Publications (18)54.22 Total impact
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Article: Development of insulin resistance during aging: involvement of central processes and role of adipokines.
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ABSTRACT: Aging in mammals associates with the development of peripheral insulin resistance. Additionally, adiposity usually increases with aging and this could play a relevant role in the gradual impairment of insulin action. In fact, fat accretion leads to changes in the expression and circulating concentrations of factors originated in adipose tissue like leptin, resistin and inflammatory cytokines which have been shown to modulate insulin signaling in insulin target tissues acting both, directly or through the central nervous system. Even insulin action on peripheral target tissues has been recently demonstrated to be partially mediated by its central action, suggesting that a decrease in central insulin action could be involved in the development of peripheral insulin resistance. In the present review we analyze the available research data on aging-associated insulin resistance making emphasis in the following aspects: 1) The time-course of development of overall insulin resistance and the evolution of changes in circulating adipokines; 2) The effect of caloric restriction and the decrease of adiposity in insulin action; 3) The influence of changes in the central action of factors like leptin or insulin in the development and maintenance of insulin resistance during aging.Current Protein and Peptide Science 06/2011; 12(4):305-15. · 2.89 Impact Factor -
Article: Development of Insulin Resistance During Aging: Involvement of Central Processes and Role of Adipokines
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ABSTRACT: Aging in mammals associates with the development of peripheral insulin resistance. Additionally, adiposity usually increases with aging and this could play a relevant role in the gradual impairment of insulin action. In fact, fat accretion leads to changes in the expression and circulating concentrations of factors originated in adipose tissue like leptin, resistin and inflammatory cytokines which have been shown to modulate insulin signaling in insulin target tissues acting both, directly or through the central nervous system. Even insulin action on peripheral target tissues has been recently demonstrated to be partially mediated by its central action, suggesting that a decrease in central insulin action could be involved in the development of peripheral insulin resistance. In the present review we analyze the available research data on aging-associated insulin resistance making emphasis in the following aspects: 1) The time-course of development of overall insulin resistance and the evolution of changes in circulating adipokines; 2) The effect of caloric restriction and the decrease of adiposity in insulin action; 3) The influence of changes in the central action of factors like leptin or insulin in the development and maintenance of insulin resistance during aging.Current Protein and Peptide Science 05/2011; 12(4):305-315. · 2.89 Impact Factor -
Article: Regulation of insulin-stimulated glucose uptake in rat white adipose tissue upon chronic central leptin infusion: effects on adiposity.
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ABSTRACT: Leptin enhances the glucose utilization in most insulin target tissues and paradoxically decreases it in white adipose tissue (WAT), but knowledge of the mechanisms underlying the inhibitory effect of central leptin on the insulin-dependent glucose uptake in WAT is limited. After 7 d intracerebroventricular leptin treatment (0.2 μg/d) of rats, the overall insulin sensitivity and the responsiveness of WAT after acute in vivo insulin administration were analyzed. We also performed unilateral WAT denervation to clarify the role of the autonomic nervous system in leptin effects on the insulin-stimulated [(3)H]-2-deoxyglucose transport in WAT. Central leptin improved the overall insulin sensitivity but decreased the in vivo insulin action in WAT, including insulin receptor autophosphorylation, insulin receptor substrate-1 tyrosine-phosphorylation, and Akt activation. In this tissue, insulin receptor substrate-1 and glucose transporter 4 mRNA and protein levels were down-regulated after central leptin treatment. Additionally, a remarkable up-regulation of resistin, together with an augmented expression of suppressor of cytokine signaling 3 in WAT, was also observed in leptin-treated rats. As a result, the insulin-stimulated glucose transporter 4 insertion at the plasma membrane and the glucose uptake in WAT were impaired in leptin-treated rats. Finally, denervation of WAT abolished the inhibitory effect of central leptin on glucose transport and decreased suppressor of cytokine signaling 3 and resistin levels in this tissue, suggesting that resistin, in an autocrine/paracrine manner, might be a mediator of central leptin antagonism of insulin action in WAT. We conclude that central leptin, inhibiting the insulin-stimulated glucose uptake in WAT, may regulate glucose availability for triacylglyceride formation and accumulation in this tissue, thereby contributing to the control of adiposity.Endocrinology 02/2011; 152(4):1366-77. · 4.46 Impact Factor -
Article: S-resistin inhibits adipocyte differentiation and increases TNFalpha expression and secretion in 3T3-L1 cells.
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ABSTRACT: S-resistin is a non-secretable resistin spliced variant described in white adipose tissue from Wistar rats. Since resistin has been implicated in adipogenesis regulation, here we have investigated the possible role of this new isoform in this process. For that, we have studied the adipocyte development in 3T3-L1 pre-adipocyte cell line stably expressing s-resistin and resistin. Both isoforms are able to restrain 3T3-L1 pre-adipocyte differentiation though affecting differently the expression pattern of pro-adipogenic transcription factors such CCAAT/enhancer binding proteins alpha and beta (C/EBPalpha and C/EBPbeta) and peroxisome proliferator-activated receptor gamma (PPARgamma), as well of proteins implicated in lipid metabolism such perilipin, fatty acid synthase (FAS), adipocyte lipid binding protein (ALBP/aP2) and carnitine palmitoyltransferase1 (CPT1). Likewise, both resistin isoforms impair insulin-stimulated glucose transport by decreasing glucose transport 4 (GLUT4) expression but to a different degree. In addition, s-resistin expressing 3T3-L1 cells display other remarkable differences. Thus, in these cells, endogenous resistin expression falls down while tumor necrosis factor alpha (TNFalpha) and interleukine 6 (IL-6) productions are increased along differentiation. These findings indicate that s-resistin isoform also impairs adipocyte differentiation affecting the expression pattern of key pro-adipogenic transcription factors and insulin sensitivity. Additionally, s-resistin may play a role in inflammatory processes.Biochimica et Biophysica Acta 10/2010; 1803(10):1131-41. · 4.66 Impact Factor -
Article: Tissue-specific PAI-1 gene expression and glycosylation pattern in insulin-resistant old rats.
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ABSTRACT: Increased levels of plasminogen activator inhibitor-1 (PAI-1) have been associated with obesity, aging, insulin resistance, and type 2 diabetes, conditions that contribute to increased cardiovascular risk. PAI-1 is expressed in a variety of tissues, but the cellular origin of plasma PAI-1 is unknown. To link insulin resistance, aging, and cardiovascular disease, we examined the expression and glycosylation pattern of PAI-1 in liver and white adipose tissue (WAT) from adult (3 mo) and insulin-resistant old (24 mo) Wistar rats. Glycosylated PAI-1 protein was also purified by affinity chromatography from endothelial culture supernatans to analyze its inhibitory activity. We also analyzed the contribution of adipocytes and stromal vascular cells from WAT to PAI-1 levels with aging. Aging caused a significant increase of PAI-1 mRNA (P < 0.001) in WAT that was predominantly due to the adipocytes and not to stroma-vascular cells, while there was no modification in liver from aged rats. Moreover, PAI-1 expression increased during preadipocyte differentiation (P < 0.001). Furthermore, we found a tissue-dependent PAI-1 glycosylation pattern: adipose tissue only expresses the glycosylated PAI-1 form, whereas the liver mainly expresses the nonglycosylated form. Finally, we also found evidences suggesting that the glycosylated PAI-1 form shows higher inhibitory activity than the nonglycosylated. Our data suggest that WAT may be a major source of the elevated plasma levels of PAI-1 in insulin-resistant old rats. Additionally, the high degree of PAI-1 glycosylation and activity, together with the significant increase in visceral fat in old rats, may well contribute to an increased cardiovascular risk associated with insulin-resistant states.AJP Regulatory Integrative and Comparative Physiology 09/2009; 297(5):R1563-9. · 3.34 Impact Factor -
Article: The expression of rat resistin isoforms is differentially regulated in visceral adipose tissues: effects of aging and food restriction.
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ABSTRACT: Two variants of the adipose hormone resistin are generated by alternative splicing in Wistar rats. Here we analyzed the expression of these resistin variants in 2 main visceral adipose depots, epididymal and retroperitoneal, as well as the resistin serum concentration during aging and food restriction. Total protein levels of resistin were also analyzed in extracts from both visceral adipose depots. Resistin variants show similar patterns of relative expression in visceral adipose tissues in 3-month-old rats, representing the short variant, s-resistin, which is 15% of the full-length transcript. However, only epididymal, but not retroperitoneal, fat pad shows a decrease in both messenger RNA and protein levels of resistin isoforms with aging. Food restriction decreases adiposity index in 8- and 24-month-old animals to values even lower than those of 3-month-old animals. Food restriction decreases resistin expression in both adipose tissues in 8-month-old but not in 24-month-old rats. Interestingly, concomitant with the improvement of insulin sensitivity asserted by homeostasis model assessment, resistin serum levels decrease only in food-restricted 8-month-old animals. In contrast, food restriction up-regulates s-resistin messenger RNA in epididymal adipose tissue, whereas no significant changes are appreciated in retroperitoneal adipose tissue. These data indicate that both forms of resistin are differentially regulated by fat depot location, aging, and even nutritional status, suggesting that alternative splicing plays a key role in this differential regulation.Metabolism: clinical and experimental 03/2009; 58(2):204-11. · 2.59 Impact Factor -
Article: Central leptin regulates total ceramide content and sterol regulatory element binding protein-1C proteolytic maturation in rat white adipose tissue.
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ABSTRACT: Obesity and type 2 diabetes are associated with insulin and leptin resistance, and increased ceramide contents in target tissues. Because the adipose tissue has become a central focus in these diseases, and leptin-induced increases in insulin sensitivity may be related to effects of leptin on lipid metabolism, we investigated herein whether central leptin was able to regulate total ceramide levels and the expression of enzymes involved in ceramide metabolism in rat white adipose tissue (WAT). After 7 d central leptin treatment, the total content of ceramides was analyzed by quantitative shotgun lipidomics mass spectrometry. The effects of leptin on the expression of several enzymes of the sphingolipid metabolism, sterol regulatory element binding protein (SREBP)-1c, and insulin-induced gene 1 (INSIG-1) in this tissue were studied. Total ceramide levels were also determined after surgical WAT denervation. Central leptin infusion significantly decreased both total ceramide content and the long-chain fatty acid ceramide species in WAT. Concomitant with these results, leptin decreased the mRNA levels of enzymes involved in de novo ceramide synthesis (SPT-1, LASS2, LASS4) and ceramide production from sphingomyelin (SMPD-1/2). The mRNA levels of enzymes of ceramide degradation (Asah1/2) and utilization (sphingomyelin synthase, ceramide kinase, glycosyl-ceramide synthase, GM3 synthase) were also down-regulated. Ceramide-lowering effects of central leptin were prevented by local autonomic nervous system denervation of WAT. Finally, central leptin treatment markedly increased INSIG-1 mRNA expression and impaired SREBP-1c activation in epididymal WAT. These observations indicate that in vivo central leptin, acting through the autonomic nervous system, regulates total ceramide levels and SREBP-1c proteolytic maturation in WAT, probably contributing to improve the overall insulin sensitivity.Endocrinology 10/2008; 150(1):169-78. · 4.46 Impact Factor -
Article: Tissue-specific effects of central leptin on the expression of genes involved in lipid metabolism in liver and white adipose tissue.
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ABSTRACT: Leptin reduces adiposity and exerts antisteatotic effects on nonadipose tissues. However, the mechanisms underlying leptin effects on lipid metabolism in liver and white adipose tissue have not been fully clarified. Here, we have studied the effects of central leptin administration on key enzymes and transcription factors involved in lipid metabolism in liver and epididymal adipose tissue. Intracerebroventricular leptin infusion for 7 d did not change leptin plasma levels but decreased triacylglyceride content in liver, epididymal adipose tissue, and plasma. In both tissues this treatment markedly decreased the expression of key enzymes of the de novo fatty acid (FA) synthesis such as acetyl-coenzyme A-carboxylase, FA synthase, and stearoyl-coenzyme A desaturase-1, in parallel with a reduction in mRNA expression of sterol regulatory element binding protein-1c in liver and carbohydrate regulatory element binding protein in adipose tissue. In addition, leptin also decreased phosphoenol-pyruvate carboxykinase-C expression in adipose tissue, an enzyme involved in glyceroneogenesis in this tissue. Central leptin administration down-regulates delta-6-desaturase expression in liver and adipose tissue, in parallel with the decrease of the expression of sterol regulatory element binding protein-1c in liver and peroxisome proliferator activated receptor alpha in adipose tissue. Finally, leptin treatment, by regulating adipose triglyceride lipase/hormone sensitive lipase/diacylglycerol transferase 1 expression, also established a new partitioning in the FA-triacylglyceride cycling in adipose tissue, increasing lipolysis and probably the FA efflux from this tissue, and favoring in parallel the FA uptake and oxidation in the liver. These results suggest that leptin, acting at central level, exerts tissue-specific effects in limiting fat tissue mass and lipid accumulation in nonadipose tissues, preventing the development of obesity and type 2 diabetes.Endocrinology 01/2008; 148(12):5604-10. · 4.46 Impact Factor -
Article: MTPA: a crustacean metallothionein that affects hepatopancreatic mitochondrial functions.
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ABSTRACT: Metallothioneins are cysteine-rich proteins, with a high capacity to bind metallic ions, and for which a precise biological role has not been established. Here we investigated the effects of MTPA, a metallothionein from the lobster Panulirus argus, on mitochondrial oxygen consumption and ROS production. An HPLC-RP-ESI-MS analysis of recombinant MTPA showed that despite its extra Cys, MTPA binds 6 Zn2+ per molecule akin to other crustacean metallothioneins with 18 Cys. The extra Cys is not involved in zinc binding, since its side-chain would be oriented to the outside of the molecule according to a preliminary model of the tridimensional structure of MTPA. MTPA-Zn2+(6) is imported into the hepatopancreatic mitochondria intermembrane space and inhibits mitochondrial oxygen consumption, increasing thereby ROS production. Nevertheless, the stimulation of ROS production by MT-bound Zn2+ is weaker compared to equivalent amounts of free Zn2+, suggesting that MTPA protects against oxidative stress. This constitutes the first report on metallothioneins effects on mitochondrial function in invertebrates and agrees with the results described for mammals, suggesting a connection between metallothioneins and energy metabolism.Archives of Biochemistry and Biophysics 12/2007; 467(1):31-40. · 2.93 Impact Factor -
Article: Effect of age and moderate food restriction on insulin sensitivity in Wistar rats: role of adiposity.
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ABSTRACT: Insulin resistance develops with ageing in humans and rodents. Here, we have studied the evolution of insulin sensitivity with ageing trying to discriminate the role of adiposity from that of ageing in this process. We performed oral glucose tolerance tests and determined overall and tissue-specific glucose utilization under euglycemic-hyper-insulinemic conditions in 3-, 8-, and 24-month-old rats fed ad libitum, and in 8- and 24-month-old rats after 3 months of calorie restriction. Body composition and adipocyte-derived cytokines such as leptin, resistin, and adiponectin were analyzed. Overall insulin sensitivity decreases with ageing. Calorie restriction improves global insulin sensitivity in 8- but not in 24-month-old rats. Insulin-stimulated glucose utilization in adipose tissues decreases in 8 months, while in oxidative muscles it reaches significance only in older rats. Calorie restriction restores adipose tissue insulin sensitivity only in 8-month-old rats and no changes are observed in muscles of 24-month-old rats. Resistin and leptin increase with ageing. Food restriction lowers resistin and increases adiponectin in 8-month-old rats and decreases leptin in both ages. Visceral and total fat increase with ageing and decrease after calorie restriction. We conclude that accretion of visceral fat plays a key role in the development of insulin resistance after sexual maturity, which is reversible by calorie restriction. With aging, accumulation of retroperitoneal and total body fat leads to impaired muscle glucose uptake and to a state of insulin resistance that is difficult to reverse.Journal of Endocrinology 08/2007; 194(1):131-41. · 3.55 Impact Factor -
Article: Altered subcellular distribution of IRS-1 and IRS-3 is associated with defective Akt activation and GLUT4 translocation in insulin-resistant old rat adipocytes.
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ABSTRACT: Insulin receptor signal transduction depends on the precise intracellular localization of signalling molecules. This study examines the compartmentalization and the insulin-induced translocation and tyrosine phosphorylation of insulin receptor substrates (IRS-1 and IRS-3) in epididymal white adipose tissue from adult and insulin-resistant old rats. We found that insulin induces the translocation of IRS-1 from plasma membrane (PM) and light microsomes (LM) to cytosol, whereas IRS-3 translocates from PM to LM and cytosol upon insulin stimulation. Old rat adipocytes are characterized by higher relative levels of IRS proteins, under basal conditions, in those fractions where they are intended to translocate in response to insulin and exhibit a higher phosphotyrosine content of IRS-1 and -3 in basal conditions and a lower maximal phosphorylation in response to insulin. Furthermore, old rat adipocytes are also characterized by a reduced ability of insulin to stimulate both, Akt/PKB activity and translocation of GLUT4 to the PM. We conclude that the lower stimulation of downstream insulin signalling involved in glucose metabolism in old rat adipocytes may be explained, at least in part, by the altered subcellular distribution of IRS-1 and -3 proteins. In addition, our data suggest that the mechanism of turning on/off insulin receptor-mediated signal is impaired with aging.Biochimica et Biophysica Acta 03/2006; 1763(2):197-206. · 4.66 Impact Factor -
Article: Cloning, tissue expression and metal inducibility of an ubiquitous metallothionein from Panulirus argus.
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ABSTRACT: Invertebrate metallothioneins (MT) have mainly been reported in digestive tissues, but data about the existence of a ubiquitous isoform expressed also in nervous tissue, are not available. Here we report the identification of a new metallothionein gene (MTPA) from the lobster Panulirus argus, putatively encoding a 59 residue polypeptide including 19 Cys. Tissue specific analysis indicated that MTPA is ubiquitously expressed in the hepatopancreas, intestine, nervous tissue and muscle, with the highest levels in the hepatopancreas and the lowest in muscle and nervous tissue. In addition, our data showed that MTPA is differentially regulated by metals: tissue explants exposed to Cd exhibited increased MTPA mRNA levels in all cases, except in muscle, with the highest effects in the nervous tissue, while Zn was effective only in the hepatopancreas. Interestingly, Cu showed no effects in any of the analyzed tissues. Taken together, these results suggest that MTPA in the hepatopancreas likely plays an important role in Cd detoxification and Zn homeostasis. The potent Cd-inducibility of MTPA in the nervous tissue might suggest a key function of this protein in protecting this highly sensitive tissue from cadmium-induced neurotoxicity.Gene 12/2005; 361:140-8. · 2.34 Impact Factor -
Article: ObRa and ObRe are differentially expressed in adipose tissue in aged food-restricted rats: effects on circulating soluble leptin receptor levels.
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ABSTRACT: In rodents, soluble leptin receptor (SLR) may be generated by alternative splicing of ObR mRNA and/or as a cleavage product of ObR membrane-anchored receptors. In this study, we investigated the contribution of both processes on the generation of SLR in 3-, 8-, and 24-month-old Wistar rats fed ad libitum (AL) or under food restriction (FR). To this end, we determined serum SLR levels and analyzed ObRa and ObRe mRNA expression under these physiological conditions. Additionally, we studied the cellular distribution of ObRa and the generation of SLR by N-ethyl-maleimide-induced shedding from ObRa membrane receptors in isolated adipocytes. Serum SLR levels were significantly increased in 8- and 24-month-old rats under FR, whereas similar amounts were found in rats of different ages fed AL. ObRa and ObRe mRNA expression in epididymal adipose tissue increased with aging. In contrast, after FR, ObRe mRNA expression decreased, whereas ObRa mRNA expression further increased compared with 8- and 24-month-old rats fed AL. Additionally, FR promoted a change in the distribution of ObRa between internal and plasma membranes in isolated adipocytes, increasing its presence at the cell surface. Finally, the generation of SLR by N-ethyl-maleimide-induced shedding from ObRa was also increased under FR. These data suggest that shedding of ObRa membrane-anchored receptors, rather than ObRe expression, might preferentially contribute to the generation of the increased levels of SLR in serum under conditions of FR.Endocrinology 12/2005; 146(11):4934-42. · 4.46 Impact Factor -
Article: Isolation and biological characterization of a 6-kDa protein from hepatopancreas of lobster Panulirus argus with insulin-like effects.
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ABSTRACT: A protein with insulin-like effects was isolated from the hepatopancreas of the lobster Panulirus argus following a classic method for mammalian insulin purification from the pancreas. After acid-alcoholic extraction and ethanol-ether precipitation followed by molecular filtration chromatography, a protein with an apparent molecular weight of 6 kDa was isolated. This protein is characterized by its ability to interact with anti-insulin antibodies and by mimicking insulin actions as the stimulation of glucose oxidation to CO(2) and lipogenesis in isolated rat adipocytes. In addition, this insulin immunoreactive protein (IIP) was able to stimulate the autophosphorylation of the insulin receptor present in rat adipocyte plasma membranes, in a dose-dependent manner. The immunological and biochemical results obtained are consistent with the hypothesis that protein(s) with insulin-like effects occur in the digestive gland of the lobster P. argus and may be of significance to control metabolic and growth related processes in crustaceans.General and Comparative Endocrinology 06/2003; 131(3):284-90. · 3.27 Impact Factor -
Article: Implicación de proteínas tirosina fosfatasas (PTP1B) en la disminución de la señal de insulina en el hipotálamo con el envejecimiento: efecto de la restricción nutricional.
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ABSTRACT: Introducción La resistencia a insulina se ha relacionado con un aumento de la expresión y/o actividad de proteínas tirosina fosfatasas, especialmente PTP1B, tanto a nivel central como periférico. Las ratas viejas presentan resistencia central a insulina debido a múltiples alteraciones en su vía de señalización. En este trabajo hemos estudiado el posible papel de las PTPs en la resistencia central a insulina durante el envejecimiento y su relación con la restricción nutricional. Material y métodos En extractos hipotalámicos de ratas Wistar macho de 3 y 24 meses de edad, y de 24 meses sometidas a restricción nutricional crónica se determinó: la actividad fosfatasa total utilizando PNPP y la capacidad de desfosforilar a un péptido fosforilado en tirosina en los sitios de autofosforilación de la cadena [beta] del receptor de insulina mediante el kit PTP assay kit 1; la activación de la PTP1B y su asociación con el receptor de insulina (RI) mediante inmunoprecipitación y western blot. Resultados A pesar de que la actividad fosfatasa total no se modifica en extractos hipotalámicos de ratas viejas, la capacidad de estos extractos para desfosforilar el péptido con la secuencia de autofosforilación en tyr del RI aumentó significativamente en ratas viejas. Además se observó un aumento de la fosforilación en tyr de PTB1B así como de su asociación con el RI en extractos hipotalámicos de ratas viejas. La restricción nutricional crónica ligeramente revirtió estos parámetros. Conclusiones En hipotálamos de animales viejos el aumento de la actividad de la PTP1B y de su asociación con el RI podría estar implicado en la menor capacidad del receptor de insulina para activarse en respuesta a insulina. Estos cambios son parcialmente restaurados con una restricción nutricional. -
Article: Central Leptin Regulates Total Ceramide Content and Sterol Regulatory Element Binding Protein-1C Proteoly tic Maturation in Rat Wh ite Adipose Tissue
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Article: The effect of aging on insulin signalling pathway is tissue dependent: Central role of adipose tissue in the insulin resistance of aging
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ABSTRACT: Insulin resistance progressively increases with age, resulting in excessively high incidence of T2D in the elderly population. To investigate the molecular mechanisms underlying insulin resistance of aging, we carried out a comparative study of insulin signalling cascade in adipose tissue, liver and skeletal muscle. We measured the protein levels in different subcellular compartments and the phosphorylation status of key components of the insulin signalling pathway in response to in vivo insulin infusion. White adipose tissue (WAT) from old rats shows altered subcellular distribution of insulin receptor (IR) and insulin receptor substrate 1 (IRS-1) and a marked reduction in the insulin-stimulated IR tyrosine phosphorylation. Furthermore, activation of Akt, as well as GLUT4 translocation to the plasma membrane, is impaired. Quadriceps muscle from old rats also has a defect in GLUT4 trafficking but, in contrast to WAT, insulin signalling at the level of IR and Akt is increased. In liver, we found no major differences in the ability of insulin to induce autophosphorylation of the IR or activation of Akt between adult and old animals. These data, therefore, show at the molecular level that insulin resistance in adipose tissue precedes the development of liver and muscle insulin resistance in aged rats.Mechanisms of Ageing and Development. -
Article: Isolation and biological characterization of a 6-kDa protein from hepatopancreas of lobster Panulirus argus with insulin-like effects
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ABSTRACT: A protein with insulin-like effects was isolated from the hepatopancreas of the lobster Panulirus argus following a classic method for mammalian insulin purification from the pancreas. After acid-alcoholic extraction and ethanol-ether precipitation followed by molecular filtration chromatography, a protein with an apparent molecular weight of 6 kDa was isolated. This protein is characterized by its ability to interact with anti-insulin antibodies and by mimicking insulin actions as the stimulation of glucose oxidation to CO2 and lipogenesis in isolated rat adipocytes. In addition, this insulin immunoreactive protein (IIP) was able to stimulate the autophosphorylation of the insulin receptor present in rat adipocyte plasma membranes, in a dose-dependent manner. The immunological and biochemical results obtained are consistent with the hypothesis that protein(s) with insulin-like effects occur in the digestive gland of the lobster P. argus and may be of significance to control metabolic and growth related processes in crustaceans.General and Comparative Endocrinology 131(3):284-290. · 3.27 Impact Factor
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2003–2011
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Universidad de Castilla-La Mancha
- Centro Regional de Investigaciones Biomédicas (CRIB)
Ciudad Real, Castille-La Mancha, Spain
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