Glyceride-Fatty Acid and Free Fatty Acid Uptake by Human Adipose Tissue in Obesity

1973 ◽  
Vol 44 (4) ◽  
pp. 18P-19P
Author(s):  
J. P. D. Wilson ◽  
R. Gutman ◽  
D. J. Galton
2018 ◽  
Vol 78 (3) ◽  
pp. 398-406 ◽  
Author(s):  
Keith N. Frayn

The present paper results from my receiving the Nutrition Society's first Blaxter Award, and describes briefly my academic history. My interest in human fat metabolism began in the Medical Research Council's Trauma Unit, studying metabolic changes in critically ill patients and their responses to nutrition. On moving to Oxford in 1986, I began to study pathways for depositing fat in adipose tissue. This involved the development of new methodologies, in particular, a technique for measurement of arterio-venous differences of metabolite concentrations across human adipose tissue beds, primarily the subcutaneous anterior abdominal depot. Our early studies showed that this tissue is dynamic in its metabolic behaviour, responding rapidly (within minutes) to changes in nutritional state. This led to an understanding of adipose tissue as playing an essential role in metabolic health, by capturing incoming dietary fatty acids, storing them as TAG and releasing them when needed, analogous to the role of the liver in glucose metabolism; we called this ‘buffering’ of fatty acid fluxes. In obesity, the mass of adipose tissue expands considerably, more than is often appreciated from BMI values. We confirmed other observations of a strong suppression of release of NEFA from adipose tissue in obesity, tending to normalise circulating NEFA concentrations. A corollary, however, is that fatty acid uptake must be equally suppressed, and this disrupts the ‘buffering’ capacity of adipose tissue, leading to fat deposition in other tissues; ectopic fat deposition. This, in turn, is associated with many metabolic abnormalities linked to obesity.


1984 ◽  
Vol 102 (3) ◽  
pp. 381-386 ◽  
Author(s):  
R. Gross ◽  
P. Mialhe

ABSTRACT To elucidate the hypolipacidaemic effect of insulin in ducks, its action on the uptake of free fatty acids (FFA) by duck hepatocytes was determined. At low doses (10 mu./l) insulin stimulated FFA uptake. This effect was not observed with higher doses of insulin (20, 30 and 50 mu./l). Growth hormone at physiological concentrations and corticosterone (14·4 nmol/l) decreased basal activity, probably by reducing glucose metabolism and consequently α-glycerophosphate (α-GP) supply. Insulin was able to reverse the inhibition induced by GH and corticosterone on both FFA uptake and α-GP production. These results therefore suggest that the hypolipacidaemic effect of insulin may be partly mediated by its action on hepatic FFA uptake. J. Endocr. (1984) 102, 381–386


2005 ◽  
Vol 288 (3) ◽  
pp. E547-E555 ◽  
Author(s):  
Ana Paola Uranga ◽  
James Levine ◽  
Michael Jensen

Oxidation and adipose tissue uptake of dietary fat can be measured by adding fatty acid tracers to meals. These studies were conducted to measure between-study variability of these types of experiments and assess whether dietary fatty acids are handled differently in the follicular vs. luteal phase of the menstrual cycle. Healthy normal-weight men ( n = 12) and women ( n = 12) participated in these studies, which were block randomized to control for study order, isotope ([3H]triolein vs. [14C]triolein), and menstrual cycle. Energy expenditure (indirect calorimetry), meal fatty acid oxidation, and meal fatty acid uptake into upper body and lower body subcutaneous fat (biopsies) 24 h after the experimental meal were measured. A greater portion of meal fatty acids was stored in upper body subcutaneous adipose tissue (24 ± 2 vs. 16 ± 2%, P < 0.005) and lower body fat (12 ± 1 vs. 7 ± 1%, P < 0.005) in women than in men. Meal fatty acid oxidation (3H2O generation) was greater in men than in women (52 ± 3 vs. 45 ± 2%, P = 0.04). Leg adipose tissue uptake of meal fatty acids was 15 ± 2% in the follicular phase of the menstrual cycle and 10 ± 1% in the luteal phase ( P = NS). Variance in meal fatty acid uptake was somewhat ( P = NS) greater in women than in men, although menstrual cycle factors did not contribute significantly. We conclude that leg uptake of dietary fat is slightly more variable in women than in men, but that there are no major effects of menstrual cycle on meal fatty acid disposal.


2014 ◽  
Vol 307 (4) ◽  
pp. E374-E383 ◽  
Author(s):  
Myriam Aouadi ◽  
Pranitha Vangala ◽  
Joseph C. Yawe ◽  
Michaela Tencerova ◽  
Sarah M. Nicoloro ◽  
...  

Proinflammatory pathways in adipose tissue macrophages (ATMs) can impair glucose tolerance in obesity, but ATMs may also be beneficial as repositories for excess lipid that adipocytes are unable to store. To test this hypothesis, we selectively targeted visceral ATMs in obese mice with siRNA against lipoprotein lipase (LPL), leaving macrophages within other organs unaffected. Selective silencing of ATM LPL decreased foam cell formation in visceral adipose tissue of obese mice, consistent with a reduced supply of fatty acids from VLDL hydrolysis. Unexpectedly, silencing LPL also decreased the expression of genes involved in fatty acid uptake (CD36) and esterification in ATMs. This deficit in fatty acid uptake capacity was associated with increased circulating serum free fatty acids. Importantly, ATM LPL silencing also caused a marked increase in circulating fatty acid-binding protein-4, an adipocyte-derived lipid chaperone previously reported to induce liver insulin resistance and glucose intolerance. Consistent with this concept, obese mice with LPL-depleted ATMs exhibited higher hepatic glucose production from pyruvate and glucose intolerance. Silencing CD36 in ATMs also promoted glucose intolerance. Taken together, the data indicate that LPL secreted by ATMs enhances their ability to sequester excess lipid in obese mice, promoting systemic glucose tolerance.


1961 ◽  
Vol 108 (1) ◽  
pp. 89-91 ◽  
Author(s):  
J. J. Spitzer ◽  
W. T. McElroy ◽  
B. Issekutz

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