Regulation of subcutaneous adipose tissue blood flow is related to measures of vascular and autonomic function

2010 ◽  
Vol 119 (8) ◽  
pp. 313-322 ◽  
Author(s):  
Jun-ichi Funada ◽  
A. Louise Dennis ◽  
Rachel Roberts ◽  
Fredrik Karpe ◽  
Keith N. Frayn

Appropriate blood vessel function is important to cardiovascular health. Adipose tissue plays an important role in metabolic homoeostasis, and subcutaneous abdominal ATBF (adipose tissue blood flow) is responsive to nutritional stimuli. This response is impaired in obesity, suggesting parallels with endothelial function. In the present study, we assessed whether regulation of ATBF is related to the regulation of endothelial function, assessed by FMD (flow-mediated vasodilatation) of the brachial artery. Impaired FMD is a marker of atherosclerotic risk, so we also assessed relationships between ATBF and a marker of atherosclerosis, common carotid artery IMT (intima-media thickness). As ATBF is responsive to sympatho-adrenal stimuli, we also investigated relationships with HRV (heart rate variability). A total of 79 healthy volunteers (44 female) were studied after fasting and after ingestion of 75 g of glucose. FMD, fasting ATBF and the responsiveness of ATBF to glucose were all negatively related to BMI (body mass index), confirming the adverse cardiovascular effects of adiposity. FMD was related to fasting ATBF (rs=0.32, P=0.008) and, at least in males, this relationship was independent of BMI (P=0.02). Common carotid artery IMT, measured in a subset of participants, was negatively related to fasting ATBF [rs=−0.51, P=0.02 (n=20)]. On the other hand, ATBF responsiveness to glucose had no relationship with either FMD or IMT. In multiple regression models, both fasting and stimulated ATBF had relationships with HRV. In conclusion, our results show that the regulation of ATBF has features in common with endothelial function, but also relationships with autonomic cardiovascular control as reflected in HRV.

1995 ◽  
Vol 269 (6) ◽  
pp. E1059-E1066 ◽  
Author(s):  
B. Stallknecht ◽  
L. Simonsen ◽  
J. Bulow ◽  
J. Vinten ◽  
H. Galbo

Trained humans (Tr) have a higher fat oxidation during submaximal physical work than sedentary humans (Sed). To investigate whether this reflects a higher adipose tissue lipolytic sensitivity to catecholamines, we infused epinephrine (0.3 nmol.kg-1.min-1) for 65 min in six athletes and six sedentary young men. Glycerol was measured in arterial blood, and intercellular glycerol concentrations in abdominal subcutaneous adipose tissue were measured by microdialysis. Adipose tissue blood flow was measured by 133Xe-washout technique. From these measurements adipose tissue lipolysis was calculated. During epinephrine infusion intercellular glycerol concentrations were lower, but adipose tissue blood flow was higher in trained compared with sedentary subjects (P < 0.05). Glycerol output from subcutaneous tissue (Tr: 604 +/- 322 nmol.100 g-1.min-1; Sed: 689 +/- 203; mean +/- SD) as well as arterial glycerol concentrations (Tr: 129 +/- 36 microM; Sed: 119 +/- 56) did not differ between groups. It is concluded that in intact subcutaneous adipose tissue epinephrine-stimulated blood flow is enhanced, whereas lipolytic sensitivity to epinephrine is the same in trained compared with untrained subjects.


1989 ◽  
Vol 257 (4) ◽  
pp. R711-R716 ◽  
Author(s):  
D. B. West ◽  
W. A. Prinz ◽  
M. R. Greenwood

Adipose tissue blood flow was measured in five depots, and plasma concentrations of glucose, insulin, and triglyceride were measured at 0, 15, 30, and 45 min after the start of a meal in unanesthetized, freely moving rats. In addition, adipose tissue lipoprotein lipase activity was measured in four depots before and 45 min after the start of a meal. Plasma glucose was significantly elevated only at the 15-min time point, and while plasma triglyceride increased these changes did not reach significance. Plasma insulin was significantly elevated at all time points after a meal. Feeding resulted in a consistent decrease of adipose tissue blood flow expressed per gram wet weight of tissue. This decrease was maximal at 30 min after the start of feeding. The decrease in adipose tissue blood flow averaged 45% at 45 min after the start of feeding for the five depots evaluated. Lipoprotein lipase activity significantly increased in the retroperitoneal and mesenteric fat depots at 45 min after the meal start, but did not change in the epididymal or dorsal subcutaneous fat depots. These results suggest that a decrease in adipose tissue blood flow is a normal result of a meal in the rat. The regional specificity of changes in adipose tissue lipoprotein lipase activity supports the concept of regional specificity of function for adipose tissue and suggests that the mesenteric and retroperitoneal depots are particularly important for the storage of triglycerides immediately after a meal.


2012 ◽  
Vol 302 (10) ◽  
pp. E1157-E1170 ◽  
Author(s):  
Richard Sotornik ◽  
Pascal Brassard ◽  
Elizabeth Martin ◽  
Philippe Yale ◽  
André C. Carpentier ◽  
...  

According to Fick's principle, any metabolic or hormonal exchange through a given tissue depends on the product of the blood flow to that tissue and the arteriovenous difference. The proper function of adipose tissue relies on adequate adipose tissue blood flow (ATBF), which determines the influx and efflux of metabolites as well as regulatory endocrine signals. Adequate functioning of adipose tissue in intermediary metabolism requires finely tuned perfusion. Because metabolic and vascular processes are so tightly interconnected, any disruption in one will necessarily impact the other. Although altered ATBF is one consequence of expanding fat tissue, it may also aggravate the negative impacts of obesity on the body's metabolic milieu. This review attempts to summarize the current state of knowledge on adipose tissue vascular bed behavior under physiological conditions and the various factors that contribute to its regulation as well as the possible participation of altered ATBF in the pathophysiology of metabolic syndrome.


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