scholarly journals Blood flow and fatty acid release by cervical adipose tissue of rabbits

1973 ◽  
Vol 235 (1) ◽  
pp. 1-8 ◽  
Author(s):  
M. J. Hardman ◽  
D. Hull
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Release ◽  
Acid Release

Control of fat cell phosphatidate phosphohydrolase by lipolytic agents

1981 ◽  
Vol 59 (1) ◽  
pp. 9-15 ◽  
Author(s):  
F. Moller ◽  
K. H. Wong ◽  
P. Green
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Cyclic Amp ◽  
Hormone Sensitive Lipase ◽  
Dibutyryl Cyclic Amp ◽  
Fat Cell ◽  
Adrenergic Antagonist ◽  
Phosphatidate Phosphohydrolase ◽  
Fatty Acid Release ◽  
Acid Release

The Mg2+-dependent phosphatidate phosphohydrolase activity increased in the microsomal and decreased in the soluble fraction of isolated rat fat cells incubated for short periods with the lipolytic hormones or agents, epinephrine, cyclic AMP, theophylline, and dibutyryl cyclic AMP. Adrenocorticotropin, on the other hand, increased not only the microsomal but also the soluble activity. The increases in microsomal activity ranged from 30 to 134% with epinephrine to almost 200% with dibutyryl cyclic AMP. The decreases in soluble activity were more modest. The effect of epinephrine was inhibited by the β-adrenergic antagonist propranolol while the α-antagonist phentolamine enhanced it. These results strongly suggest that the fat cell phosphatidate phosphohydrolase is controlled through the β-adrenergic receptor and the activity of adenylate cyclase. Lipolysis, as measured by fatty acid release, was stimulated in a similar pattern as the microsomal activity suggesting parallel activation of the hormone sensitive lipase and phosphatidate phosphohydrolase. It is speculated that the activation of this lipogenic enzyme by lipolytic stimuli may represent a mechanism whereby fatty acid release from adipose tissue may be modulated and intracellular fatty acid accumulation maybe counteracted during accelerated lipolysis in adipose tissue.

scholarly journals Factors regulating subcutaneous adipose tissue storage, fibrosis, and inflammation may underlie low fatty acid mobilization in insulin-sensitive obese adults

2017 ◽  
Vol 313 (4) ◽  
pp. E429-E439 ◽  
Author(s):  
Douglas W. Van Pelt ◽  
Lisa M. Guth ◽  
Abigail Y. Wang ◽  
Jeffrey F. Horowitz
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Subcutaneous Adipose Tissue ◽  
Obese Adults ◽  
Tissue Samples ◽  
Pathway Activation ◽  
Fatty Acid Release ◽  
Acid Release ◽  
Subcutaneous Adipose ◽  
Fatty Acid Mobilization

Although the rate of fatty acid release from adipose tissue into the systemic circulation is very high in most obese adults, some obese adults maintain relatively low rates of fatty acid release, which helps protect them against the development of systemic insulin resistance. The primary aim of this study was to identify factors in adipose tissue that may underlie low vs. high rates of fatty acid mobilization in a relatively homogeneous cohort of obese adults. We measured systemic fatty acid rate of appearance (FA Ra) via 13C-palmitate isotope dilution, and we obtained subcutaneous abdominal adipose tissue samples from 30 obese adults (BMI: 38 ± 1 kg/m2, age: 30 ± 2 yr) after an overnight fast. We then measured insulin sensitivity using a hyperinsulinemic-euglycemic clamp. Confirming our previous work, insulin sensitivity was inversely proportional to FA Ra ( R2 = 0.50; P < 0.001). Immunoblot analysis of subcutaneous adipose tissue samples revealed that, compared with obese adults with high FA Ra, those with low FA Ra had lower markers of lipase activation and higher abundance of glycerol-3-phosphate acyltransferase, which is a primary enzyme for fatty acid esterification. Microarray and pathway analysis provided evidence of lower fibrosis and lower SAPK/JNK pathway activation in obese adults with low FA Ra compared with those with high FA Ra. Our findings suggest that alterations in factors regulating triglyceride storage in adipose tissue, along with lower fibrosis and inflammatory pathway activation, may underlie maintenance of a relatively low FA Ra in obesity, which may help protect against the development of insulin resistance.

FAT/CD36 regulates PEPCK expression in adipose tissue

2013 ◽  
Vol 304 (5) ◽  
pp. C478-C484 ◽  
Author(s):  
Zhongxiao Wan ◽  
Sarthak Matravadia ◽  
Graham P. Holloway ◽  
David C. Wright
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Mrna Expression ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Fatty Acid Uptake ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Expression Of Genes ◽  
Fatty Acid Release ◽  
Acid Release

Fatty acid translocase (FAT)/CD36 has been extensively studied for its role in facilitating fatty acid uptake. Recent findings have also demonstrated that this protein regulates adipocyte lipolysis and may modulate fatty acid reesterification. As FAT/CD36 has been shown to control the expression of genes involved in fatty acid oxidation in adipocytes, we reasoned that this protein might also control the expression of enzymes involved in fatty acid reesterification. In adipose tissue from FAT/CD36 knockout (KO) mice, we found that glycerol and fatty acid release were reduced and this was associated with reductions in adipose triglyceride lipase. Decreases in lipolysis were paralleled by increases in the free fatty acid-to-glycerol ratio and reductions in primary and fractional rates of fatty acid reesterfication in cultured adipose tissue from FAT/CD36 KO mice. Reductions in reesterfication were associated with decreases in the mRNA expression and protein content of phosphoenolpyruvate carboxykinase (PEPCK). To determine if reductions in lipolysis could lead to decreases in PEPCK mRNA expression, we treated cultured mouse adipose tissue with the lipase inhibitor CAY10499 (2 μM) and found that this resulted in an ∼50% reduction in PEPCK mRNA expression. Treatment with hexarelin (10 μM, 12 h), a CD36 agonist, increased PEPCK mRNA expression independent of lipolysis. Collectively, our results provide novel evidence that FAT/CD36 regulates PEPCK in adipose tissue and that this could be secondary to reductions in lipolysis.

Sign in / Sign up

Export Citation Format

Share Document