Correlation ofA2bARandKLF4/KLF15with Obesity-Dyslipidemia Induced Inflammation in Uygur Population

Abstract

In this paper, the researchers collected visceral adipose tissue from the Uygur population, which were divided into two groups: the normal control group (NC, n = 50, 18.0 kg/m2 ≤ BMI ≤ 23.9 kg/m2) and the obese group (OB, n = 45, BMI ≥ 28 kg/m2), and then use real-time PCR to detect the mRNA expression level of key genes involved in inflammation signaling pathway. The findings suggest that, in obese status, the lower expression level of A2bAR, KLF4, and KLF15 of visceral adipose tissue may correlate with obese-dyslipidemia induced inflammation in Uygur population.

Krüppel-Like Factors

“…Despite the prominent role of KLF15 in promoting adipocyte differentiation, Klf15 expression is decreased in WAT and BAT of wild-type mice fed a high-fat diet, as well as in db/db mice (171) . This finding is consistent with reports of reduced Klf15 expression in the visceral adipose tissue of obese individuals 171 , 172 . The relationship between reduced KLF15 expression and increased adiposity remains to be investigated.…”

“…KLF4 78 , 79 , KLF5 (83) , KLF6 91 , 92 , KLF8 (82) , KLF9 80 , 81 , KLF13 (84) , and KLF15 (85) promote adipocyte differentiation and adipose tissue expansion, whereas KLF2 (89) , KLF3 (87) , KLF7 (88) , and KLF16 (93) have the opposite effect ( Figure 4 ). Moreover, KLF3 (87) , KLF11 (126) , KLF14 (115) , and KLF15 171 , 172 promote weight gain.…”

Different lipid profiles, insulin sensitivity, and insulin resistance among Han, Uygur, and Kazak men with normal glucose tolerance in Xinjiang, China

“…According to a study by Zhang Jun et al [ 27 ], at the same BMI, Uygurs have greater waist to hip ratio values, abdominal visceral fat content, and diabetes risk than Kazaks. These differences were mainly associated with the distribution of adipose tissue in the body, changes in metabolic activity, and adipokine secretion by the adipose tissue [ 27 , 28 ]. Once again, genetics and lifestyle habits could play roles in those differences, but additional studies are necessary.…”

Distinct Molecular Mechanisms Analysis of Obesity Based on Gene Expression Profiles

“…GO enrichment analysis for up regulated genes was implemented. Enriched genes such as AMOT (angiomotin) [131], CCDC80 [132], CXCL10 [133], ERBB2 [134], KLF4 [135], LEP (leptin) [136], MFGE8 [137], SLIT2 [138], TNMD (tenomodulin) [139], ADAMTS5 [140], ELN (elastin) [141], HTRA1 [142], LUM (lumican) [143], MFAP5 [144] and IL1RN [145] were responsible for progression of obesity. Enriched genes such as ANGPT1 [146], NOTCH3 [147] and TGFBR2 [148] were associated with development of hypertension, but these genes may be responsible for progression of obesity.…”