Abstract
White adipose tissue has distinctive angiogenic properties. White adipocytes are capable
of producing vascular endothelial growth factor (VEGF) in response to insulin and
catecholamines. Recognizing the dual functions of adipose tissue as an endocrine/metabolic
organ and fuel storage depot with an inimitable ability to adjust its organ mass,
our aim was to determine whether fasting would affect adipocyte VEGF165 production. Rats were fed ad libitum, then fasted for 24 hours, and then refed after the 24-hour fast. The isolated white
adipocytes from each group and blood endocrine/metabolic profiles were examined at
each stage, yielding three sets of results. Using cultured adipocytes, fasting caused
a two-fold increase in VEGF165 formation compared to fed rats that normalized after refeeding. Likewise, freshly
prepared adipocytes manifested a three-fold augmentation in adipocyte VEGF165 mRNA expression and a 60 % increase the transcriptional regulator hypoxia-inducible
factor 1 (HIF-1α) that normalized after refeeding. Blood studies revealed the expected
fasting-related alterations in glucose, β-hydroxybutyrate and corticosterone. Plasma
VEGF concentrations were attenuated by 26 % with fasting, and did not normalize with
refeeding. Multiple linear regression analyses uncovered statistically significant
inverse correlations between plasma VEGF and blood β-hydroxybutyrate or serum corticosterone.
Blood glucose, in contrast, correlated directly with plasma VEGF. We will discuss
the potential role of enhanced adipocyte VEGF formation during starvation in light
of the known actions of this factor on vascular endothelial mitogenesis and permeability.
Key words
Fasting - Adipose tissue - Vascular permeability - Hypoxia-inducible factor 1
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G. Mick
University of Alabama at Birmingham · Dept. of Pediatrics · Endocrinology
1600 7th Ave South ACC 608 · Birmingham · AL 35233 · USA ·
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