Lipid metabolism in omental adipose tissue during operative surgery1

Samra, Jaswinder S.; Sved, Paul; Sullivan, David; Hugh, Thomas J.; Smith, Ross C.

doi:10.1016/j.jss.2004.08.032

Cited by 5 publications

(5 citation statements)

References 24 publications

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“…It is interesting to note that the NEFA concentrations found in this vein (presumably draining almost exclusively visceral fat) were very similar to that in veins which drain subcutaneous abdominal fat (∼1500 µmol/l) [12]. In contrast with these in vitro studies, the in vivo studies of Samra et al [11] found that the suppression of lipolysis in the intra-abdominal fat depot in response to glucose-stimulated hyperinsulinaemia was almost complete, suggesting that the intra-abdominal fat depot behaves in an identical fashion with other fat depots. These findings corroborate the studies of Jensen and coworkers because the extra-abdominal fat depot is almost invariably greater in mass compared with the intra-abdominal fat depot.…”

Section: Introductionmentioning

confidence: 60%

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Adipose tissue function in the insulin-resistance syndrome

Tan¹,

Karpe²

2005

Biochem. Soc. Trans

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Insulin resistance is often seen as a consequence of obesity and there are several possible links between adipose tissue function and insulin resistance determined in other organs such as skeletal muscle or liver. One such link is the regulation of NEFA (non-esterified fatty acid) delivery to the rest of the body. Simplistically, an expanded adipose tissue mass delivers more NEFA to the systemic circulation and these fatty acids compete for substrate utilization in skeletal muscle, which in turn reduces glucose utilization. This increases blood glucose concentration and provides the stimulus for increased insulin secretion and hyperinsulinaemia is a key feature of the insulin-resistance syndrome. However, there is abundant evidence that adipose tissue is exquisitely insulin sensitive and hyperinsulinaemia may therefore lead to a constant lipolytic inhibition in adipose tissue. Consequently, the main function of adipose tissue, to rapidly switch between fat uptake and fat release, will be hampered. Adipose tissue blood flow is the conveyor of signals and substrates to and from the adipose tissue. In healthy people adipose tissue blood flow is much enhanced by food intake, whereas in insulin-resistant subjects this response is blunted. This is another facet of unresponsiveness of adipose tissue in the insulin-resistance syndrome.

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Section: Introductionmentioning

confidence: 60%

“…However, Samra et al [11] recently sampled blood from veins draining omental fat tissue during abdominal surgery. However, Samra et al [11] recently sampled blood from veins draining omental fat tissue during abdominal surgery.…”

Section: Introductionmentioning

confidence: 99%

Adipose tissue function in the insulin-resistance syndrome

Tan¹,

Karpe²

2005

Biochem. Soc. Trans

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“…Although a NEFA enzyme assay was commercially available and has been used previously for various applications including monitoring adipocyte metabolism in vitro [4–7, 22] and in vivo (in plasma),[23, 24] the enzyme assay was designed for absorbance-based detection. Conversion of the NEFA assay to fluorescence detection was desirable for on-chip monitoring and automation to improve sensitivity in microfluidic channels.…”

Section: Resultsmentioning

confidence: 99%

Reversibly sealed multilayer microfluidic device for integrated cell perfusion and on-line chemical analysis of cultured adipocyte secretions

et al. 2010

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A three-layer microfluidic device was developed that combined perfusion of cultured cells with on-line chemical analysis for near real-time monitoring of cellular secretions. Two layers were reversibly sealed to form a cell chamber that could allow cells grown on coverslips to be loaded directly into the chip. The outlet of the chamber was in fluidic contact with a third layer that was permanently bonded. Perfusate from the cell chamber flowed into this third layer where a fluorescence enzyme assay for non-esterified fatty acid (NEFA) was performed on-line. The device was used to monitor efflux of NEFAs from cultured adipocytes with 83 s temporal resolution. Perfusion of murine 3T3-L1 cultured adipocytes resulted in an average basal concentration of 24.2 ± 2.4 μM NEFA (SEM, n = 6) detected in the effluent corresponding to 3.31 × 10−5 nmol cell−1 min−1. Upon pharmacological treatment with a β-adrenergic agonist to stimulate lipolysis, a 6.9 ± 0.7-fold (SEM, n = 6) sustained increase in NEFA secretion was observed. This multilayer device was capable of monitoring NEFA from ~6 250 adipocytes This multilayer device provides a versatile platform that could be adapted for use with other cell types to study corresponding cellular secretions.

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“…In vitro, the degree of inhibition of lipolysis and stimulation of fatty acid re-esterification seen when adipocytes are exposed to insulin depends on the source of adipocytes: those from visceral adipose tissue show a blunted response to insulin compared with those from subcutaneous adipose tissue [13,14]. In contrast with these in vitro studies, the in vivo studies of Samra et al [11] found that the suppression of lipolysis in the intra-abdominal fat depot in response to glucose-stimulated hyperinsulinaemia was almost complete, suggesting that the intra-abdominal fat depot behaves in an identical fashion with other fat depots.…”

Section: Introductionmentioning

confidence: 97%

“…However, Samra et al [11] recently sampled blood from veins draining omental fat tissue during abdominal surgery. It is interesting to note that the NEFA concentrations found in this vein (presumably draining almost exclusively visceral fat) were very similar to that in veins which drain subcutaneous abdominal fat (∼1500 µmol/l) [12].…”

Section: Introductionmentioning

confidence: 99%