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boschmann b-55p manualPlease add several products to your cart. Please add several products to your cart. Real easy transaction. We will reply within 2 business days.Energizing check OKEnergizing check OKG-Mach McGard M12xP1.5 Tune-up woofer with built-in TS-WX88A amplifier. To walk through. Please add several products to your cart. Please add several products to your cart. The staff at the Sasebo location was very helpful, Thank you again! We will reply within 2 business days.Body. Power supply wiring. Wired remote control there. Operation check OK. Scratches. DirtBody. DirtPrevious term genuine. Cutting bright. TOYO (Toyo)Late version. Tail lens. Outside Tune-up woofer with built-in TS-WX88A amplifier. XJ-1 series is made with materials containing elements mined from the core of the earth, which are meticulously isolated, tested and recombined to suc. XJ2 Series drivers will give you improved musical realism by attribute of many of its unique properties and strengths. The specially formulated, extre. For more offers and benefits, you can also subscribe to our online Newsletter. Most of the manufacturers reserve the right to change the product characteristics or complement without notice. Please refine the important parameters by the selling assistant when making a purchase. Any publication or copying (full or partial) without a reference to the source page is prohibited. Cambridge, 1976. Cornell University Press: Ithaca, New York, 1972. Dublin: Jeremy Pepyat, 1709. Paris: Libraire C. Reinwald, 1902. Berkeley: Univ. California Press, 1956. Chicago, 1935. London: Cambridge Press, 1977. Uppsala, 1964. Uppsala, 1964. Camridge, MA: MIT Press, 1986. Oxford Univ. Press, 2003. MA: MIT Press, 1983. Cambridge, MA: MIT Press, 1975 Hove (UK): LEA, 1994. New York, Willy, 1949. Leipzig, Voss, 1866. Studium Generale. 1957. B. 10. S. 231-337. New York: Springer, 1960. New York: Holt, 1890. Uppsala: Almqvist and Wiksell, 1950. Englwood Cliffs. N. Y.: Prentice-Hall, 1973. The brain's art of mindfulness.

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Cambridge, Mass.: Harward University Press, 1995. Paris, 1968. Neuropsychologic 1988. V. 26(3). P. 453-463. London: Methuen, 1963. Hillsdale, NJ: Erlbaum, 1992. New York: Appleton-Centuiy-Crofts, 1967. Philadelphia: Sanders, 1950. Cambridge, MA: MIT Press, 1998. Paris, 1947. Hillsdale, NJ: Erlbaum. 1978. Englewood Cliffs, N.J.: Prentice-Hall, 1989. Boston: Heath, 1901. P. 273. North Holland: Elsevier Science. B.V. 1994. P. 3-18. Minneapolis: University of Minnesota Press, 1965. New York: Macmillan, 1918. London: Methuen, 1978. Psychological Monographs. 1933. V. 44. P. 95-117. Hillsdale, NJ: Erlbaum, 1990. The Hagye: Mouton, 1970. Leipzig: Wintersche, 1862. Synthesis and Photoresponsive Behaviors of Weil-Defined Azobenzene-Containing Polymers via RAFT Polymerization. Macromolecules 2007. V. 40. P. 48094817. Synthesis of Double Side-Chain Liquid Crystalline Block Copolymers Using RAFT Polymerization and the Orientational Cooperative Effect. Macromolecules 2008. V. 41. P. 3823-3831. A handbook of dietary practices. Toronto - Philadelphia: Mayo, 1988. - 636 p. 279. Pennington Ch.R. Malnutrition in hospital practice. CABI Publishing. - 2003. - 824 p. 295. Suchner U., Senftieben U., Eckart T. et al. Enteral versus parenteral: nutrition effects on gastrointestinal function and metabolism. Dialysate concentrations of ethanol, glycerol, glucose, and lactate were measured for estimating blood flow. Isoproterenol increased blood flow and lipolysis at both sites and those effects could be returned to baseline values by the addition of Ang II in aSAT but not fSAT.Discussion: In conclusion, our data indicate that in addition to its well-known vasoconstricting effect, Ang II inhibits lipolysis in adipose tissue, whereby femoral fat depots seem to be more sensitive to this effect than abdominal depots.Keywords: blood flow, glycolysis, lipolysis, metabolism, microdialysis Do you want to read the rest of this article. Request full-text Advertisement Citations (63) References (31). Indeed, the vasocontrictive effect of Ang II has also been demonstrated in adipose tissue. Infusion of Ang II, using the microdialysis technique, resulted in a reduction in adipose tissue blood flow (ATBF), which was more pronounced in femoral subcutaneous than in abdominal subcutaneous adipose tissue (110). The Ang II-induced reduction in ATBF could result in accumulation of free fatty acids (FFAs) or a decrease in intracellular pH, as demonstrated by a rise in lactate concentration in the dialysate (110), thereby inhibiting lipolysis (111)... Infusion of Ang II, using the microdialysis technique, resulted in a reduction in adipose tissue blood flow (ATBF), which was more pronounced in femoral subcutaneous than in abdominal subcutaneous adipose tissue (110). The Ang II-induced reduction in ATBF could result in accumulation of free fatty acids (FFAs) or a decrease in intracellular pH, as demonstrated by a rise in lactate concentration in the dialysate (110), thereby inhibiting lipolysis (111). In addition, accumulation of FFA could lead to an increased fatty acid re-esterification... Therefore, there is an apparent discrepancy between an Ang II-induced reduction in glucose uptake, as suggested by Boschmann et al. (110), and a concomitant increase in fatty acid re-esterification.. Possible involvement of the adipose tissue renin-angiotensin system in the pathophysiology of obesity and obesity-related disorders Article Mar 2003 OBES REV Gijs H Goossens Ellen Blaak Marleen van Baak Angiotensin II (Ang II), acting on the AT1 and AT2 receptors in mammalian cells, is the vasoactive component of the renin-angiotensin system (RAS). Several components of the RAS have been demonstrated in different tissues, including adipose tissue. In the first part of this review, we will describe the production of Ang II, the different receptors through which Ang II exerts its effects and summarize the concomitant intracellular signalling cascades. Thereafter, potential Ang II-induced mechanisms, which may be associated with obesity and obesity-related disorders, will be considered. Finally, we will focus on the different pharmaceutical agents that interfere with the RAS and highlight the possible implications of these drugs in the treatment of obesity-related disorders. View Show abstract. In the last two decades, a full renin-angiotensin system has been demonstrated in adipose tissue (8), but so far most of the data on the metabolic action of Ang II have been obtained from in vitro (9) or ex vivo studies (10,11). Recent studies addressing the in vivo effects of Ang II reported contrasting results on lipolysis and adipose blood flow (12) (13)(14). Concordant are the results on body weight loss in rats after chronic Ang II infusion, even at low doses (15)(16)(17)(18)(19). In fact, in situ Ang II administration has been found to either stimulate lipolysis without changes in blood flow (13) or inhibit lipolysis with reduction of adipose blood flow (12)... Contrasting results are reported on the in situ acute effect of Ang II on lipolysis and adipose blood flow (12)(13)(14), whereas no data, until now, have been available on the effect of chronic Ang II infusion. In fact, in situ Ang II administration has been found to either stimulate lipolysis without changes in blood flow (13) or inhibit lipolysis with reduction of adipose blood flow (12). It has been proposed that Ang II could have antilipolytic effects at physiological concentrations but lipolytic actions at supraphysiological concentrations (14).. Sympathetic Modulation by Carvedilol and Losartan Reduces Angiotensin II-Mediated Lipolysis in Subcutaneous and Visceral Fat Article Full-text available Jun 2005 J CLIN ENDOCR METAB Aderville Cabassi Pietro Coghi Paolo Govoni Enrico Fiaccadori Advanced heart failure is characterized by increased activation of the renin-angiotensin system and the development of cachexia. Angiotensin II (Ang II) has been proposed as a lipid metabolism regulator. Higher sustained interstitial glycerol and norepinephrine levels were found after 7 and 12 d of Ang II infusion. Triglyceride to DNA content ratio and adipocyte diameter were reduced in sc and visceral (retroperitoneal and epididymal) fat tissues of Ang II-infused rats, whose body weight was lower and blood pressure higher. Losartan, an Ang II receptor 1 blocker, and carvedilol, an alpha1-nonselective-beta1,2,3-adrenergic blocker, but not doxazosin, an alpha1-selective-adrenergic blocker, lowered glycerol and norepinephrine levels, preventing lipolysis and weight loss. Our results indicate that Ang II stimulates lipolysis in sc and visceral adipocytes by sympathetic activation and beta-adrenergic-receptor stimulation. Nonselective-beta-adrenergic and Ang II-receptor1 blockade markedly attenuated the rise of norepinephrine, preventing catabolic effects. The metabolic benefits of carvedilol and losartan, in addition to recognized protective cardiovascular effects, may be relevant in cachectic patients with advanced heart failure. Adipocytes also express and secrete angiotensinogen and angiotensin-II, which may relate to vasomotor control. 71 Innervation of white adipose tissue One obvious signalling pathway relevant to regulation of net fat deposition would be via the autonomic nervous system. Both sympathetic (adrenergic) 21 ( Figure 4) and parasympathetic (cholinergic) 72 activation affect adipose tissue lipolysis... This group includes TNFa, plasminogen activator inhibitor-1 and components of the renin-angiotensin system. 71, 129 It remains to be established which of these are secreted into the systemic circulation by adipose tissue. For example, although adipocytes secrete TNFa, and this cytokine can induce insulin resistance, 130 it may act more as a paracrine than as an endocrine Integrative physiology of human adipose tissue Article Full-text available Sep 2003 INT J OBESITY Keith Frayn Fredrik Karpe Barbara A Fielding Simon Coppack 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. Increased RAS activity has been associated with insulin resistance and decreased glucose uptake in various tissues, including adipose tissue. The accelerated adipose tissue growth and fat cell hypertrophy during the onset of obesity precedes adipocyte dysfunction. One of the features of adipocyte dysfunction is dysregulated adipokine secretion, which leads to an imbalance of pro-inflammatory, pro-atherogenic versus anti-inflammatory, insulin-sensitizing adipokines. The production of renin-angiotensin system (RAS) components by adipocytes is exacerbated during obesity, contributing to the systemic RAS and its consequences. Increased adipose tissue RAS has been described in various models of diet-induced obesity (DIO) including fructose and high-fat feeding. Up-regulation of the adipose RAS by DIO promotes inflammation, lipogenesis and reactive oxygen species generation and impairs insulin signaling, all of which worsen the adipose environment. Consequently, the increase of circulating RAS, for which adipose tissue is partially responsible, represents a link between hypertension, insulin resistance in diabetes and inflammation during obesity. However, other nutrients and food components such as soy protein attenuate adipose RAS, decrease adiposity, and improve adipocyte functionality. Here, we review the molecular mechanisms by which adipose RAS modulates systemic RAS and how it is enhanced in obesity, which will explain the simultaneous development of metabolic syndrome alterations. Finally, dietary interventions that prevent obesity and adipocyte dysfunction will maintain normal RAS concentrations and effects, thus preventing metabolic diseases that are associated with RAS enhancement. Microarray analysis of the complete genome of aliskiren-treated neonatal-rat cardiomyocytes, with RT-qPCR and immunoblot confirmation assays in rat and human primary cardiomyocytes, showed that aliskiren up-regulated mRNA and increased protein expression of several enzymes important in lipid and glucose metabolism and in cholesterol biosynthesis. Cardiomyocyte cell-cycle and viability were unaffected by aliskiren. View Show abstract. 14,15 Other actions of Ang II, such as vasoconstriction, also apply to adipose tissue. Drug treatments show dose and duration in weeks.. Selective reduction in body fat mass and plasma leptin induced by angiotensin-converting enzyme inhibition in rats Article Full-text available Aug 2008 Michael L Mathai S Naik Andrew J Sinclair R S Weisinger There is emerging evidence that angiotensin stimulates adipocyte differentiation and lipogenesis. This study tested the hypothesis that inhibition of angiotensin II by treatment with an angiotensin-converting enzyme inhibitor, perindopril, would reduce fat mass in rats. After a 12-day baseline, rats were divided into two groups: one was untreated and the other received perindopril (1.2 mg kg(-1) per day) in drinking water for 26 days. In total, 16 male Sprague-Dawley rats aged 10 weeks at the start of the study. Plasma leptin was measured in samples collected at baseline, half-way through and at the end of treatment. Body weight, food and water intake were measured daily throughout the experiment. Body fat mass, bone and lean mass were determined by dual energy X-ray absorptiometry (DEXA) at the end of the treatment period. Daily food intake was the same in both groups throughout the study. The association of the T allele with adipocyte size is in line with the role of AGT gene expression in adipocyte growth, as previously reported in animals (14,32). Besides its lipogenic effect (5), AngII could also elicit a hemodynamic and lipolytic response in adipose tissue, as previously reported (33). Using the microdialysis technique, Boschmann et al. (33) demonstrated that perfusion of AngII led to a decrease in blood flow and in lipolysis in adipose tissue from healthy men... Besides its lipogenic effect (5), AngII could also elicit a hemodynamic and lipolytic response in adipose tissue, as previously reported (33). Using the microdialysis technique, Boschmann et al. (33) demonstrated that perfusion of AngII led to a decrease in blood flow and in lipolysis in adipose tissue from healthy men. Although the effect of AngII on blood flow or lipolytic activity was moderate, this effect could be amplified in adipose tissue from obese subjects because of an increased overall metabolic activity.. Adipose Angiotensinogen Secretion, Blood Pressure, and AGT M235T Polymorphism in Obese Patients Article Full-text available Apr 2004 Obes Res Lydie Prat-Larquemin Jean-Michel Oppert Karine Clement Annie Quignard-Boulange To investigate AGT secretion in cultured adipocytes from obese patients and its relationship with obesity-related phenotypes, blood pressure, and the M235T polymorphism in the AGT gene. A subcutaneous abdominal adipose tissue biopsy was used for adipocyte size determination and quantification of AGT secretion in the medium of cultured adipocytes. AGT M235T genotype was determined using polymerase chain reaction-restriction fragment length polymorphism. The aim of this work was to study the expression of renin-angiotensin system genes in adipose tissue of obese hypertensive subjects and the hormonal regulation of these genes. Differential expression of renin-angiotensin system genes in subcutaneous abdominal adipocytes of 12 lean normotensive, eight obese normotensive, and 10 obese hypertensive women was determined in a cross-sectional study. In vitro hormonal regulation of these genes was studied in primary human adipocytes obtained by breast reduction from healthy women. In the clinical study, 24-h ambulatory blood pressure measurement and anthropometry were used to characterize the volunteers, and adipocytes were obtained by subcutaneous needle biopsy. The in vitro regulation of renin-angiotensin system genes by hydrocortisone, insulin, thyroxin, estradiol and angiotensin II on primary cultured human mammary adipocytes was studied by quantitative reverse transcriptase polymerase chain reaction (RT-PCR). While expression of the angiotensinogen gene was significantly lower in adipocytes from both obese groups, the renin, angiotensin-converting enzyme and angiotensin II type 1 receptor genes were significantly upregulated in obese hypertensives. Hydrocortisone increased angiotensin II type 1 receptor gene and protein expression in a time- and dose-dependent manner in human adipocytes, but had no significant influence on other renin-angiotensin system genes. Expression of these genes was not significantly affected by any of the other tested hormones. Renin-angiotensin system genes are differentially regulated in human obesity and hypertension. The role of the adipose-tissue renin-angiotensin system in the development of obesity-associated hypertension or metabolic disease clearly warrants further study. In fact, the effects of angiotensin II on glucose metabolism have been recently studied in different cells. The infusion of angiotensin II into the abdominal subcutaneous adipose tissue reduces glucose uptake (14). Adipocytes contain the renin-angiotensin system (RAS), which regulates signalling pathways that control angiogenesis via Akt in an autocrine fashion. Soya protein (Soy) consumption modifies the gene expression pattern in adipose tissue, resulting in an improved adipocyte function. Therefore, the aim of the present work is to study whether dietary Soy regulates the expression of RAS and angiogenesis-related genes and its association with the phosphorylated state of Akt in the adipose tissue of obese rats. Animals were fed a 30 Soy or casein (Cas) diet containing 5 or 25 fat for 160 d. mRNA abundance was studied in the adipose tissue, and Akt phosphorylation and hormone release were measured in the primary adipocyte culture. The present results show that Soy treatment in comparison with Cas consumption induces lower angiotensin release and increased insulin-stimulated Akt activation in adipocytes. Furthermore, Soy consumption varies the expression of RAS and angiogenesis-related genes, which maintain cell size and vascularity in the adipose tissue of rats fed a high-fat diet. Thus, adipocyte hypertrophy and impaired angiogenesis, which are frequently observed in dysfunctional adipose tissue, were avoided by consuming dietary Soy. Taken together, these findings suggest that Soy can be used as a dietary strategy to preserve adipocyte functionality and to prevent obesity abnormalities. The role of angiotensin II (AII) as a stimulator or inhibitor on lipolytic activity remains unclear in the literature 1, 2. Noradrenaline (NOR) has an important role in the energy metabolism of adipose tissue and exhibited a positive stimulus for lipolytic and glycolytic activity, increasing lactate and glycerol production 3,4.. Signaling downstream cascade crosstalk induced by noradrenaline on angiotensin II metabolic activity in adipocytes Conference Paper Full-text available Dec 2019 Camila Morais Dora Maria Grassi Kassisse Filipy Borghi Priscila Cristina da Silva The role of angiotensin II (AII) on lipolytic metabolism is still controversial in the literature. Diversely, noradrenaline (NOR) is an important stimulator of lipolysis and glycolysis in adipocytes. Spontaneously hypertensive rats (SHR) have lower body weight and smaller adipocytes when compared to its control, Wistar-Kyoto, with higher basal lactate production by area and volume. We aimed in this work to evaluate the influence in downstream cascate of AII and NOR, co-incubated or not, in the production of glycerol and lactate in three different strains. The combination of NOR and AII potentiated the lipolytic activity by decreasing the glucose metabolism to lactate. This effect may be associated with the NOR activity on adrenergic receptors or by the AII activity blockade at AT1 receptors, highlighting the antilipolytic activity of this receptor and the crosstalk between downstream cascade induced by these agonists. In the fedstate, this increased Agt production gives rise to Ang II production, which induces local vasoconstriction in the adipose tissue via its effect on AT 1. This leads to reduced lipolysis (Boschmann et al., 2001). Conversely, fasting leads to lower Agt and Ang II levels, giving rise to local vasodilation resulting in increased lipolysis.. The adipose tissue renin-angiotensin system and metabolic disorders: A review of molecular mechanisms Article Full-text available Jul 2012 Nishan Sudheera Kalupahana Naima Moustaid-Moussa The renin-angiotensin system (RAS) is classically known for its role in regulation of blood pressure, fluid and electrolyte balance. In this system, angiotensinogen (Agt), the obligate precursor of all bioactive angiotensin peptides, undergoes two enzymatic cleavages by renin and angiotensin converting enzyme (ACE) to produce angiotensin I (Ang I) and angiotensin II (Ang II), respectively. The contemporary view of RAS has become more complex with the discovery of additional angiotensin degradation pathways such as ACE2. All components of the RAS are expressed in and have independent regulation of adipose tissue. Mice with adipose-specific Agt overproduction have a 30 increase in plasma Agt levels and develop hypertension and insulin resistance, while mice with adipose-specific Agt knockout have a 25 reduction in Agt plasma levels, demonstrating endocrine actions of adipose RAS. Emerging evidence also points towards a role of RAS in regulation of energy balance. Because adipose RAS is overactivated in many obesity conditions, it is considered a potential candidate linking obesity to hypertension, insulin resistance and other metabolic derangements. Most randomized clinical trials have demonstrated that RAS blockade reduces the incidence of type 2 diabetes, which has been explained by improved insulin secretion and insulin sensitivity. In this review, an overview of the mechanisms that may underlie the association between the RAS and type 2 diabetes will be provided, with focus on skeletal muscle and adipose tissue function. This will include discussion of several human studies performed in our laboratory to investigate the metabolic and hemodynamic effects of the RAS, combining in vivo measurements of whole-body and tissue metabolism with molecular and immunohistochemical approaches. Available data suggest that the detrimental effects of the RAS on insulin secretion are mediated by a reduction in pancreatic blood flow and induction of islet fibrosis, oxidative stress as well as inflammation, whereas both impaired skeletal muscle function and adipose tissue dysfunction may underlie RAS-induced insulin resistance. Thus, although future studies in humans are warranted, current evidence supports that targeting the RAS in intervention studies may improve metabolic and cardiovascular function in conditions of insulin resistance like obesity and type 2 diabetes. Studies using the microdialysis technique demonstrated site-specific differences in the local action of Ang II in human adipose-tissue. Article Jul 2003 INT J BIOCHEM CELL B Stefan Engeli Petra Schling Kerstin Gorzelniak Arya Mitra Sharma Overfeeding of rodents leads to increased local formation of angiotensin II due to increased secretion of angiotensinogen from adipocytes. Whereas angiotensin II promotes adipocyte growth and preadipocyte recruitment, increased secretion of angiotensinogen from adipocytes also directly contributes to the close relationship between adipose-tissue mass and blood pressure in mice. In contrast, angiotensin II acts as an antiadipogenic substance in human adipose tissue, and the total increase in adipose-tissue mass may be more important in determining human plasma angiotensinogen levels than changes within the single adipocyte. However, as increased local formation of angiotensin II in adipose tissue may be increased especially in obese hypertensive subjects, a contribution of the adipose-tissue renin-angiotensin system to the development of insulin resistance and hypertension is conceivable in humans, but not yet proven. Insulin resistance may be aggravated by the inhibition of preadipocyte recruitment, which results in the redistribution of triglycerides to the liver and skeletal muscle, and blood pressure may be influenced by local formation of angiotensin II in perivascular adipose tissue. Thus, although the mechanisms are still speculative, the beneficial effects of ACE-inhibition and angiotensin-receptor blockade on the development of type 2 diabetes in large clinical trials suggest a pathophysiological role of the adipose-tissue renin-angiotensin system in the metabolic syndrome. Ang II is an active mediator of lipolysis in a time-dependent manner. Short term treatment of Ang II inhibits lipolysis in human adipose tissue and adipocytes through the AT1 receptor (Boschmann et al., 2001; Goossens et al., 2004Goossens et al.,, 2007. However, long term infusion of Ang II markedly increased lipolysis in rats (Cabassi et al., 2005).. Angiotensinogen Gene Silencing Reduces Markers of Lipid Accumulation and Inflammation in Cultured Adipocytes Article Full-text available Mar 2013 Wenting X Carroll Suzanne L Booker Nishan Sudheera Kalupahana Naima Moustaid-Moussa Inflammatory adipokines secreted from adipose tissue are major contributors to obesity-associated inflammation and other metabolic dysfunctions. We and others have recently documented the contribution of adipose tissue renin-angiotensin system to the pathogenesis of obesity, inflammation, and insulin resistance. This was tested using 3T3-L1 adipocytes, stably transfected with Agt-shRNA or scrambled Sc-shRNA as a control. Transfected preadipocytes were differentiated and used to investigate the role of adipose Agt through microarray and PCR analyses and adipokine profiling. As expected, Agt gene silencing significantly reduced the expression of Agt and its hormone product angiotensin II (Ang II), as well as lipid accumulation in 3T3-L1 adipocytes. Microarray studies identified several genes involved in lipid metabolism and inflammatory pathways which were down-regulated by Agt gene inactivation, such as glycerol-3-phosphate dehydrogenase 1 (Gpd1), serum amyloid A 3 (Saa3), nucleotide-binding oligomerization domain containing 1 (Nod1), and signal transducer and activator of transcription 1 (Stat1). Further, silencing of Agt gene significantly lowered expression of pro-inflammatory adipokines including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-?), and monocyte chemotactic protein-1 (MCP-1). In conclusion, this study directly demonstrates critical effects of Agt in adipocyte metabolism and inflammation and further support a potential role for adipose Agt in the pathogenesis of obesity-associated metabolic alterations. Although the detailed mechanism of how mTOR inhibition interferes with body weight regulation is rather unclear, present data suggest that this effect is mediated by both central and peripheral mechanisms. These findings in ADPKD patients are in contrast to well-documented effects of hypothalamic mTOR on regulation of energy homeostasis and eating behavior in rodents. In a number of rodent models, the mTOR inhibitor rapamycin induces increased food intake, which is accompanied by increased body weight. However, animal data are inconsistent.