Peripheral fat metabolism during infusion of an exogeneous triacylglycerol emulsion

Samra, Jaswinder S.; Giles, Sarah L.; Summers, L. K. M.; Evans, Rhys; Arner, Peter; Humphreys, S. M.; Clark, M. L.; Frayn, Keith N.

doi:10.1038/sj.ijo.0800664

Cited by 24 publications

(27 citation statements)

References 41 publications

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“…The duration of the infusion suggests that this may be due to direct gene transactivation, probably by PPA R-2. Interesti n g l y, mean plasma leptin levels were unaffected by the 5-h Intralipid plus heparin (2.8 ± 0.4 ng/ml) or saline infusion (2.9 ± 0.9 ng/ml) in comparison with baseline (3.2 ± 0.6 and 3.2 ±1.0 ng/ml, respectively), thus confirming the results obtained by Samra et al (26).…”

Section: R E S U Lt Ssupporting

confidence: 88%

“…Under our experimental conditions, it is unlikely that NEFA-induced leptin gene expression influenced the rate of lipolysis, since it has been shown that increased NEFA availability from an extracellular source inhibits intracellular lipolysis (26,39). The intracellular role of N E FA-induced leptin gene expression may rather be that of modulating the expression of other genes involved in the regulation of cell metabolism.…”

Section: Discussionmentioning

confidence: 84%

“…Under similar experimental conditions, a 5-h exogenous triacylglycerol emulsion infusion failed to increase plasma leptin concentrations or leptin release from adipose tissue (26). The reason why leptin mRNA is affected by NEFA infusion whereas circulating leptin levels are not remains to be explained.…”

Section: Discussionmentioning

confidence: 89%

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Induction of fatty acid translocase/CD36, peroxisome proliferator-activated receptor-gamma2, leptin, uncoupling proteins 2 and 3, and tumor necrosis factor-alpha gene expression in human subcutaneous fat by lipid infusion.

et al. 2000

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Little is known about the mechanisms involved in the preferential channeling of different fuels to fat and how the target tissue participates in this process. Dietary fatty acids have been shown to act as signaling molecules that bind and activate a new class of nuclear receptors, the peroxisome proliferator-a c t ivated receptors (PPARs). PPA R-is particularly interesting because it may have the potential to link particular fatty acids with a program of gene expression involved in lipid storage and metabolism. We investigated whether a nutrient-sensing pathway is activated by an increased availability of lipid fuels in nine normal weight male volunteers. Using reverse transcriptase-polymerase chain reaction analysis, the mRNA expression of fatty acid translocase (FAT ) / C D 3 6 , P PA R-2, leptin, uncoupling protein (UCP)-2 and U C P-3, and tumor necrosis factor (TNF)-was investigated in gluteal subcutaneous fat biopsies before and after 5 h infusions of saline or Intralipid (Pharmacia and Upjohn, Milan, Italy) plus heparin, which does not modify insulinemia. Marked increases in FAT/CD36 (724 ± 18%; P < 0.05), PPA R-2 (200 ± 8%; P < 0.05), leptin (110 ± 13%; P < 0.05), UCP-2 (120 ± 7%; P < 0.05), UCP-3 (80 ± 5%; P < 0.05), and TNFmRNA (130 ± 12%; P < 0.05) were observed in comparison with pretreatment levels, whereas there was no change after saline infusion. These data suggest that the in vivo gene expression of FAT / C D 3 6 , P PA R-2, leptin, UCP-2, UCP-3, and TNF-in subcutaneous adipose tissue is regulated by circulating lipids independent of insulin and that prolonged hyperlipidemia may therefore contribute to increased fat metabolism and storage as a result of the increased expression of these proteins. D i a b e t e s 4 9 :3 1 9-324, 2000

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Section: R E S U Lt Ssupporting

confidence: 88%

Section: Discussionmentioning

confidence: 84%

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Induction of fatty acid translocase/CD36, peroxisome proliferator-activated receptor-gamma2, leptin, uncoupling proteins 2 and 3, and tumor necrosis factor-alpha gene expression in human subcutaneous fat by lipid infusion.

et al. 2000

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“…They concluded that changes in leptin concentration were not correlated with changes in FFA concentration. Samra et al 34 showed consistent leptin release, with no change over time, following the onset of an Intralipid triacylglycerol (TG) infusion. These authors observe, however, that the TG extraction by adipose tissue was much less that that observed when TG concentration is elevated by ingestion of a fatty meal.…”

Section: Discussionmentioning

confidence: 99%

Leptin does not respond to 48 h fat deposition or mobilization in women

et al. 2003

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OBJECTIVE:To test the hypothesis that acute responses of plasma leptin concentration to energy balance manipulation are mediated by fat flux. DESIGN: Ten healthy women aged 31-63 y, mass 48-113.5 kg, fat mass 8.5-62.5 kg, were studied for 3 days in a whole-body calorimeter on two occasions. After a control day (D1) during which energy balance was maintained, diet was manipulated to induce fat deposition (FD) or mobilization (FM) of 50 g/day for 2 days (D2 & D3). A difference totalling of 194718.6 g fat was achieved between manipulations without significant effects on carbohydrate or protein balance. Fasting plasma leptin was measured on D2 and D4. RESULTS: After the control day plasma leptin concentration averaged 19.0179.8 ng/ml, and was found to be linearly related to body fat mass. After 2 days manipulation of fat balance, leptin concentrations were 21.4710.3 ng/ml (FD) and 21.2711.3 ng/ ml (FM). There was no significant difference between treatments in either control day or postmanipulation leptin concentrations, nor did the treatments induce any differences in glucose or insulin concentration responses. CONCLUSION: Although in states of energy balance leptin concentration is linearly related to fat mass, acute modulation of leptin concentration during energy imbalance is not mediated by fat flux.

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“…This is clearly an unphysiological situation, but if it is mimicked acutely by intravenous infusion of a TG emulsion, producing no detectable increase in plasma insulin, there is a marked decrease in NEFA release from adipose tissue, reflecting a suppression of HSL activity. 168,169 This experiment seems to imply that there is some signal that responds to increased nutrient availability to regulate net fat storage independently of insulin, and in this case presumably also independently of the SNS.…”

Section: Pulsatilitymentioning

confidence: 96%

Integrative physiology of human adipose tissue

et al. 2003

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Adipose tissue is now recognised as a highly active metabolic and endocrine organ. Great strides have been made in uncovering the multiple functions of the adipocyte in cellular and molecular detail, but it is essential to remember that adipose tissue normally operates as a structured whole. Its functions are regulated by multiple external influences such as autonomic nervous system activity, the rate of blood flow and the delivery of a complex mix of substrates and hormones in the plasma. Attempting to understand how all these factors converge and regulate adipose tissue function is a prime example of integrative physiology. Adipose tissue metabolism is extremely dynamic, and the supply of and removal of substrates in the blood is acutely regulated according to the nutritional state. Adipose tissue possesses the ability to a very large extent to modulate its own metabolic activities, including differentiation of new adipocytes and production of blood vessels as necessary to accommodate increasing fat stores. At the same time, adipocytes signal to other tissues to regulate their energy metabolism in accordance with the body's nutritional state. Ultimately adipocyte fat stores have to match the body's overall surplus or deficit of energy. This implies the existence of one (or more) signal(s) to the adipose tissue that reflects the body's energy status, and points once again to the need for an integrative view of adipose tissue function.

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Peripheral fat metabolism during infusion of an exogeneous triacylglycerol emulsion

Cited by 24 publications

References 41 publications

Induction of fatty acid translocase/CD36, peroxisome proliferator-activated receptor-gamma2, leptin, uncoupling proteins 2 and 3, and tumor necrosis factor-alpha gene expression in human subcutaneous fat by lipid infusion.

Induction of fatty acid translocase/CD36, peroxisome proliferator-activated receptor-gamma2, leptin, uncoupling proteins 2 and 3, and tumor necrosis factor-alpha gene expression in human subcutaneous fat by lipid infusion.

Leptin does not respond to 48 h fat deposition or mobilization in women

Integrative physiology of human adipose tissue

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