Cardiovascular complications of obesity are on the rise; therefore, this study set out to determine if adipose-specific ablation of vascular endothelial growth factor-A (VEGF-A) plays a role in the maintenance of aortic structure and function.
This study provides experimental evidence of the possible correlation between AT miR-20b-miR-296-Let-7f with obesity and T2D, which might involve vascular endothelial growth factor and WNT-dependent pathways that are regulated by six different genes, suggesting a novel signaling pathway that could be important for understanding the mechanisms underlying the AT dysfunction associated with obesity and T2D.
We previously reported that universal repression of vascular endothelial growth factor (VEGF) leads to brown-like adipocyte development in white adipose tissues, and that these mice are resistant to obesity (Lu X et al.Endocrinology 153: 3123-3132, 2012).
Our results show a significantly higher immunohistochemical expression of VEGF and eNOS in the endothelium of placentas from obese women than in controls, whereas the immunoexpression of iNOS was comparable in the two groups.
It is not known to what extent inflammation precedes the development of obesity.MethodsIn a cohort of 882 infants born before 28 weeks of gestation, we examined relationships between concentrations of 25 inflammation-related proteins in blood obtained during the first two postnatal weeks and body mass index at 2 years of age.ResultsAmong children delivered for spontaneous indications (n=734), obesity was associated with elevated concentrations of four proteins (IL-1β, IL-6, TNF-R1, and MCP-1) on the first postnatal day; one protein (IL-6) on postnatal day 7; and two proteins (ICAM-3 and VEGF-R1) on postnatal day 14.
(2018) provide mechanistic insight on the role of obesity in the development of anti-VEGF drug resistance in human patients and murine models of breast cancer.
Abdominal adipose tissue (AbdAT) levels of thirteen microRNAs (miRNAs), SFRP4, and VEGF in lean nondiabetic subjects (<i>n</i> = 7), subjects with obesity (<i>n</i> = 5), and subjects with obesity and type 2 diabetes (T2DM) (<i>n</i> = 5) were measured by qPCR.
Our results suggested that high vascular endothelial growth factor levels were significantly associated with overweight in Japanese males but high vascular endothelial growth factor levels did not necessarily cause obesity.
Loss of TPCs can lead to obesity and hypercholesterolemia, and to a slow-down of intracellular virus and bacterial toxin trafficking, it can affect VEGF-induced neoangiogenesis, autophagy, human hair pigmentation or the acrosome reaction in sperm.
BCa presence was associated to elevated levels of IR (glucose, triglycerides) and tumor-derived (VEGF) markers, especially in overweight/obese patients.
In conclusion, exercise initiates increases in factors related to angiogenic processes and may promote alterations in macrophage inflammation in SAT.<b>NEW & NOTEWORTHY</b> Acute exercise in overweight/obese adults increased subcutaneous adipose tissue (SAT) mRNA expression of VEGFA, an important regulator of angiogenesis and capillary growth.
Similarly, a strong interdependence with vascular endothelial growth factor (VEGF) gene expression was also described; in fact, LPIN1 and VEGF expression levels were significantly decreased with obesity to a similar extent.
The VEGF -460 genotype was predictive of retinopathy, even after controlling for blood pressure, glycemic control, duration of diabetes, and obesity (P = 0.02).