BACKGROUND: While body mass index (BMI) is the most widely used indicator as a measure of obesity factors in post-transplantation diabetes mellitus (PTDM), body composition is a more accurate measure of obesity. This study aims to investigate the effects of Computed tomography (CT)--based morphemic factors on PTDM and establish a prediction model for PTDM after kidney transplantation.
METHODS: The pre-transplant data and glycemic levels of kidney transplant recipients (June 2021 to July 2023) were retrospectively and prospectively collected. Univariate and multivariate analyses were conducted to analyze the relationship between morphemic factors and PTDM at one month, six months, and one year after hospital discharge. Subsequently, a one-year risk prediction model based on morphemic factors was developed.
RESULTS: The study consisted of 131 participants in the one-month group, where Hemoglobin A1c (HbA1c) (p = 0.02) was identified as the risk factor for PTDM. In the six-month group, 129 participants were included, and the intermuscular adipose tissue (IMAT) area (p = 0.02) was identified as the risk factor for PTDM. The one-year group had 128 participants, and the risk factors for PTDM were identified as body mass index (BMI) (p = 0.02), HbA1c (p = 0.01), and IMAT area (p = 0.007). HbA1c (%) and IMAT area were included in the risk prediction Model for PTDM in the one-year group with AUC = 0.716 (95 % CI 0.591-0.841, p = 0.001).
CONCLUSIONS: Compared to BMI and other morphemic factors, this study demonstrated that the IMAT area was the most potential predictor of PTDM.
UNASSIGNED: Chictr.org (ChiCTR2300078639).

Epigenetic alterations play a pivotal role in conditions influenced by environmental factors such as overweight and obesity. Many of these changes are tissue-specific, which entails a problem in its study since obtaining human tissue is a complex and invasive practice. While blood is widely used as a surrogate biomarker, it cannot directly extrapolate the evidence found in blood to tissue. Moreover, the intricacies of metabolic diseases add a new layer of complexity, as obesity leads to significant alterations in adipose tissue, potentially causing associated pathologies that can disrupt existing correlations seen in healthy individuals. Here, our objective was to determine which epigenetic markers exhibit correlations between blood and adipose tissue, regardless of the metabolic status. We collected paired blood and adipose tissue samples from 64 patients with morbidity obesity and non-obese and employed the MethylationEPIC 850 K array for analysis. We found that only a small fraction, specifically 4.3% (corresponding to 34,825 CpG sites), of the sites showed statistically significant correlations (R ≥ 0.6) between blood and adipose tissue. Within this subset, 5327 CpG sites exhibited a strong correlation (R ≥ 0.8) between blood and adipose tissue. Our findings suggest that the majority of epigenetic markers in peripheral blood do not reliably reflect changes occurring in visceral adipose tissues. However, it is important to note that there exists a distinct set of epigenetic markers that can indeed mirror changes in adipose tissue within blood samples. KEY MESSAGES: More than 8% of methylation sites exhibit similarity between blood and adipose tissues, regardless of BMI The correlation percentage between blood and adipose tissue is strongly influenced by gender The principal genes implicated in this correlation are related to metabolism or the immunological system.

Excessive visceral adipose tissue (VAT) is a significant risk factor for various diseases. Diet plays a crucial role in controlling obesity. This study examined the association between the Dietary Approaches to Stop Hypertension (DASH) diet and VAT in 9027 adults using data from the National Health and Nutrition Examination Survey. Linear regression models were used to explore this association, with subgroup analyses included. Results showed a significant inverse association between DASH scores and VAT area, even after adjusting for covariates (β = -2.18, 95% CI: -3.10, -1.27). Participants in the highest DASH score tertile had significantly lower VAT areas compared to those in the lowest tertile (β = -7.2, 95% CI: -10.40, -4.01). This inverse association was most pronounced in middle-aged participants. Further prospective cohort studies are necessary to confirm these findings.

BACKGROUND: Aging is a complex biological process characterized by obesity and immunosenescence throughout the organism. Immunosenescence involves a decline in immune function and the increase in chronic-low grade inflammation, called inflammaging. Adipose tissue expansion, particularly that of visceral adipose tissue (VAT), is associated with an increase in pro-inflammatory macrophages that play an important role in modulating immune responses and producing inflammatory cytokines. The leukotriene B4 receptor 1 (BLT1) is a regulator of obesity-induced inflammation. Its ligand, LTB4, acts as a chemoattractant for immune cells and induces inflammation. Studies have shown that BLT1 is crucial for cytokine production during lipopolysaccharide (LPS) endotoxemia challenge in younger organisms. However, the expression patterns and function of BLT1 in older organisms remains unknown.
RESULTS: In this study, we investigated BLT1 expression in immune cell subsets within the VAT of aged male and female mice. Moreover, we examined how antagonizing BLT1 signaling could alter the inflammatory response to LPS in aged mice. Our results demonstrate that aged mice exhibit increased adiposity and inflammation, characterized by elevated frequencies of B and T cells, along with pro-inflammatory macrophages in VAT. BLT1 expression is the highest in VAT macrophages. LPS and LTB4 treatment result in increased BLT1 in young and aged bone marrow-derived macrophages (BMDMs). However, LTB4 treatment resulted in amplified Il6 from aged, but not young BMDMs. Treatment of aged mice with the BLT1 antagonist, U75302, followed by LPS-induced endotoxemia resulted in an increase in anti-inflammatory macrophages, reduced phosphorylated NFκB and reduced Il6.
CONCLUSIONS: This study provides valuable insights into the age- and sex- specific changes in BLT1 expression on immune cell subsets within VAT. This study offers support for the potential of BLT1 in modulating inflammation in aging.

Excess visceral adipose tissue (VAT) plays a crucial role in leading to obesity-related diseases. However, the association between fruit intake (excluding fruit juice) and VAT is not well-known. We aim to further explore this association in a large population. We hypothesized that higher intact fruit intake would be inversely associated with VAT. A total of 9582 adult participants from the National Health and Nutrition Examination Survey and the Food Patterns Equivalents Database 2011-2018 were included. Weighted linear regression models were utilized to evaluate the association between intact fruit intake (from two 24-hour dietary recalls) and VAT area (measured by dual-energy X-ray absorptiometry). Subgroup analysis was conducted to test the robustness of the results. Restricted cubic spline analysis was performed to find the nonlinear association. The median of intact fruit intake was 0.32 cup-equivalent (eq)/d, and the mean of VAT was 104.87 ± 1.23 cm2. Intact fruit intake (increased by 1 cup-eq/d) demonstrated an inverse association with VAT area across three adjusted models, with β(95% confidence interval) values of -7(-8.49, -5.51), -6(-7.50, -4.51), and -3.02(-4.11, -1.94) in model 1, model 2, and model 3, respectively. Subgroup analysis revealed no interactions were found among age, sex, ethnicity, body mass index, and physical activity subgroups. Restricted cubic spline revealed the inverse association was more significant when intact fruit intake was less than 1.7 cups-eq/d. These findings suggest that increasing intact fruit consumption could be an effective public health strategy to mitigate VAT accumulation and associated health risks, advancing our understanding of dietary impacts on adiposity.

BACKGROUND: Albuminuria is considered an early and sensitive marker of kidney dysfunction, but also an independent cardiovascular risk factor. Considering the possible relationship among metabolic liver disease, cardiovascular disease and chronic kidney disease, we aimed to evaluate the risk of developing albuminuria regarding the presence of epicardial adipose tissue and the steatotic liver disease status.
METHODS: A retrospective long-term longitudinal study including 181 patients was carried out. Epicardial adipose tissue and steatotic liver disease were assessed by computed tomography. The presence of albuminuria at follow-up was defined as the outcome.
RESULTS: After a median follow up of 11.2 years, steatotic liver disease (HR 3.15; 95% CI, 1.20-8.26; p = 0.02) and excess amount of epicardial adipose tissue (HR 6.12; 95% CI, 1.69-22.19; p = 0.006) were associated with an increased risk of albuminuria after adjustment for visceral adipose tissue, sex, age, weight status, type 2 diabetes, prediabetes, hypertriglyceridemia, hypercholesterolemia, arterial hypertension, and cardiovascular prevention treatment at baseline. The presence of both conditions was associated with a higher risk of developing albuminuria compared to having steatotic liver disease alone (HR 5.91; 95% CI 1.15-30.41, p = 0.033). Compared with the first tertile of visceral adipose tissue, the proportion of subjects with liver steatosis and abnormal epicardial adipose tissue was significantly higher in the second and third tertile. We found a significant correlation between epicardial fat and steatotic liver disease (rho = 0.43 [p < 0.001]).
CONCLUSIONS: Identification and management/decrease of excess adiposity must be a target in the primary and secondary prevention of chronic kidney disease development and progression. Visceral adiposity assessment may be an adequate target in the daily clinical setting. Moreover, epicardial adipose tissue and steatotic liver disease assessment may aid in the primary prevention of renal dysfunction.

The relationship between immunoglobulin A (IgA) levels and chronic liver disease remains poorly understood. The present study evaluated the clinical significance of IgA in 478 new patients who visited the Outpatient Clinic of Nagasaki Harbor Medical Center (Nagasaki, Japan). Serum IgA levels in comparison to liver stiffness (LS), as measured using a FibroScan® device, were evaluated in 358 patients. Furthermore, in 270 patients, the associations between serum IgA levels and body composition were analyzed using computed tomography. The IgA levels of patients in the groups with Child-Pugh classification B and C (CPGBC), alcoholic liver disease (ALD), steatotic liver disease (SLD) or diabetes were higher than the IgA levels of patients in the groups with CPGA, non-ALD, non-SLD or no diabetes, respectively. Logistic regression analysis showed that CPGBC, ALD, high IgG (>1,700 mg/dl), high macrophage galactose-specific lectin-2 binding protein glycosylation isomer (M2BPGi) (>1 cut-off index) and diabetes were contributing factors for high serum IgA level (>410 mg/dl). The ratio of IgA level divided by IgG level was highest in patients with ALD, followed by those with metabolic dysfunction-associated SLD (MASLD) and non-SLD. In SLD, IgA level was associated more with LS than M2BPGi and fibrosis-4 (FIB-4) in multiple regression analysis. In the receiver operating characteristic analysis, IgA level, M2BPG, and FIB-4 had similar area under the curve values for discriminating high LS (>8 kPa) from low LS (≤8 kPa) in SLD. IgA levels were also associated with visceral fat, and this association was only found in women. In conclusion, elevated IgA is an indicator of liver fibrosis that also reflects the presence of diabetes and an increased visceral fat level. Therefore, IgA is considered a useful marker of liver disease severity in the current era of increased SLD.

Visceral white adipose tissues (WAT) regulate systemic lipid metabolism and inflammation. Dysfunctional WAT drive chronic inflammation and facilitate atherosclerosis. Adipose tissue-associated macrophages (ATM) are the predominant immune cells in WAT, but their heterogeneity and phenotypes are poorly defined during atherogenesis. The scavenger receptor CD36 mediates ATM crosstalk with other adipose tissue cells, driving chronic inflammation. Here, we combined the single-cell RNA sequencing technique with cell metabolic and functional assays on major WAT ATM subpopulations using a diet-induced atherosclerosis mouse model (Apoe-null). We also examined the role of CD36 using Apoe/Cd36 double-null mice. Based on transcriptomics data and differential gene expression analysis, we identified a previously undefined group of ATM displaying low viability and high lipid metabolism and labeled them as \"unhealthy macrophages\". Their phenotypes suggest a subpopulation of ATM under lipid stress. We also identified lipid-associated macrophages (LAM), which were previously described in obesity. Interestingly, LAM increased 8.4-fold in Apoe/Cd36 double-null mice on an atherogenic diet, but not in Apoe-null mice. The increase in LAM was accompanied by more ATM lipid uptake, reduced adipocyte hypertrophy, and less inflammation. In conclusion, CD36 mediates a delicate balance between lipid metabolism and inflammation in visceral adipose tissues. Under atherogenic conditions, CD36 deficiency reduces inflammation and increases lipid metabolism in WAT by promoting LAM accumulation.

BACKGROUND: The Chinese visceral adiposity index (CVAI) is a new index to evaluate visceral adipose tissue in the Chinese population. Arterial stiffness (AS) is a kind of degeneration of the large arteries, and obesity is an essential contributing factor to AS. Our study aimed to explore the longitudinal association between CVAI and the risk of AS and to compare the predictive power of CVAI, body mass index (BMI), and waist circumference (WC) for AS.
METHODS: Between 2010 and 2020, a total of 14,877 participants participating in at least two brachial-ankle pulse wave velocity (baPWV) measurements from the Kailuan study were included. The Cox proportional hazard regression models were performed to evaluate the longitudinal association between CVAI and the risk of AS. The area under the receiver operating characteristic (ROC) curve was calculated to compare the predictive power of CVAI, BMI, and WC for AS.
RESULTS: After adjusting for potential confounding factors, CVAI was significantly associated with the risk of AS. Compared with the first CVAI quartile, the hazard ratios (HR) and 95% CI of the second, third, and fourth quartiles were 1.30 (1.09-1.56), 1.37 (1.15-1.63), and 1.49 (1.24-1.78), respectively. The area under ROC curve of CVAI was 0.661, significantly higher than BMI (AUC: 0.582) and WC (AUC: 0.606).
CONCLUSIONS: CVAI may be a reliable indicator to identify high-risk groups of AS in the Chinese general population, and the predictive power of CVAI for AS was better than BMI and WC.

UNASSIGNED: Filipino Americans (FAs) are at high risk for developing type 2 diabetes despite other Asian phenotypes. Evidence suggests that pro-inflammatory interleukin-18 (IL-18) and anti-inflammatory adiponectin biomarkers associated with visceral adipose tissue (VAT) may explain this risk.
UNASSIGNED: This study aimed to quantify the biomarkers in relation to standard ranges of VAT or typical circulating concentration ranges reported in the literature of IL-18 and adiponectin, examine relationships of these markers, and determine if they were different among those participants without diabetes, prediabetes, and diabetes.
UNASSIGNED: A cross-sectional study was used to enroll FAs without diabetes, prediabetes, or diabetes. VAT was measured using the InBody 570© Body Composition Analyzer. Blood samples were obtained to assess plasma concentrations of IL-18 and adiponectin using enzyme-linked immunosorbent assay. All analyses were conducted using a 5% type I error rate. Mean ±SD and percentages were used to describe the sample and data where appropriate. Pearson\'s correlations (R) were calculated to determine the relationships between VAT and IL-18 in each group. Analysis of variance was used to determine differences in VAT, IL-18, and adiponectin among groups. Further, nonparametric procedures examined the differences in adiponectin among those within groups.
UNASSIGNED: Seventy-five participants were enrolled. Biomarkers above the typical concentration range were observed for VAT, IL-18, and adiponectin. Adiponectin significantly differed among groups with lower values in the diabetes group vs. the nondiabetes group.
UNASSIGNED: The findings indicate that while inflammation-related biomarkers, such as adiponectin, correlate with VAT and may serve as indicators of increased risk of type 2 diabetes in FAs, correlation alone does not establish causality.