Native fructose extracted from apple improves glucose tolerance in mice

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Fructose is one of the most abundant monosaccharide in nature. It is also the sweetest naturally occurring carbohydrate. Since decades, fructose used for food preparations is not provided by fruit or vegetable but by a chemical process of starch or inulin conversion. We processed a new method of fructose extraction from apple and investigated the acute and long term effect of this carbohydrate on glucose metabolism in C57Bl6/j mice. By using the glycemic index (GI), we have shown that one of the sugars obtained from apple, FructiLight, has a very low impact on glycemic and insulin response during acute treatment compared to other sugars. This carbohydrate, essentially constituted by fructose, has also beneficial properties when administrated for long term treatment. Indeed, as two other sugars extracted from apple (FructiSweetApple and FructiSweet67), FructiLight exposure during 21 weeks in beverage has promoted an enhancement of glucose tolerance compared to glucose treatment without affecting food intake and weight. All these results indicate that apple-extracted sugars and more precisely fructose from these fruits could be a promising way to produce new food and sweet beverages (AU)

Caffeine reduces TNFalpha up-regulation in human adipose tissue primary culture

Adipose tissue secretions play an important role in the development of obesityrelatedpathologies such as diabetes. Through inflammatory cytokines production,adipose tissue stromavascular fraction cells (SVF), and essentially macrophages, promoteadipocyte insulin resistance by a paracrine way. Since xanthine family compoundssuch as caffeine were shown to decrease inflammatory production by humanblood cells, we investigated the possible effect of caffeine on Tumor Necrosis Factoralpha (TNFalpha) and Interleukin-6 (IL-6) expression by human adipose tissue primary culture.For that purpose, human subcutaneous adipose tissue obtained from healthynon-obese women (BMI: 26.7 ± 2.2 kg/m2) after abdominal dermolipectomy, wassplit into explants and cultured for 6 hours with or without caffeine. Three differentconcentrations of caffeine were tested (0.5ìg/mL, 5ìg/mL and 50ìg/mL). After 6hours of treatment, explants were subjected to collagenase digestion in order to isolateadipocytes and SVF cells. Then, TNFalpha and IL-6 mRNA were analysed by realtimePCR alternatively in adipocytes and SVF cells. In parallel, we checked geneexpression of markers involved in adipocyte differenciation and in SVF cells inflammationand proliferation. Our findings show a strong and dose dependent down-regulationof TNF-alpha gene expression in both adipocyte and SVF cells whereas IL-6 wasonly down regulated in SVF cells. No effect of caffeine was noticed on the othergenes studied. Thus, caffeine, by decreasing TNFá expression, could improve adiposetissue inflammation during obesity (AU)

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Caffeine reduces TNFá up-regulation in humanadipose tissue primary culture

Adipose tissue secretions play an important role in the development of obesityrelatedpathologies such as diabetes. Through inflammatory cytokines production,adipose tissue stromavascular fraction cells (SVF), and essentially macrophages, promoteadipocyte insulin resistance by a paracrine way. Since xanthine family compoundssuch as caffeine were shown to decrease inflammatory production by humanblood cells, we investigated the possible effect of caffeine on Tumor Necrosis Factorá (TNFá) and Interleukin-6 (IL-6) expression by human adipose tissue primary culture.For that purpose, human subcutaneous adipose tissue obtained from healthynon-obese women (BMI: 26.7 ± 2.2 kg/m2) after abdominal dermolipectomy, wassplit into explants and cultured for 6 hours with or without caffeine. Three differentconcentrations of caffeine were tested (0.5ìg/mL, 5ìg/mL and 50ìg/mL). After 6hours of treatment, explants were subjected to collagenase digestion in order to isolateadipocytes and SVF cells. Then, TNFá and IL-6 mRNA were analysed by realtimePCR alternatively in adipocytes and SVF cells. In parallel, we checked geneexpression of markers involved in adipocyte differenciation and in SVF cells inflammationand proliferation. Our findings show a strong and dose dependent down-regulationof TNF-á gene expression in both adipocyte and SVF cells whereas IL-6 wasonly down regulated in SVF cells. No effect of caffeine was noticed on the othergenes studied. Thus, caffeine, by decreasing TNFá expression, could improve adiposetissue inflammation during obesity (AU)

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Expanding role for the apelin/APJ system in physiopathology

Apelin is a bioactive peptide known as the ligand of the G protein-coupled receptorAPJ. Diverse active apelin peptides exist under the form of 13, 17 or 36 aminoacids, originated from a common 77-amino-acid precursor. Both apelin and APJmRNA are widely expressed in several rodent and human tissues and have functionaleffects in both the central nervous system and peripheral tissues. Apelin has beenshown to be involved in the regulation of cardiovascular functions, fluid homeostasis,vessel formation and cell proliferation. More recently, apelin has been describedas an adipocyte-secreted factor (adipokine), up-regulated in obesity. By acting as circulatinghormone or paracrine factor, adipokines are involved in physiological regulations(fat depot development, energy storage, metabolism or eating behavior) or inthe promotion of obesity-associated disorders (type 2 diabetes and cardiovasculardysfunctions). In this regard, expression of apelin gene in adipose tissue is increasedby insulin and TNFalpha. This review will consider the main roles of apelin in physiopathologywith particular attention on its role in energy balance regulation and inobesity-associated disorders (AU)

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Expanding role for the apelin/APJ systemin physiopathology

Apelin is a bioactive peptide known as the ligand of the G protein-coupled receptorAPJ. Diverse active apelin peptides exist under the form of 13, 17 or 36 aminoacids, originated from a common 77-amino-acid precursor. Both apelin and APJmRNA are widely expressed in several rodent and human tissues and have functionaleffects in both the central nervous system and peripheral tissues. Apelin has beenshown to be involved in the regulation of cardiovascular functions, fluid homeostasis,vessel formation and cell proliferation. More recently, apelin has been describedas an adipocyte-secreted factor (adipokine), up-regulated in obesity. By acting as circulatinghormone or paracrine factor, adipokines are involved in physiological regulations(fat depot development, energy storage, metabolism or eating behavior) or inthe promotion of obesity-associated disorders (type 2 diabetes and cardiovasculardysfunctions). In this regard, expression of apelin gene in adipose tissue is increasedby insulin and TNFá. This review will consider the main roles of apelin in physiopathologywith particular attention on its role in energy balance regulation and inobesity-associated disorders (AU)

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Increased monoamine oxidase and semicarbazide-sensitive amine oxidase activities in white adipose tissue of obese dogs fed a high-fat diet

Adipocytes express two types of amine oxidases: the cell surface semicarbazidesensitive amine oxidase (SSAO) and the mitochondrial monoamine oxidase (MAO). In human abdominal subcutaneous adipose tissue, it has been reported that SSAO substrates stimulate glucose transport and inhibit lipolysis while MAO activity is decreased in obese patients when compared to age-matched controls. However, no information has been reported on visceral WAT. To further investigate the obesity-induced regulations of MAO and SSAO in white adipose tissue (WAT) from different anatomical locations, enzyme activities and mRNA abundance have been determined on tissue biopsies from control and high-fat fed dogs, an obesity model already described to be associated with arterial hypertension and hyperinsulinemia. MAO activity was increased in the enlarged omental WAT of diet-induced obese dogs, but not in their mesenteric WAT, another intra-abdominal fat depot. Subcutaneous WAT did not exhibit any change in MAO activity, as did the richest MAO-containing tissue: liver. Similarly, SSAO was increased in omental WAT of diet-induced obese dogs, but was not modified in other WAT and in aorta. The increase in SSAO activity observed in omental WAT likely results from an increased expression of the AOC3 gene since mRNA abundance and maximal benzylamine oxidation velocity were increased. Finally, plasma SSAO was decreased in obese dogs. Although the observed regulations differ from those found in subcutaneous WAT of obese patients, this canine model shows a tissue- and site-specific regulation of peripheral MAO and SSAO in obesity (AU)

Los adipocitos expresan dos tipos de amino-oxidasa: la amino oxidasa sensible a semicarbazida de la superficie celular (SSAO) y la monoamino oxidasa mitocondrial (MAO). En el tejido adiposo subcutáneo abdominal de humanos se ha descrito que los sustratos de la SSAO estimulan el transporte de glucosa e inhiben la lipólisis, mientras que la actividad MAO disminuye en pacientes obesos cuando se compara con controles de su propia edad. Sin embargo, no existe información sobre lo que ocurre en el tejido adiposo visceral. Se investiga, por tanto, sobre la influencia de la obesidad en la regulación de la MAO y SSAO en el tejido adiposo blanco (WAT) de diferentes localizaciones anatomicas, su actividad enzimatica y la riqueza de RNAm en biopsias tisulares procedentes de perros control y tratados con dieta rica en grasa. Este modelo de obesidad ya había sido previamente descrito asociado a hipertensión arterial e hiperinsulinemia. La actividad MAO se incrementó en WAT omental hipertrofiado de perros tratados con dieta rica en grasa, pero este efecto no se apreciaba en su correspondiente tejido adiposo mesentérico, otro depósito graso intra-abdominal. En el tejido adiposo subcutáneo no se pusieron de manifiesto cambios en la actividad MAO, ni tampoco en un tejido como el hígado, muy rico en MAO.De forma similar, la actividad SSAO se incrementó en el WAT omental de perros con obesidad inducida por la dieta, pero no se modificaba en otros WAT y en la aorta. El incremento encontrado en la actividad de la SSAO en el WAT (..) (AU)

Influence of high-fat diet on amine oxidase activity in white adipose tissue of mice prone or resistant to diet-induced obesity

Decreased monoamine oxidase (MAO) activity has been observed in adipose tissue of obese patients. Since substrates of MAO and semicarbazide-sensitive amine oxidase (SSAO) can modify adipocyte metabolism, this work investigates whether changes in amine oxidase activity may occur during white adipose tissue (WAT) development. We evaluated MAO and SSAO activities in WAT of high-fat diet (HFD) and low-fat diet fed mice. To distinguish the effect of HFD on its own from the effect of fat mass enlargement, obesity-prone transgenic line of the FVBn strain lacking b3-adrenergic receptors (AR) but expressing human b3-AR and a2-AR (mb3-/-, hb3+/+, ha2+/-) was compared to its obesity-resistant control (mb3-/-, hb3+/+). As already reported, the former mice became obese while the latter resisted to HFD. No significant change in SSAO or MAO activity was found in WAT of both strains after HFD when expressing oxidase activity per milligram of protein. However, when considering the overall capacity of the fat depots to oxidize tyramine or benzylamine, there was an increase in MAO and SSAO activity only in the enlarged WAT of HFD-induced obese mice. Therefore, the comparison of these models allowed to demonstrate that the higher amine oxidase capacity hold in enlarged fat stores of obese mice is more likely the consequence of increased fat cell number rather than the result of an increased expression of MAO or SSAO in the adipocyte

En trabajos previos se describe que la actividad monoamino oxidasa (MAO) en el tejido adiposo disminuye en pacientes obesos. Dado que los sustratos de la MAO y de la amino oxidasa sensible a semicarbazida (SSAO) pueden modificar el metabolismo de los adipocitos, se investiga en este trabajo si se producen cambios en la actividad amino oxidasa durante el desarrollo del tejido adiposo blanco. Para ello, se evalúa el efecto de la dieta rica en grasa (HFD) respecto de la dieta control sobre la actividad MAO y SSAO en tejido adiposo de ratones transgénicos que no expresan sus propios receptores adrenérgicos b3 y que son de dos líneas diferentes: los que expresan los receptores adrenérgicos humanos b3 Y a2 (mb3 -/-, hb3+/+, ha2+/-) y que son no susceptibles a la obesidad y los que sólo expresan los b3 humanos (mb3 -/-, hb3+/+) y que son resistentes a la obesidad. Los resultados no muestran cambios significativos por efecto de la dieta en ninguno de los dos grupos de ratones sobre la actividad MAO y SSAO cuando se expresa referida a mg de proteína. Sin embargo, cuando se considera la capacidad total de los depósitos grasos para oxidar tiramina o benzilamina, so observa un aumento significativo en ambas actividades MAO y SSAO sólo en el incrementado tejido adiposo blanco de los ratones obesos por efecto de la dieta HFD. Por tanto, estos datos indican que la mayor actividad amino oxidasa de los depósitos grasos de los ratones obesos es probablemente debida al aumento del número de células adiposas, mas que a un incremento de la expresión de MAO y SSAO en los adipocitos

Effects of oral administration of benzylamine on glucose tolerance and lipid metabolism in rats

Repeated administration of benzylamine plus vanadate have been reported to exhibit anti-hyperglycemic effects in different models of diabetic rats. Likewise oral treatment with Moringa oleifera extracts which contain the alkaloïd moringine, identical to benzylamine, has also been shown to prevent hyperglycemia in alloxan-induced diabetic rats. With these observations we tested whether prolonged oral administration of benzylamine could interact with glucose and/or lipid metabolism. Seven week old male Wistar rats were treated for seven weeks with benzylamine 2.9 g/l in drinking water and were submitted to glucose tolerance tests. A slight decrease in water consumption was observed in benzylamine-treated animals while there was no change in body and adipose tissue weights at the end of treatment. Blood glucose and plasma insulin, triacylglycerol or cholesterol levels were not modified. However, benzylamine treatment resulted in a decrease in plasma free fatty acids in both fed and fasted conditions. Benzylamine treatment improved glucose tolerance as shown by the reduction of hyperglycemic response to intra-peritoneal glucose load. Oral benzylamine treatment did not alter the response of adipocytes to insulin nor to insulin-like actions of benzylamine plus vanadate, via in vitro activation of glucose transport or inhibition of lipolysis. This work demonstrates for the first time that oral administration of benzylamine alone influences glucose and lipid metabolism. However, these results obtained in normoglycemic rats require to be confirmed in diabetic models

En ratas diabéticas, la administración crónica de la combinación benzilamina más vanadato ejerce un efecto antidiabético. Recientemente se ha descrito en ratas diabéticas inducidas por aloxan una reducción de la glucemia tras el tratamiento oral con extracto de Moringa oleifera, que contiene el alcaloide moringina, idéntico a la benzilamina. Por ello, se investiga en este trabajo el efecto del tratamiento prolongado por via oral con sólo benzilamina sobre el metabolismo de la glucosa y/o los lípidos. Ratas macho Wistar de 7 semanas se trataron durante 7 semanas con benzilamina 2.9 g/l en el agua de la bebida. Al finalizar el tratamiento, las ratas fueron sometidos a un test de tolerancia a la glucosa, inyectada por via intraperitoneal. Se recogió plasma para la determinación bioquímica y se aislaron adipocitos para estudiar la lipólisis y la captación de glucosa. El tratamiento oral con benzilamina no modifica el peso corporal ni el de la grasa, ni los niveles plasmáticos de glucosa, insulina, triacilglicerol y colesterol. Sin embargo, mejora la tolerancia a la glucosa, pues reduce la respuesta hiperglucémica a la inyección intra-peritoneal de glucosa y reduce los niveles de acidos grasos, tanto en situación de ayuno como tras la ingesta. El tratamiento oral con benzilamina no modifica en el adipocito los efectos de insulina o benzilamina más vanadato sobre la activación del transporte de glucosa o la inhibición de la lipolisis. Este trabajo demuestra por vez primera que la administración oral de benzilamina influye sobre el metabolismo de los lípidos y de la glucosa. Sin embargo, estos resultados obtenidos en ratas normoglicémicas deben ser confirmados en modelos diabéticos

Amine oxidase substrates for impaired glucose tolerance correction

Amine oxidases are widely distributed from microorganisms to vertebrates and produce hydrogen peroxide plus aldehyde when catabolizing endogenous or xenobiotic amines. Novel roles have been attributed to several members of the amine oxidase families, which cannot be anymore considered as simple amine scavengers. Semicarbazide-sensitive amine oxidase (SSAO) is abundantly expressed in mammalian endothelial, smooth muscle, and fat cells, and plays a role in lymphocyte adhesion to vascular wall, arterial fiber elastic maturation, and glucose transport, respectively. This latter role was studied in detail and the perspectives of insulin-like actions of amine oxidase substrates discussed in the present review. Independent studies have demonstrated that SSAO substrates and monoamine oxidase substrates mimic diverse insulin effects in adipocytes: glucose transport activation, lipogenesis stimulation and lipolysis inhibition. These substrates also stimulate in vitro adipogenesis. Acute in vivo administration of amine oxidase substrates improves glucose tolerance in rats, mice and rabbits, while chronic treatments with benzylamine plus vanadate exert an antihyperglycaemic effect in diabetic rats. Dietary supplementations with methylamine, benzylamine or tyramine have been proven to influence metabolic control in rodents by increasing glucose tolerance or decreasing lipid mobilisation, without noticeable changes in the plasma markers of lipid peroxidation or protein glycation, despite adverse effects on vasculature. Thus, the ingested amines are not totally metabolized at the intestinal level and can act on adipose and vascular tissues. In regard with this influence on metabolic control, more attention must be paid to the composition or supplementation in amines in foods and nutraceutics

Las amino-oxidasas (AO) están ampliamente distribuidas, desde microorganismos hasta vertebrados, y producen peróxido de hidrógeno y aldehído al catabolizar aminas biógenas o exógenas. Datos recientes ponen de manifiesto que las AO no pueden considerarse exclusivamente como depuradoras de aminas. La amino-oxidasa sensible a semicarbazida (SSAO) es muy abundante en ciertas células de mamíferos como las endoteliales, la célula muscular lisa y los adipocitos, donde desempeña un papel importante en la adhesión de los linfocitos a las paredes vasculares, la maduración de las fibras elásticas arteriales, y el transporte de glucosa, respectivamente. Este último efecto es el que se presenta en esta revisión donde, además, se discuten las perspectivas abiertas como consecuencia de sus acciones insulino-miméticas. Los sustratos de SSAO y de monoamino-oxidasa mimetizan varios efectos de la insulina en los adipocitos: activación del transporte de glucosa y de la lipogénesis e inhibición de la lipólisis. También estimulan in vitro la adipogénesis. La administración aguda in vivo de sustratos de AO mejora la tolerancia a la glucosa en ratas, ratones y conejos, y los tratamientos crónicos con benzilamina y vanadato tienen un efecto antihiperglucemiante en ratas diabéticas. Suplementos en la dieta con metilamina, benzilamina o tiramina han puesto de manifiesto una acción beneficiosa sobre el control metabólico en roedores a través de un aumento en la tolerancia a la glucosa o una disminución de la movilización lipídica, sin cambios notables en los marcadores plasmáticos de peroxidación lipídica o de glicación proteica, a pesar de unos efectos aterogénicos indeseables. Por tanto, las aminas ingeridas no se degradan totalmente a nivel de la barrera intestinal y pueden actuar sobre el tejido adiposo y vascular. En relación con esta influencia sobre el control metabólico, se concluye que es necesario prestar atención a la composición o adición como suplementos de estas aminas a los alimentos y medicamentos