scholarly journals Distribution of Abdominal Visceral and Subcutaneous Adipose Tissue and Metabolic Syndrome in a Korean Population

Diabetes Care ◽  
2011 ◽  
Vol 34 (2) ◽  
pp. 504-506 ◽  
Author(s):  
S. Kim ◽  
B. Cho ◽  
H. Lee ◽  
K. Choi ◽  
S. S. Hwang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Korean Population ◽  
Subcutaneous Adipose

scholarly journals Influence of birth weight on gene regulators of lipid metabolism and utilization in subcutaneous adipose tissue and skeletal muscle of neonatal pigs

Reproduction ◽  
2009 ◽  
Vol 138 (3) ◽  
pp. 609-617 ◽  
Author(s):  
P J Williams ◽  
N Marten ◽  
V Wilson ◽  
J C Litten-Brown ◽  
A M Corson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Subcutaneous Adipose Tissue ◽  
Morphological Changes ◽  
Fatty Acid Binding ◽  
Obesity And Diabetes ◽  
Subcutaneous Adipose

Epidemiological studies suggest that low-birth weight infants show poor neonatal growth and increased susceptibility to metabolic syndrome, in particular, obesity and diabetes. Adipose tissue development is regulated by many genes, including members of the peroxisome proliferator-activated receptor (PPAR) and the fatty acid-binding protein (FABP) families. The aim of this study was to determine the influence of birth weight on key adipose and skeletal muscle tissue regulating genes. Piglets from 11 litters were ranked according to birth weight and 3 from each litter assigned to small, normal, or large-birth weight groups. Tissue samples were collected on day 7 or 14. Plasma metabolite concentrations and the expression ofPPARG2,PPARA,FABP3, andFABP4genes were determined in subcutaneous adipose tissue and skeletal muscle. Adipocyte number and area were determined histologically. Expression ofFABP3and4was significantly reduced in small and large, compared with normal, piglets in adipose tissue on day 7 and in skeletal muscle on day 14. On day 7,PPARAandPPARG2were significantly reduced in adipose tissue from small and large piglets. Adipose tissue from small piglets contained more adipocytes than normal or large piglets. Birth weight had no effect on adipose tissue and skeletal muscle lipid content. Low-birth weight is associated with tissue-specific and time-dependent effects on lipid-regulating genes as well as morphological changes in adipose tissue. It remains to be seen whether these developmental changes alter an individual's susceptibility to metabolic syndrome.

scholarly journals The level of SCD1 in subcutaneous adipose tissue is associated with the presence of metabolic syndrome in morbidly obese patients

2016 ◽  
Author(s):  
Sara Garcia-Serrano ◽  
Carolina Gutierrez-Repiso ◽  
Francisca Rodriguez-Pacheco ◽  
Ailec Ho-Plagaro ◽  
Eva Garcia-Escobar ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Morbidly Obese ◽  
Obese Patients ◽  
Subcutaneous Adipose

scholarly journals Subcutaneous adipose tissue biology in metabolic syndrome

2018 ◽  
Vol 33 (1) ◽  
Author(s):  
Ishwarlal Jialal ◽  
Sridevi Devaraj
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Interleukin 1 ◽  
Plasminogen Activator Inhibitor ◽  
Retinol Binding Protein ◽  
Plasminogen Activator Inhibitor 1 ◽  
Amyloid A ◽  
Subcutaneous Adipose

AbstractMetabolic syndrome (MetS) is a common global problem that comprises the cardio-metabolic cluster and predisposes to both diabetes and cardiovascular diseases. Although the pathogenic mechanisms have not been elucidated, both increased inflammation and insulin resistance play a pivotal role. It appears that both monocyte/macrophages and adipose tissue (AT) conspire to accentuate both the pro-inflammatory state and increased insulin resistance. Whilst there are scant data on visceral adipose tissue (VAT) and epicardial adipose tissue (EAT) biology, there are data on subcutaneous adipose tissue (SAT) dysregulation. There is a significant increase in macrophages and crown-like structures in the SAT of patients with MetS. With respect to adipokines, there is an increase in plasma leptin, plasminogen activator inhibitor-1, retinol-binding protein-4 (RBP-4), chemerin, serum amyloid-A, C-reactive protein (CRP), interleukin-1, -6, -8, lipopolysaccharide, fetuin A (FetA) and a decrease in adiponectin and omentin-1. All of the abnormalities in plasma were also confirmed for SAT-secreted adipokines except for adiponectin and RBP-4 which derive largely from VAT. As many of these biomediators correlate with both insulin resistance and increased inflammation, we can posit that dysregulation of SAT is detrimental and contributes to both the pathogenesis of MetS and its sequalae. Furthermore, as future directions, much work is needed with respect to VAT/EAT biology, autophagy, sirtuins, the gut microbiome, browning of AT, to further elucidate this common syndrome and identify potential therapeutic targets to forestall its serious complications.

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