Adipose Accumulation Research Articles

N6,N6‐Dimethyl‐l‐Lysine: An Anti‐Obesity Metabolite of Lactiplantibacillus plantarum R2‐5 From Longevity Area Revealed by Multi‐Omics Analysis

ABSTRACTLactobacilli bacteria, as probiotics, show significant potential for lipid reduction. Current research into their lipid‐lowering effects is in the early stages, with mechanisms largely unexplored. In this study, mice were induced with a high‐fat diet (HFD) and treated with Lactiplantibacillus plantarum R2‐5 (LPR2‐5) via oral gavage. After 12 weeks, the LPR2‐5‐treated group exhibited substantial improvements in body weight and lipid abnormalities, with significant reductions in liver and abdominal fat accumulation. (LPR2‐5 can reduce serum total cholesterol [TC] by 25.7%, lower triglycerides [TG] by 45%, decrease low‐density lipoprotein cholesterol [LDL‐C] by 30%, and double high‐density lipoprotein cholesterol [HDL‐C].) Analysis of gut microbiota diversity demonstrated that LPR2‐5 intervention altered the gut microbiome, increasing the abundance of short‐chain fatty acid (SCFA)‐producing bacteria (Lactobacillus, Roseburia) and potentially beneficial microbes (Turicibacter, Christensenella), while inhibiting obesity‐associated bacteria (Alistipes, Bilophila), thus altering metabolic activity in the gut. Using multi‐omics techniques, key metabolic pathways and metabolites were identified. The lipid‐lowering mechanism involved a notable increase in N6,N6‐dimethyl‐l‐lysine, a precursor for carnitine synthesis, enhancing carnitine production in the liver and promoting β‐oxidation of long‐chain fatty acids, thereby effectively reducing early stage adipose accumulation.

Kombucha enables to inhibit digestive enzymes activity and adipocyte differentiation of OP9 cells.

Obesity is a global challenging epidemic caused by surplus adipose accumulation or energy intake, and available medications are quite limited. Studies focused on identifying potent anti-adipogenic pharmaceuticals and functional foods have gained great interests. This study evaluated the obesity prevention potential of oolong tea kombucha (OTK) and yellow tea kombucha (YTK) by in vitro experiments. The results showed that the total polyphenol content in OTK and YTK increased by 50.00% and 47.49% after fermentation, and the antioxidative capacity of kombucha was enhanced by 7.57% and 7.83% as well. After fermentation, the inhibitory activity of OTK and YTK on α-amylase and lipase was increased by 53.15% and 64.43%, and 45.24% and 39.74%, respectively. The anti-adipogenic effects evaluated by using mouse OP9 cell model indicated that both OTK and YTK could downregulate the expression levels of FABP4, PPARγ, C/EBPα, and SERBP-1C which are involved with adipocyte differentiation. Taken together, kombucha showed great potential in regulating glucose and lipid metabolism by inhibiting digestive enzymes and adipocyte differentiation, which could be a functional beverage in aiding obesity prevention or treatments. However, further animal or clinical experiments are needed to verify its potential in obesity intervention. PRACTICAL APPLICATION: This study showed that kombucha showed great potential in preventing obesity, which provided an alternative functional beverage for obesity intervening or prevention.

Change in adiposity indices after 1 year of peritoneal dialysis: a single-center cohort study.

Weight gain is common after starting peritoneal dialysis (PD). Several adiposity indices have been developed recently as potential indicators of visceral adiposity and lipid accumulation. We aim to investigate the prevalence and prognostic implications of the change in adiposity indices after 1year of PD. We recruited 110 patients treated with PD for 12months. Adiposity indices, including triglyceride glucose index, lipid accumulation product, visceral adiposity index and conicity index, were measured at baseline and then 1year after PD started. The relation between their changes (Δ) and other clinical and biochemical parameters, as well as survival and hospitalization rates were analyzed. After 1year of PD, more than half of the patients had increased adiposity indices. The change in adipose tissue mass significantly correlated with the concomitant changes in triglyceride glucose index (ΔTyGI) (r=0.25, P =.01), lipid accumulation product (ΔLAP) (r=0.27, P =.007) and visceral adiposity index (ΔVAI) (r=0.26, P =.01). ΔTyGI significantly correlated with the change in insulin resistance as represented by homeostasis model assessment of insulin resistance (HOMA-IR) (r=0.22, P =.02), while ΔLAP and change in conicity index (ΔCI) correlated with the changes in various anthropometric parameters. However, no indices variation was associated with patient survival, technique survival or hospitalization rate. Increased adiposity indices were common after 1year of PD. The changes in adiposity indices had variable correlation with the change in adipose tissue mass, insulin resistance and anthropometric parameters. Further studies are required to identify simple metabolic parameters with a prognostic impact that could be suitable for serial monitoring.

Irisin Improves Preeclampsia by Promoting Embryo Implantation and Vascular Remodeling.

Preeclampsia is a pregnancy-specific disorder with unclear pathogenesis. Irisin, a recently identified exercise-induced factor, significantly influences lipid metabolism and cardiovascular function. Nonetheless, its role in trophoblast development during human placentation and the related intracellular signaling pathways remain poorly understood. We assessed peripheral blood irisin expression in early pregnancy among patients with preeclampsia and its correlation with key clinical indicators. In trophoblast cell lines and mice, we used exogenous irisin and viral knockdown to investigate functional changes. Phosphorylation-specific antibody arrays and dual-luciferase reporter assays were used to explore downstream molecular mechanisms, which were subsequently validated in trophoblast cell lines and relevant gene knockout mice. In early pregnancy, patients with preeclampsia exhibit decreased peripheral blood irisin levels, occurring earlier than traditional predictive markers, such as PLGF (placental growth factor) and sFlt-1 (soluble fms-like tyrosine kinase-1). Furthermore, irisin concentration is positively correlated with proteinuria and abnormal blood pressure during pregnancy. Exogenous irisin significantly enhanced trophoblast cell migration, invasion, and proliferation while inhibiting apoptosis. It also increased STAT (signal transducers and activators of transcription) 4 phosphorylation and its binding to the GLUT (glucose transporter)-3 promoter, resulting in elevated GLUT-3 expression and glucose uptake in trophoblast cells. In vivo, increased peripheral irisin promoted embryo implantation, vascular remodeling, and enhanced glucose uptake, whereas reduced irisin resulted in a preeclampsia-like phenotype characterized by elevated blood pressure, proteinuria, renal-placental dysfunction, adipose accumulation, and restricted fetal growth. Peripheral irisin improves preeclampsia by promoting embryo implantation and vascular remodeling through the activation of the STAT4/GLUT-3 pathway. Reduced peripheral irisin may contribute to preeclampsia-like pathologies. This study supports the advocacy for appropriate exercise during early pregnancy and provides new insights for preeclampsia prevention.

Retinol metabolism signaling participates in microbiota-regulated fat deposition in obese mice

Obesity is a global pandemic threatening public health, excess fat accumulation and overweight are its characteristics. In this study, the interplay between gut microbiota and retinol metabolism in modulating fat accumulation was verified. We observed gut microbiota depletion reduced the body weight and the ratios of white adipose tissues (WATs) to body weight in high-fat diet (HFD) fed-mice. The kyoto encyclopedia of genes and genomes (KEGG) analysis and protein-protein interaction (PPI) network of RNA-seq results indicated that retinol metabolism signaling may be involved in the microbiota-regulated fat deposition. Furthermore, activated retinol metabolism signaling by all-trans retinoic acid (atRA) supplementation reduced body weight and WAT accumulation in obese mice. 16S rRNA gene sequencing of the ileal microbiota suggested that atRA supplementation increased the microbial diversity and induced the growth of beneficial bacteria including Parabacteroides, Bacteroides, Clostridium_XVIII, Bifidobacterium, Enterococcus, Bacillus, Leuconostoc, and Lactobacillus in obese mice. Spearman correlation showed that the microbiota altered by atRA were associated with body and WAT weights. Together, this study reveals the interaction between the gut microbiota and retinol metabolism signaling in regulating adipose accumulation and obesity. It is expected of this finding to provide new insights to prevent and develop therapeutic measures of obesity-related metabolic syndrome.

Employing single-cell RNA sequencing coupled with an array of bioinformatics approaches to ascertain the shared genetic characteristics between osteoporosis and obesity.

This study examined the relationship between obesity (OB) and osteoporosis (OP), aiming to identify shared genetic markers and molecular mechanisms to facilitate the development of therapies that target both conditions simultaneously. Using weighted gene co-expression network analysis (WGCNA), we analyzed datasets from the Gene Expression Omnibus (GEO) database to identify co-expressed gene modules in OB and OP. These modules underwent Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and protein-protein interaction analysis to discover Hub genes. Machine learning refined the gene selection, with further validation using additional datasets. Single-cell analysis emphasized specific cell subpopulations, and enzyme-linked immunosorbent assay (ELISA), protein blotting, and cellular staining were used to investigate key genes. WGCNA revealed critical gene modules for OB and OP, identifying the Toll-like receptor (TLR) signalling pathway as a common factor. TLR2 was the most significant gene, with a pronounced expression in macrophages. Elevated TLR2 expression correlated with increased adipose accumulation, inflammation, and osteoclast differentiation, linking it to OP development. Our study underscores the pivotal role of TLR2 in connecting OP and OB. It highlights the influence of TLR2 in macrophages, driving both diseases through a pro-inflammatory mechanism. These insights propose TLR2 as a potential dual therapeutic target for treating OP and OB.

Body mass index across development and adolescent hair cortisol: the role of persistence, variability, and timing of exposure.

Research suggests a putative role of the glucocorticoid stress hormone cortisol in the accumulation of adiposity. However, obesity and weight fluctuations may also wear and tear physiological systems promoting adaptation, affecting cortisol secretion. This possibility remains scarcely investigated in longitudinal research. This study tests whether trajectories of body mass index (BMI) across the first 15 years of life are associated with hair cortisol concentration (HCC) measured two years later and whether variability in BMI and timing matter. BMI (kg/m2) was prospectively measured at twelve occasions between age 5 months and 15 years. Hair was sampled at age 17 in 565 participants. Sex, family socioeconomic status, and BMI measured concurrently to HCC were considered as control variables. Latent class analyses identified three BMI trajectories: "low-stable" (59.2%, n = 946), "moderate" (32.6%, n = 507), and "high-rising" (8.2%, n = 128). BMI variability was computed by dividing the standard deviation of an individual's BMI measurements by the mean of these measurements. Findings revealed linear effects, such that higher HCC was noted for participants with moderate BMI trajectories in comparison to low-stable youth (β = 0.10, p = 0.03, 95% confidence interval (CI) = [0.02-0.40]); however, this association was not detected in the high-rising BMI youth (β = -0.02, p = 0.71, 95% CI = [-0.47-0.32]). Higher BMI variability across development predicted higher cortisol (β = 0.17, p = 0.003, 95% CI = [0.10-4.91]), additively to the contribution of BMI trajectories. BMI variability in childhood was responsible for that finding, possibly suggesting a timing effect. This study strengthens empirical support for BMI-HCC association and suggests that more attention should be devoted to BMI fluctuations in addition to persistent trajectories of BMI.

Resveratrol inhibits white adipose deposition by the ESR1-mediated PI3K/AKT signaling pathway

Excessive adipose accumulation is the primary cause of obesity. Resveratrol (RES), a natural polyphenolic compound, has garnered significant attention for its anti-obesity properties. However, the precise mechanisms by which RES influences fat deposition have not yet been explored. In this study, the aim was to identify the target proteins and associated pathways of RES in order to elucidate the mechanisms by which RES reduces fat deposition. In this study, mice were administered 400 mg/kg of RES via gavage for 12 weeks. We found that while 400 mg/kg RES had no impact on the growth of the mice, it significantly reduced the weight of various white adipose tissues, as well as the serum and liver concentrations of total cholesterol and triglycerides. Network pharmacology identified 15 potential targets of RES and highlighted the PI3K/AKT signaling pathway as a key pathway. Molecular docking and dynamic simulations suggested that ESR1 might be the target protein through which RES exerts its anti-fat deposition effects. In vitro experiments revealed that ESR1 promotes the proliferation and inhibits the differentiation of 3 T3-L1 adipocytes, and suppresses the PI3K/AKT signaling pathway. Silencing the ESR1 gene altered the ability of RES to inhibit cell differentiation via the PI3K/AKT pathway. Gene expression results in subcutaneous adipose tissue, epididymal fat tissue, and liver tissue of mice were consistent with observations in cells. In summary, RES reduces white fat deposition by directly targeting the ESR1 protein and inhibiting the PI3K/AKT signaling pathway. Our findings provide new insights into the potential use of RES in the prevention and treatment of obesity.

Lipidomic perturbations of normal-weight adiposity phenotypes and their mediations on diet–adiposity associations

Background & aimsNormal-weight obesity (NWO) and normal-weight central obesity (NWCO) have been linked to higher cardiometabolic risks, but their etiological bases and attributable dietary factors remain unclear. In this study we therefore aimed to identify lipidomic signatures and dietary factors related to NWO and NWCO and to explore the mediation associations of lipids in diet–adiposity associations. MethodsUsing a high-coverage targeted lipidomic approach, we quantified 1245 serum lipids in participants with NWO (n = 150), NWCO (n = 150), or propensity-score-matched normal-weight controls (n = 150) based on the Regional Ethnic Cohort Study in Northwest China. Consumption frequency of 28 major food items was recorded using a food frequency questionnaire. ResultsProfound lipidomic perturbations of NWCO relative to NWO were observed, and 249 (dominantly glycerolipids) as well as 48 (dominantly glycerophospholipids) lipids were exclusively associated with NWCO or NWO. Based on strong lipidomic signatures identified by a LASSO model, phospholipid biosynthesis was the top enriched pathway of NWCO, and sphingolipid metabolism was the top pathway of NWO. Remarkably, sphingolipids were positively associated with NWO and NWCO, but lyso-phosphatidylcholines were negatively associated with them. Rice, fruit juice, and carbonated drink intakes were positively associated with the risk of NWCO. Both global and individual lipidomic signatures, including SE(28:1_22:6) and HexCer(d18:1/20:1), mediated these diet-NWCO associations (mediation proportion: 15.92%–26.10%). ConclusionsDifferential lipidomic signatures were identified for overall and abdominal adiposity accumulation in normal-weight individuals, underlining their core mediation roles in dietary contributions to adiposity deposition.

Mung bean protein pre-fibrils are superior than the mature fibrils in stabilizing HIPEs and controlling the lipid digestion to inhibit in vivo adipose accumulation

Excessive consumption of lipids is one of the major reasons for the prevalence of obesity. Interfacial engineering of food emulsions is highly expected to control the digestion and absorption of lipids, consequently to inhibit adipose expansion. However, this strategy is restricted mainly due to the lack of effective food emulsifiers. In the present study, the mung bean protein fibrils with short worm-like morphology were demonstrated to have superior capabilities than the mature ones in stabilizing high internal phase emulsions (HIPEs) and consequently inhibiting the lipid digestion to control in vivo adipose accumulation. The short worm-like pre-fibrils showed a faster adsorption kinetics to the oil/water interface to reduce the interfacial tension to a substantially lower level compared with the mature fibrils. The HIPEs stabilized by the worm-like pre-fibrils showed a wider range of oil phase volume fractions and protein fibril concentrations, which showed the characteristic connected polygon oil droplets network microstructure due to the squeezing of oil droplets. In comparison, the HIPEs stabilized by the mature mung bean protein fibrils were unstable, undergoing ostwald ripening with the appearance of big oil droplets shortly after the preparation. Consequently, significantly less free fatty acids were released from the HIPEs stabilized by the worm-like pre-fibrils compared with the mature ones in the in vitro stimulating digestion assay. Interestingly, compared with the HIPEs emulsified by the mature amyloid-like fibrils (HIPEs-M group), long-term oral administration of mice with the HIPEs stabilized by the worm-like pre-fibrils (HIPEs-W group) resulted in significantly lower body weight and substantially inhibited adipose expansion. The genes related to lipolysis were over-expressed and the expression of the lipogenesis genes were down-regulated in adipose tissue in HIPEs-W group compared with those in HIPEs-M group. Furthermore, fecal lipid content in HIPEs-W group was higher than that in HIPEs-M group; and the expression of genes related to lipid adsorption in intestine, such as FATP4, FABP-1, PPAR-α, MTTP-1 and CPT1A was down-regulated. Therefore, restriction of lipid digestion and absorption in intestine could serve as the mechanism for the inhibition of in vivo adipose expansion caused by the HIPEs stabilized by the worm-like fibrils compared with the mature fibrils.

The association between visceral adipose accumulation and hyperuricemia risk among Chinese elder individuals: A nationwide prospective cohort study

BackgroundLipid accumulation product (LAP), visceral adiposity index (VAI) and Chinese visceral adiposity index (CVAI) are proposed indices of visceral adipose accumulation. This study aimed to explore their relationship and temporal changes with hyperuricemia (HUA) development in a Chinese population. MethodsA total of 4268 participants aged ≥45 years from the baseline survey of the China Health and Retirement Longitudinal Study were followed up for 4 years (from 2011 to 2015). The relationships among VAI, LAP, CVAI and HUA were analyzed using logistic regression. The predictive abilities of the VAI, LAP and CVAI for HUA were compared using receiver operating characteristic curves. Nonlinear relationships between the indices and HUA were analyzed using restricted cubic spline regression. ResultsDuring the four-year follow-up, 415 (9.72 %) patients experienced incident HUA . Elevated baseline VAI (odds ratio (OR): 1.19 (95 % confidence interval (95 %CI: 1.10, 1.29)), LAP (OR: 1.21 (95 % CI: 1.09, 1.34)) and CVAI (OR: 1.19 (95 % CI: 1.02, 1.40)) were significantly correlated with increased HUA risk (all P < 0.05). Compared to individuals with consistently low VAI,CVAIor LAP levels, those with elevated or consistently high levels of these indicators are more likely to have HUA. The area under curve (AUC) was slightly greater and more significant for the CVAI (AUC=0.641) than for the VAI (AUC=0.604) and LAP (AUC=0.628) (P < 0.05). ConclusionVAI, LAP and CVAI can predict HUA, with CVAI more efficient than VAI and LAP. Early management can lessen the burden of HUA in Chinese people aged 45 years or older with elevated CVAI levels.

Remission of type 2 diabetes: position statement of the Italian society of diabetes (SID)

AbstractThe primary cause of the pandemic scale of type 2 diabetes (T2D) is the excessive and/or abnormal accumulation of adiposity resulting from a chronic positive energy balance. Any form of weight loss dramatically affects the natural history of T2D, favoring prevention, treatment, and even remission in the case of significant weight loss. However, weight regain, which is often accompanied by the recurrence or worsening of obesity complications such as T2D, is an inevitable biological phenomenon that is an integral part of the pathophysiology of obesity. This can occur not only after weight loss, but also during obesity treatment if it is not effective enough to counteract the physiological responses aimed at restoring adiposity to its pre-weight-loss equilibrium state. Over the past few years, many controlled and randomized studies have suggested a superior efficacy of bariatric surgery compared to conventional therapy in terms of weight loss, glycemic control, and rates of T2D remission. Recently, the therapeutic armamentarium in the field of diabetology has been enriched with new antihyperglycemic drugs with considerable efficacy in reducing body weight, which could play a pathogenetic role in the remission of T2D, not through the classical incretin effect, but by improving adipose tissue functions. All these concepts are discussed in this position statement, which aims to deepen the pathogenetic links between obesity and T2D, shift the paradigm from a “simple” interaction between insulin resistance and insulin deficiency, and evaluate the efficacy of different therapeutic interventions to improve T2D management and induce diabetes remission whenever still possible.

Multiomics reveals the ameliorating effect and underlying mechanism of aqueous extracts of polygonatum sibiricum rhizome on obesity and liver fat accumulation in high-fat diet-fed mice

BackgroundPolygonatum sibiricum polysaccharides protect against obesity and NAFLD. However, the potential effects of PS rhizome aqueous extracts (PSRwe) on adiposity and hepatic lipid accumulation remains unexplored. PurposeElucidating the impact and underlying mechanism of PSRwe on HFD-induced obesity and liver fat depostition. Study design56 male mice, aged eight weeks, were divided into seven groups: Positive, four doses of PSRwe, Model, and Control. HFD was fed for eight weeks, followed by alternate-day gavage of orlistat and PSRwe for an additional eight-week period. Integrative analysis encompassing multiomics, physiological and histopathological, and biochemical indexes was employed. MethodsBody weight (BW); liver, fat and Lee's indexes; TC, TG, LDL-C, HDL-C, AST, ALT, FFA, leptin, and adiponectin in the liver and blood; TNFα, IL-6, and LPS in the colon, plasma, and liver; H&E, PAS and oil red O staining on adipose and liver samples were examined. OGTT and ITT were conducted The gut microbiome, microbial metabolome, colonic and liver transcriptome, plasma and liver metabolites were investigated. ResultsPSRwe at the dosage of 7.5 mg/kg demonstrated significant and consistent reduction in BW and hepatic fat deposition than orlistat. PSRwe significantly decreased TC, TG, LDL-C, LEP, FFA levels in blood and liver. PSRwe significantly enhanced the relative abundance of probiotics including Akkermansia muciniphila, Bifidobacterium pseudolongum, Lactobacillus reuteri, and metabolic pathways including glycolysis and fatty acids β-oxidation. The 70 up-regulated microbial metabolites in PSRwe-treated mice mainly involved in nucleotides and amino acids metabolism, while 40 decreased metabolites primarily associated with lipid metabolism. The up-regulated colonic differentially expressed genes (DEGs) participate in JAK-STAT/PI3K-Akt/FoxO signaling pathway, serotonergic/cholinergic/glutamatergic synapses, while the down-regulated DEGs predominantly focused on fat absorption and transport. The up-regulated liver DEGs mainly concentrated on fatty acid oxidation and metabolism. Liver metabolisms revealed 131 differential metabolites, among which carnitine and oxidized lipids significantly increased in PSRwe-treated mice. In plasma, the 58 up-regulated metabolites mainly participate in co-factors/vitamins metabolism while 154 down-regulated ones in fatty acids biosynthesis. Comprehensive multiomics association analysis revealed significant associations between gut microbiota and colonic/liver gene expression, and suggested exogenous and endogenous betaine may be active compound in alleviating HFD-induced symptoms. ConclusionPSRwe effectively mitigate HFD-induced obesity and hepatic steatosis by increasing beneficial bacteria, reducing colonic fat digestion/absorption, increasing hepatic lipid metabolism, and elevating betaine levels.

Distinct Gut Microbiota and Arachidonic Acid Metabolism in Obesity-Prone and Obesity-Resistant Mice with a High-Fat Diet.

An imbalance of energy intake and expenditure is commonly considered as the fundamental cause of obesity. However, individual variations in susceptibility to obesity do indeed exist in both humans and animals, even among those with the same living environments and dietary intakes. To further explore the potential influencing factors of these individual variations, male C57BL/6J mice were used for the development of obesity-prone and obesity-resistant mice models and were fed high-fat diets for 16 weeks. Compared to the obesity-prone mice, the obesity-resistant group showed a lower body weight, liver weight, adipose accumulation and pro-inflammatory cytokine levels. 16S rRNA sequencing, which was conducted for fecal microbiota analysis, found that the fecal microbiome's structural composition and biodiversity had changed in the two groups. The genera Allobaculumbiota, SMB53, Desulfovibrio and Clostridium increased in the obesity-prone mice, and the genera Streptococcus, Odoribacter and Leuconostoc were enriched in the obesity-resistant mice. Using widely targeted metabolomics analysis, 166 differential metabolites were found, especially those products involved in arachidonic acid (AA) metabolism, which were significantly reduced in the obesity-resistant mice. Moreover, KEGG pathway analysis exhibited that AA metabolism was the most enriched pathway. Significantly altered bacteria and obesity-related parameters, as well as AA metabolites, exhibited strong correlations. Overall, the phenotypes of the obesity-prone and obesity-resistant mice were linked to gut microbiota and AA metabolism, providing new insight for developing an in-depth understanding of the driving force of obesity resistance and a scientific reference for the targeted prevention and treatment of obesity.

Investigating a novel surrogate indicator of adipose accumulation in relation to erectile dysfunction

IntroductionAlthough previous studies have linked obesity and erectile dysfunction, the novel surrogate indicators of adipose accumulation are more essential and dependable factors to consider. Therefore, the primary objective of the current investigation was to examine and clarify the association between metabolic score for visceral fat (METS-VF) and erectile dysfunction.MethodsFirstly, multivariate logistic regression analysis, smoothed curve fitting, and threshold effect analysis were employed to investigate the association between METS-VF and erectile dysfunction. Mediation analysis was also performed to evaluate the mediating role of homocysteine and inflammation. After that, subgroup analysis was carried out to examine the stability of the correlation of METS-VF with erectile dysfunction in various population settings. Furthermore, the area under the receiver operating characteristic (ROC) curve and eXtreme Gradient Boosting (XGBoost) algorithm were utilized to assess the capability of identifying METS-VF in comparison to the other four obesity-related indicators in identifying erectile dysfunction.ResultsAfter adjusting for all confounding factors, METS-VF was strongly and favourablely correlated with erectile dysfunction. With each additional unit rise in METS-VF, the prevalence of erectile dysfunction increased by 141%. A J-shaped relationship between METS-VF and erectile dysfunction was discovered through smoothed curve fitting. Marital status, physical activity, and smoking status can potentially modify this association. This finding of the ROC curve suggests that METS-VF had a powerful identifying capacity for erectile dysfunction (AUC = 0.7351). Homocysteine and inflammation mediated 4.24% and 2.81%, respectively.ConclusionThe findings of the current investigation suggest that METS-VF can be considered a dependable identifying indicator of erectile dysfunction.

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.

Abstract MP71: Novel Association Between Parity and Skeletal Muscle Adiposity in Middle-Aged and Older African Caribbean Women

Objective: Pregnancy and parity (number of children born to a women) are associated with alterations in metabolism and lifestyle, which may affect women’s short- and long-term cardiometabolic health. Greater skeletal muscle adiposity (myosteatosis) is recognized as a major risk factor for cardiometabolic diseases, especially in African ancestry individuals. While lifetime parity has been previously associated with greater central obesity years after childbearing ceased, it remains unclear whether parity is associated with myosteatosis. Methods: We examined the association of parity (0, 1, 2, 3, 4+) with myosteatosis and general and central obesity among 1,119 African Caribbean women, aged 40-84 years, recruited from 2019 to 2023 without regard to health status. Calf myosteatosis area was measured by CT-derived intermuscular adipose tissue (IMAT, mm 2 ) and skeletal muscle density (mg/cm 3 , with a lower density indicating more adiposity). Multivariable linear regression models were used to estimate the adjusted means of IMAT, muscle density, BMI, and waist circumference for each parity group. Results: The mean age of women who reported ever being pregnant (N=969) was 55.8 (SD=9.0) years. They were obese on average (BMI=32.1 (SD=6.8) kg/m 2 ), and had given birth to an average of 3 (SD=2.3) children. In multivariable models, higher parity was significantly associated with higher IMAT and lower muscle density, after accounting for age, BMI, physical activity, and comorbidities (see Table). Parity showed no associations with BMI or waist circumference. Conclusions: Parity may be associated with greater accumulation of adiposity in skeletal muscle, despite no link with general or central adiposity among African Caribbean women. Our novel findings, if confirmed in prospective studies, might highlight the need for tailored strategies for maintaining healthy muscles in multiparous women of African ancestry. Table. Adjusted population marginal means (95% CI) for myosteatosis by parity groups in African Caribbean women a

Immune metabolic mechanisms of acupuncture in improving glycolipid metabolic disorders explored through pancreatic adipose tissue.

Pancreatic adipose tissue serves as a crucial structural basis for the development of glycolipid metabolic disorders. Understanding the mechanisms underlying pancreatic adipose tissue infiltration and regulatory strategies is essential for early intervention in glycolipid metabolic disorders. Pancreatic adipose tissue functions as a significant medium linking systemic immune metabolism, while the pancreatic vascular system emerges as a novel target for sensing pancreatic immune responses and maintaining the body's energy homeostasis, collectively participating in the development of glycolipid metabolic disorders. Acupuncture possesses potential effects in modulating the interaction between resident macrophages and adipocytes in the pancreas, leading to the reversible reduction of excessive pancreatic adipose accumulation, with its action being vascular-dependent.

Aging from adipose accumulation of antibodies.

IgG accumulation in white adipose tissue contributes to aging-associated metabolic dysfunction.

Abstract 1501 The reduction of adiposity and hepatic lipid accumulation by bilirubin is dependent on its hormonal function

Abstract 1501 The reduction of adiposity and hepatic lipid accumulation by bilirubin is dependent on its hormonal function