Short- and long-term insulin-like effects of monoamine oxidases and semicarbazide-sensitive amine oxidase substrates in cultured adipocytes

Carpéné, Christian; Daviaud, Danièle; Boucher, Jérémie; Bour, Sandy; Visentin, Virgile; Grès, Sandra; Duffaut, Carine; Fontana, E.; Testar, Xavier; Saulnier-Blache, Jean Sébastien; Valet, Philippe

doi:10.1016/j.metabol.2006.06.011

Cited by 35 publications

(19 citation statements)

References 37 publications

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“…Monoamine oxidases are highly expressed in endothelial and smooth muscle cells and adipocytes, and their expression is induced during adipocyte differentiation (5) and is known to stimulate adipogenesis (15). Furthermore, monoamine oxidase substrates mimic diverse insulin effects in adipocytes, including activation of glucose transport, stimulation of lipogenesis, and inhibition of lipolysis (8,31,45). Thus, Dex-induced amine oxidases have many potential roles in adipose tissue function, including adipogenesis and adipocyte metabolism as well as stress/defense response.…”

Section: Dex Increases Expression Of Genes Involved In Protection Agamentioning

confidence: 99%

Pathways regulated by glucocorticoids in omental and subcutaneous human adipose tissues: a microarray study

Lee

Gong

Burkey

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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Glucocorticoids (GC) are powerful regulators of adipocyte differentiation, metabolism, and endocrine function and promote the development of upper body obesity, especially visceral fat stores. To provide a comprehensive understanding of how GC affect adipose tissue and adipocyte function, we analyzed patterns of gene expression (HG U95 Affymetrix arrays) after culture of abdominal subcutaneous (Abd sc) and omental (Om) adipose tissues from severely obese subjects (3 F, 1 M) in the presence of insulin or insulin (7 nM) plus dexamethasone (Dex, 25 nM) for 7 days. About 20% (561 genes in Om and 569 genes in sc) of 2,803 adipose expressed genes were affected by long-term GC. While most of the genes (90%) were commonly regulated by Dex in both depots, 26 in Om and 34 in Abd sc were affected by Dex in only one depot. 60% of the commonly upregulated genes were involved in metabolic pathways and were expressed mainly in adipocytes. Dex suppressed genes in immune/ inflammatory (IL-6, IL-8, and MCP-1, expressed in nonadipocytes) and proapoptotic pathways, yet induced genes related to the acute-phase response (SAA, factor D, haptoglobin, and RBP4, expressed in adipocytes) and stress/defense response. Functional classification analysis showed that Dex also induced expression levels of 22 transcription factors related to insulin action and lipogenesis (LXR␣, STAT5␣, SREBP1, and FoxO1) and immunity/adipogenesis (TSC22D3) while suppressing 17 transcription factors in both depots. Overall, these studies reveal the powerful effects of GC on gene networks that regulate many key functions in human adipose tissue.OBESITY, particularly visceral and upper body obesity, is associated with increased risk for obesity-related comorbidities, including type 2 diabetes and cardiovascular diseases. Glucocorticoids (GC) are powerful regulators of fat deposition and distribution, as is most clearly shown by the visceral obesity associated with Cushing's syndrome. In human obesity, the prereceptor activation of cortisone to cortisol via 11␤-hydroxysteroid dehydrogenase (HSD1) is upregulated in both omental (Om) and abdominal subcutaneous (Abd sc) adipose tissues (26,34,36), and this difference is exaggerated after culture with GC (26). The resulting increases in local cortisol generation are thought to promote fat deposition, most markedly in visceral depots but also in Abd sc adipose tissue. However, very little is known about the molecular mechanisms that mediate depot differences in the effects of GC on adipocyte function. Our previous studies of leptin and lipoprotein lipase demonstrated differences in sensitivity and responsiveness to GC effects in Om and Abd sc (18,35). In the present study, we used microarray approaches to compare the global effects of long-term culture with GC on gene expression in Om and Abd sc tissues.Nutritional state affects cortisol production as well as responsiveness to cortisol. Administration of GC in the overnight-fasted state (low insulin) has catabolic effects on adipocytes [increased lipolysis (13)] and doe...

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Section: Dex Increases Expression Of Genes Involved In Protection Agamentioning

confidence: 99%

Pathways regulated by glucocorticoids in omental and subcutaneous human adipose tissues: a microarray study

Lee

Gong

Burkey

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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“…When confluent cells were induced to differentiate by 50 nM insulin with medium changed daily during 8 days. Cells were starved from serum overnight prior to glucose transport assay that consisted in a 45-min preincubation with the tested compounds followed by a 10-min incubation with a 2-DG isotopic dilution (140 nmoles; 500000 dpm/well) and a determination of the internalized radioactivity as previously defined (4). Table I, two study groups were constituted.…”

Section: Chemicalsmentioning

confidence: 99%

Lack of direct insulin-like action of visfatin/Nampt/PBEF1 in human adipocytes

2009

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Visfatin, a protein identified as a secretion product of visceral fat in humans and mice, is also expressed in different anatomical locations, and is known as pre-B cell-colony enhancing factor (PEBF1). It is also an enzyme displaying nicotinamide phosphoribosyltransferase activity (Nampt). The evidence that levels of visfatin correlate with visceral fat mass has been largely debated and widely extended to other regulations in numerous clinical studies and in diverse animal models. On the opposite, the initial findings regarding the capacity of visfatin/Nampt/PEBF1 to bind and to activate the insulin receptor have been scarcely reproduced, and even were contradicted in recent reports. Since the putative insulin mimicking effects of visfatin/Nampt/PEBF1 have never been tested on mature human adipocytes, at least to our knowledge, we tested different human visfatin batches on human fat cells freshly isolated from subcutaneous abdominal fat and exhibiting high insulin responsiveness. Up to 10 nM, visfatin was devoid of clear activatory action on glucose transport in human fat cells while, in the same conditions, insulin increased by more than threefold the basal 2-deoxyglucose uptake. Moreover, visfatin was unable to mimic the lipolysis inhibition induced by insulin. Visfatin definitively cannot be considered as a direct activator of insulin signalling in human fat cells. Nevertheless itsin vivo effects on insulin release and on glucose handling deserve to further study the role of this multifunctional extracellular enzyme in obese and diabetic states.

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“…In fact, it has been recently reported that VHFD mice respond to a single injection of hexaquis(benzylammonium) decavanadate, which is a complex salt of vanadium and benzylamine, by an improvement of glucose tolerance (9). Although the demonstration of insulin-like actions of vanadate plus benzylamine is of interest, it remained to be clarified whether benzylamine alone is also able to act on a rodent model of diabetes for at least two reasons: 1) vanadium is potently toxic and, in spite of increasing its bioavailability at the targets of insulin mimicry, it may alter overall phosphorus metabolism; 2) the presence of vanadate does not improve the insulin-like effects of benzylamine in human adipocytes (13) or murine preadipocytes (7). Thus, it might be suspected that the synergism observed between the amine and the transition metal in the diabetic models studied so far could not be easily extrapolated to diabetic patients.…”

Section: Discussionmentioning

confidence: 99%

Influence of acute and chronic administration of benzylamine on glucose tolerance in diabetic and obese mice fed on very high-fat diet

Iffiú-Soltész

Prévot

Grès

et al. 2007

J. Physiol. Biochem.

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The combination of vanadate plus benzylamine has been reported to stimulate glucose transport in rodent adipocytes and to mimic other insulin actions in diverse studies. However, benzylamine alone activates glucose uptake in human fat cells and increases glucose tolerance in rabbits. The aim of this work was to unravel the benzylamine antihyperglycemic action and to test whether its chronic oral administration could restore the defective glucose handling of mice rendered slightly obese and diabetic by very high-fat diet (VHFD). When VHFD mice were i.p. injected with benzylamine at 0.7 to 700 micromol/kg before glucose tolerance test, they exhibited reduced hyperglycemic response without alteration of insulin secretion. Whole body glucose turnover, as assessed by the glucose isotopic dilution technique, was unchanged in mice perfused with benzylamine (total dose of 75 micromol/kg). However, their in vivo glycogen synthesis rate was increased. Benzylamine appeared therefore to directly facilitate glucose utilisation in peripheral tissues. When given chronically at 2000 or 4000 micromol/kg/d in drinking water, benzylamine elicited a slight reduction of water consumption but did not change body weight or adiposity and did not modify oxidative stress markers. Benzylamine treatment improved glucose tolerance but failed to normalize the elevated glucose fasting plasma levels of VHFD mice. There was no influence of benzylamine ingestion on lipolytic activity, basal and insulin-stimulated glucose uptake, and on inflammatory adipokine expression in adipocytes. The improvement of glucose tolerance and the lack of adverse effects on adipocyte metabolism, reported here in VHFD mice allow to consider orally given benzylamine as a potential antidiabetic strategy which deserves to be further studied in other diabetic models.

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Short- and long-term insulin-like effects of monoamine oxidases and semicarbazide-sensitive amine oxidase substrates in cultured adipocytes

Cited by 35 publications

References 37 publications

Pathways regulated by glucocorticoids in omental and subcutaneous human adipose tissues: a microarray study

Pathways regulated by glucocorticoids in omental and subcutaneous human adipose tissues: a microarray study

Lack of direct insulin-like action of visfatin/Nampt/PBEF1 in human adipocytes

Influence of acute and chronic administration of benzylamine on glucose tolerance in diabetic and obese mice fed on very high-fat diet

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