Enlarged adipocytes from subcutaneous vs. visceral adipose tissue differentially contribute to metabolic dysfunction and atherogenic risk of patients with obesity

Abstract

Morphological characteristics and source of adipose tissue as well as adipokines may increase cardiometabolic risk. This study aimed to explore whether adipose tissue characteristics may impact metabolic and atherogenic risks. Subcutaneous Adipose Tissue (SAT), Visceral Adipose Tissue (VAT) and peripheral blood were obtained from obese patients submitted to bariatric surgery. Adipose tissue (morphometry), plasma adiponectin, TNF-α, resistin (multiplexing) and biochemical chemistry were analyzed; as well as endothelial dysfunction (Flow Mediated Dilation, FMD) and atherogenesis (Carotid Intima Media Thickness, CIMT). Subgroups divided by adipocyte size and source were compared; as well as correlation and multivariate analysis. Sixty patients 36.6% males, aged 44 years-old, BMI 46.7 kg/m2 were included. SAT’s adipocytes showed a lower range of size expandability than VAT’s adipocytes. Independent from their source, larger adipocytes were associated with higher glucose, lower adiponectin and higher CIMT. Particularly, larger adipocytes from SAT were associated with higher blood pressure, lower insulin and HDL-cholesterol; and showed positive correlation with glucose, HbA1c, systolic/diastolic values, and negatively correlated with insulin and adiponectin. VAT’s larger adipocytes particularly associated with lower resistin and lower FMD values. Gender and Diabetes Mellitus significantly impacted the relation of adipocyte size/source with the metabolic and atherogenic risk. Multivariable analysis suggested hypertension-resistin-HbA1c interactions associated with SAT’s larger adipocytes; whereas potential insulin-adiponectin associations were observed for VAT’s larger adipocytes. Adipocyte morphology and source are differentially related with cardiometabolic and atherogenic risk in population with obesity, which are potentially affected by gender and Diabetes Mellitus.

Apolipoprotein CIII Reduction Protects White Adipose Tissues against Obesity-Induced Inflammation and Insulin Resistance in Mice

“…Focusing on WAT there was a hypertrophy of adipocytes in both SAT and VAT from Scr-treated obese mice. The difference in size and that VAT has larger adipocytes than SAT are in line with previous observations [ 21 , 22 , 23 ]. The adipocytes normalized their size in both tissues after ASO treatment.…”

“…The adipocytes normalized their size in both tissues after ASO treatment. There are suggestions that the size difference is a determining factor for a pathogenic or protective role associated with VAT and SAT, respectively [ 21 , 22 , 23 ]. It has been demonstrated that obese subjects without metabolic complications have, in contrast to obese with metabolic impairments, smaller and more numerous adipocytes in WAT accompanied with a lower degree of inflammation [ 23 ].…”

“…It has been demonstrated that obese subjects without metabolic complications have, in contrast to obese with metabolic impairments, smaller and more numerous adipocytes in WAT accompanied with a lower degree of inflammation [ 23 ]. In a population of 60 patients with obesity, where two-thirds of them met the criteria for the metabolic syndrome, large adipocytes from SAT were associated with a worse gluco-metabolic profile than large adipocytes from VAT [ 22 ]. As a possible explanation for this difference, it was suggested that because adipocytes from SAT show a lower expandability which limits the ability of lipid storage, lipid accumulation occurs in other tissues (hepatocytes, myocytes, β-cells), which causes impaired metabolism such as insulin resistance [ 22 ].…”

The Effect of Magnesium Supplementation on Endothelial Function: A Randomised Cross-Over Pilot Study

“…BMI only became significant after adding saturated fat intake and age suggesting that part of the reason BMI may be positively associated with FMD may be due its correlation with saturated fat and age and adjusting for these reveals the unexpected positive association. Although in a cross-sectional study larger visceral adipocytes were associated with lower FMD there was no association between BMI and visceral adipose size [36]. Thus an increased BMI may not necessarily have an adverse effect.…”

Cardiac-derived TGF-β1 confers resistance to diet-induced obesity through the regulation of adipocyte size and function

“…To elucidate the mechanisms responsible for altered response to high-fat diet observed in TGF-β1 mutant mice, we performed unbiased RNA expression analysis in pgWAT. This depot was chosen as visceral white adipose depot is most critical for metabolic dysfunction in response to diet challenges [ 17 , 18 ]. This analysis revealed a profound impact of TGF-β1 on the transcriptome of pgWAT under both control and high-fat diet conditions ( Figure 4 A, Table S2 and Table S3 ).…”