diet for the weight maintenance phase.

Lycium barbarum polysaccharide ameliorates the accumulation of lipid droplets in adipose tissue via an ATF6/SIRT1-dependent mechanism.

Lipid droplets (LDs) are dynamic organelles that store neutral lipids and are closely linked to obesity. Previous studies have suggested that Lycium barbarum polysaccharide (LBP) supplements can ameliorate obesity, but the underlying mechanisms remain unclear. In this study, we hypothesize that LBP alleviates LD accumulation in adipose tissue (AT) by inhibiting fat-specific protein 27 (Fsp27) through an activating transcription factor-6 (ATF6)/small-molecule sirtuin 1 (SIRT1)-dependent mechanism. LD accumulation in AT is induced in high-fat diet (HFD)-fed mice, and differentiation of 3T3-L1 preadipocytes (PAs) is induced. The ability of LBP to alleviate LD accumulation and the possible underlying mechanism are then investigated both in vivo and in vitro. The influences of LBP on the expressions of LD-associated genes ( ATF6 and Fsp27) are also detected. The results show that HFD and PA differentiation markedly increase LD accumulation in ATs and adipocytes, respectively, and these effects are markedly suppressed by LBP supplementation. Furthermore, LBP significantly activates SIRT1 and decreases ATF6 and Fsp27 expressions. Interestingly, the inhibitory effects of LBP are either abolished or exacerbated when ATF6 is overexpressed or silenced, respectively. Furthermore, SIRT1 level is transcriptionally regulated by LBP through opposite actions mediated by ATF6. Collectively, our findings suggest that LBP supplementation alleviates obesity by ameliorating LD accumulation, which might be partially mediated by an ATF6/SIRT1-dependent mechanism.

Peculiarities of the clinical picture and diagnosis of dirofilariasis in the maxillofacial area: a series of cases from practice

Dirofilariasis is a helminthiasis that occurs in carnivorous animals (dogs, cats, foxes, wolves, etc.) and less often in humans, although according to some authors it is believed that the number of infected animals approximately corresponds to the number of infected people. Dirofilariasis of the maxillofacial area is not a widespread condition, its cases are described in short series, therefore, the aim of this work is to share our own experience of managing patients with this rare condition.The work presents our own experience in the management of 14 dirofilariasis patients with lesions of the maxillofacial area, of them there are 3 men and 11 women aged 29 to 54. Most patients sought help in the late autumn, winter and spring periods and only 2 people in the summer period. All patients were examined by a dentist, and an ultrasound examination of the area with a formation was performed. According to the clinical manifestations, the disease began acutely in nine patients and had a picture of inflamed atheroma (2 – in the zygomatic area, 1 – in the parotid, 2 – in the infraorbital area, 2 – in the temporal area, and 2 – in the area of the nasal bridge). All patients were operated on and tumor-like formations in dense membranes were removed, inside which one live nematode 11-18 cm long was found. In 3 observations, fragments of dead, partially lysed nematodes were removed from the oral cavity, the capsules of which imitated a migrating granuloma. According to the location – 5 capsules with dirofilaria were located in the subcutaneous fatty tissue, 3 – in the submucosal layer of the gums fused to the periosteum of the upper jaw, 1 – in the submucous layer of the lower jaw, 2 – in the fibers of the temporalis muscle and 1 – in the fibers of the buccal muscle. In each case, the localization of the nematode was close to the places of accumulation of adipose tissue or large blood vessels. In the postoperative period complex therapy was prescribed, including symptomatic anti-inflammatory and desensitizing agents, and consultation with infectionist was recommended. Thus, according to our observations, dirofilariasis most often affects areas of the face in which there are large vessels and accumulation of fatty tissue. In connection with the prevalence of dirofilariosis in humans and the predominant localization of parasitic infection in the face area, dentists, ophthalmologists and otolaryngologists need to be familiar with this pathology and show definite vigilance. Treatment dirofilariosis patients should be carried out comprehensively, together with parasitologists, with surgical excision of the lesion and appropriate drug therapy.

Evaluation of Lipids and Lipid-Related Transcripts in Human and Ovine Theca Cells and an in Vitro Mouse Model Exposed to the Obesogen Chemical Tributyltin.

Exposure to obesogenic chemicals has been reported to result in enhanced adipogenesis, higher adipose tissue accumulation, and reduced ovarian hormonal synthesis and follicular function. We have reported that organotins [tributyltin (TBT) and triphenyltin (TPT)] dysregulate cholesterol trafficking in ovarian theca cells, but, whether organotins also exert lipogenic effects on ovarian cells remains unexplored. We investigated if environmentally relevant exposures to organotins [TBT, TPT, or dibutyltin (DBT)] induce lipid dysregulation in ovarian theca cells and the role of the liver X receptor (LXR) in this effect. We also tested the effect of TBT on oocyte maturation and neutral lipid accumulation, and lipid-related transcript expression in cumulus cells and preimplantation embryos. Primary theca cell cultures derived from human and ovine ovaries were exposed to TBT, TPT, or DBT (1, 10, or ). The effect of these chemical exposures on neutral lipid accumulation, lipid abundance and composition, lipid homeostasis-related gene expression, and cytokine secretion was evaluated using liquid chromatography-mass spectrometry (LC-MS), inhibitor-based methods, cytokine secretion, and lipid ontology analyses. We also exposed murine cumulus-oocyte complexes to TBT and evaluated oocyte maturation, embryo development, and lipid homeostasis-related mRNA expression in cumulus cells and blastocysts. Exposure to TBT resulted in higher intracellular neutral lipids in human and ovine primary theca cells. In ovine theca cells, this effect was dose-dependent, independent of cell stage, and partially mediated by LXR. DBT and TPT resulted in higher intracellular neutral lipids but to a lesser extent in comparison with TBT. More than 140 lipids and 9 cytokines were dysregulated in TBT-exposed human theca cells. Expression of genes involved in lipogenesis and fatty acid synthesis were higher in theca cells, as well as in cumulus cells and blastocysts exposed to TBT. However, TBT did not impact the rates of oocyte maturation or blastocyst development. TBT induced dyslipidemia in primary human and ovine theca cells, which may be responsible for some of the TBT-induced fertility dysregulations reported in rodent models of TBT exposure. https://doi.org/10.1289/EHP13955.