FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2081730949> ?p ?o ?g. }

• W2081730949 endingPage "S118" @default.
• W2081730949 startingPage "S112" @default.
• W2081730949 abstract "Leptin and adiponectin are adipokines with respective pro-atherogenic and anti-atherogenic properties, defining the plasma leptin/adiponectin ratio as a novel marker for atherosclerosis. In non-renal patients, both hyperleptinemia and hypoadiponectinemia are associated with cardiovascular complications. In peritoneal dialysis (PD) patients, the leptin/adiponectin ratio is markedly elevated, which is consistent with their increased cardiovascular risk. As glucose metabolism regulates adipokines, we hypothesized that glucose and/or other PD fluid components may affect adipokine production balance. This review summarizes the available data arising from research in this area. In 3T3-L1 adipocytes, glucose-based PD4 1.36% significantly increased leptin secretion vs amino-acid-based (AA) and icodextrin (ICOD)-based PD fluids. In contrast, adiponectin secretion was significantly reduced by PD4 1.36% vs glucose-free dialysates. Glucose concentration in PD fluids was shown to determine leptin secretion. Preliminary data from PD patients showed that a single 6-h dwell with PD4 3.86% glucose acutely increased plasma leptin vs AA (P<0.05). The reduction in glucose load in a standard PD regimen was associated with an improvement in the plasma leptin/adiponectin ratio at 6 months. pH-neutral PD fluids increased leptin secretion in vitro vs acidic PD fluids, without effect on adiponectin. Whether this effect may have an impact on plasma leptin levels in PD patients is unknown. In conclusion, glucose-based PD fluids worsen the adipokine production balance in vitro while glucose-free solutions improve it. In PD patients, hypertonic glucose-based PD fluids may increase plasma leptin levels. Glucose-sparing PD regimens appear to improve the leptin/adiponectin ratio. However, their potential to reduce cardiovascular complications needs to be demonstrated. Leptin and adiponectin are adipokines with respective pro-atherogenic and anti-atherogenic properties, defining the plasma leptin/adiponectin ratio as a novel marker for atherosclerosis. In non-renal patients, both hyperleptinemia and hypoadiponectinemia are associated with cardiovascular complications. In peritoneal dialysis (PD) patients, the leptin/adiponectin ratio is markedly elevated, which is consistent with their increased cardiovascular risk. As glucose metabolism regulates adipokines, we hypothesized that glucose and/or other PD fluid components may affect adipokine production balance. This review summarizes the available data arising from research in this area. In 3T3-L1 adipocytes, glucose-based PD4 1.36% significantly increased leptin secretion vs amino-acid-based (AA) and icodextrin (ICOD)-based PD fluids. In contrast, adiponectin secretion was significantly reduced by PD4 1.36% vs glucose-free dialysates. Glucose concentration in PD fluids was shown to determine leptin secretion. Preliminary data from PD patients showed that a single 6-h dwell with PD4 3.86% glucose acutely increased plasma leptin vs AA (P<0.05). The reduction in glucose load in a standard PD regimen was associated with an improvement in the plasma leptin/adiponectin ratio at 6 months. pH-neutral PD fluids increased leptin secretion in vitro vs acidic PD fluids, without effect on adiponectin. Whether this effect may have an impact on plasma leptin levels in PD patients is unknown. In conclusion, glucose-based PD fluids worsen the adipokine production balance in vitro while glucose-free solutions improve it. In PD patients, hypertonic glucose-based PD fluids may increase plasma leptin levels. Glucose-sparing PD regimens appear to improve the leptin/adiponectin ratio. However, their potential to reduce cardiovascular complications needs to be demonstrated. The adipose tissue is now recognized as an active endocrine organ, involved in the regulation of energy homeostasis and metabolism.1.Kershaw E.E. Flier J.S. Adipose tissue as an endocrine organ.J Clin Endocrinol Metab. 2004; 89: 2548-2556Crossref PubMed Scopus (3371) Google Scholar Adipocytes secrete a number of hormones and cytokines, namely adipokines, including leptin, adiponectin, tumor necrosis factor-α, interleukin-6, resistin, and visfatin, which are implicated in important pathophysiological mechanisms determining health and disease. Leptin and adiponectin have well-defined actions in humans. Leptin is a 167-amino-acid (AA)-circulating protein encoded by the ob gene, which signals the body's nutritional status to the brain to regulate energy balance.2.Halaas J.L. Gajiwala K.S. Maffei M. et al.Weight-reducing effects of the plasma protein encoded by the obese gene.Science. 1995; 269: 543-546Crossref PubMed Scopus (4103) Google Scholar Leptin also has distinct cytokine properties, such as the stimulation of inflammation and modulation of the immune system.3.Gainsford T. Willson T.A. Metcalf D. et al.Leptin can induce proliferation, differentiation and functional activation of hemopoietic cells.Proc Natl Acad Sci USA. 1996; 93: 14564-14568Crossref PubMed Scopus (653) Google Scholar Adiponectin is a 244-AA protein produced by the apM1 gene, which has insulin-sensitizing, anti-inflammatory, and anti-atherogenic properties.4.Ouchi N. Kihara S. Arita Y. et al.Novel modulator for endothelial adhesion molecules. Adipocyte-derived plasma protein adiponectin.Circulation. 1999; 100: 2473-2476Crossref PubMed Scopus (1895) Google Scholar In patients with end-stage renal disease (ESRD), adipokines accumulate in plasma, mainly because of the loss of renal clearance.5.Nordfors L. Lonnqvist F. Heimburger O. et al.Low leptin gene expression and hyperleptinemia in chronic renal failure.Kidney Int. 1998; 54: 1267-1275Abstract Full Text Full Text PDF PubMed Scopus (166) Google Scholar,6.Huang J.W. Yen C.J. Chiang H.W. et al.Adiponectin in peritoneal dialysis patients: a comparison with hemodialysis patients and subjects with normal renal function.Am J Kidney Dis. 2004; 43: 1047-1055Abstract Full Text Full Text PDF PubMed Scopus (101) Google Scholar However, an important determinant of plasma levels of adipokines is fat mass, even in patients with various stages of renal insufficiency.5.Nordfors L. Lonnqvist F. Heimburger O. et al.Low leptin gene expression and hyperleptinemia in chronic renal failure.Kidney Int. 1998; 54: 1267-1275Abstract Full Text Full Text PDF PubMed Scopus (166) Google Scholar,6.Huang J.W. Yen C.J. Chiang H.W. et al.Adiponectin in peritoneal dialysis patients: a comparison with hemodialysis patients and subjects with normal renal function.Am J Kidney Dis. 2004; 43: 1047-1055Abstract Full Text Full Text PDF PubMed Scopus (101) Google Scholar Plasma leptin level is strongly correlated with fat mass.7.Considine R.V. Sinha M.K. Heiman M.L. et al.Serum immunoreactive-leptin concentrations in normal-weight and obese humans.N Engl J Med. 1996; 334: 292-295Crossref PubMed Scopus (5306) Google Scholar Thus, ESRD patients have hyperleptinemia, which is further magnified by high fat mass.8.Heimburger O. Lonnqvist F. Danielsson A. et al.Serum immunoreactive leptin concentrations and its relation to the body fat content in chronic renal failure.J Am Soc Nephrol. 1997; 8: 1423-1430PubMed Google Scholar In contrast, plasma adiponectin level is inversely correlated with adipose tissue mass,9.Arita Y. Kihara S. Ouchi N. et al.Paradoxical decrease of an adipose-specific protein, adiponectin, in obesity.Biochem Biophys Res Commun. 1999; 257: 79-83Crossref PubMed Scopus (3923) Google Scholar and patients with ESRD display moderate hyperadiponectinemia, which may be mitigated in obese patients. Other factors such as gender, sex hormone levels, and factors associated with ESRD such as inflammation, hyperinsulinemia, and acidosis, may superimpose modulation of either leptin10.Grunfeld C. Zhao C. Fuller J. et al.Endotoxin and cytokines induce expression of leptin, the ob gene product, in hamsters.J Clin Invest. 1996; 97: 2152-2157Crossref PubMed Scopus (807) Google Scholar, 11.Bradley R.L. Cheatham B. Regulation of ob gene expression and leptin secretion by insulin and dexamethasone in rat adipocytes.Diabetes. 1999; 48: 272-278Crossref PubMed Scopus (172) Google Scholar, 12.Teta D. Bevington A. Brown J. et al.Effects of acidosis on leptin secretion from 3T3-L1 adipocytes and on serum leptin in the uraemic rat.Clin Sci. 1999; 97: 363-368Crossref PubMed Scopus (27) Google Scholar and/or adiponectin13.Fasshauer M. Klein J. Neumann S. et al.Hormonal regulation of adiponectin gene expression in 3T3-L1 adipocytes.Biochem Biophys Res Commun. 2002; 290: 1084-1089Crossref PubMed Scopus (565) Google Scholar,14.Yu J.G. Javorschi S. Hevener A.L. et al.The effects of thiazolidinediones on plasma adiponectin levels in normal, obese and type 2 diabetic subjects.Diabetes. 2002; 51: 2968-2974Crossref PubMed Scopus (634) Google Scholar production to determine final plasma levels. Peritoneal dialysis (PD) is characterized by gain of fat mass, extraordinarily raised plasma leptin15.Pérez Fontán M. Rodríguez-Carmona A. Cordido F. García-Buela J. Hyperleptinemia in uremic patients undergoing conservative management, peritoneal dialysis and hemodialysis: a comparative analysis.Am J Kidney Dis. 1999; 34: 824-831Abstract Full Text Full Text PDF PubMed Scopus (75) Google Scholar and moderate hyperadiponectinemia6.Huang J.W. Yen C.J. Chiang H.W. et al.Adiponectin in peritoneal dialysis patients: a comparison with hemodialysis patients and subjects with normal renal function.Am J Kidney Dis. 2004; 43: 1047-1055Abstract Full Text Full Text PDF PubMed Scopus (101) Google Scholar and, thus, represents a distinct condition for the study of adipokine metabolism. Glucose metabolism is a major factor regulating both leptin16.Mueller W.M. Gregoire F.M. Stanhope K.L. et al.Evidence that glucose metabolism regulates leptin secretion from cultured rat adipocytes.Endocrinology. 1998; 139: 551-558Crossref PubMed Scopus (354) Google Scholar and adiponectin.17.Hazel M. Cooksey R.C. Jones D. et al.Activation of the hexosamine signaling pathway in adipose tissue results in decreased serum adiponectin and skeletal muscle insulin resistance.Endocrinology. 2004; 145: 2118-2124Crossref PubMed Scopus (55) Google Scholar As glucose is a key element in the composition of most PD fluids, we hypothesized that glucose-based PD solutions and/or a regimen high in glucose may regulate plasma levels of leptin and adiponectin in these patients. Because adipokines have pleiotropic actions, that is, on insulin sensitivity, inflammation, immunity, and atherosclerosis, the adipokine balance in PD may thus have an impact on patient outcome. The aims of this article are the following: (1) to review the biological and clinical actions of adipokines, with a focus on the cardiovascular system; (2) to introduce the notion of the leptin/adiponectin ratio as a novel marker for cardiovascular risk; and (3) to discuss the effects of PD fluids on adipokine production balance in vitro and on leptin/adiponectin ratio in PD patients. It is hypothesized that modulation of the adipokine profile by using a glucose-sparing PD regimen could reduce cardiovascular risk in PD patients. Leptin was first described as the monogenic mutation responsible for the morbidly obese phenotype observed in the ob/ob mouse.18.Zhang Y. Proenca R. Maffei M. et al.Positional cloning of the mouse obese gene and its human homologue.Nature. 1994; 372: 425-432Crossref PubMed Scopus (11221) Google Scholar After secretion from adipose tissue into plasma, this 16-kDa protein crosses the blood-brain barrier and interacts with specific leptin receptors (Ob-Rb) in the hypothalamus to limit food intake.2.Halaas J.L. Gajiwala K.S. Maffei M. et al.Weight-reducing effects of the plasma protein encoded by the obese gene.Science. 1995; 269: 543-546Crossref PubMed Scopus (4103) Google Scholar Leptin also increases energy expenditure through a stimulatory effect on the sympathetic nervous system.19.Friedman J.M. Halaas J.L. Leptin and the regulation of body weight in mammals.Nature. 1998; 395: 763-770Crossref PubMed Scopus (4320) Google Scholar Obese patients have high not low leptin levels, suggesting that obesity may be associated with leptin resistance.7.Considine R.V. Sinha M.K. Heiman M.L. et al.Serum immunoreactive-leptin concentrations in normal-weight and obese humans.N Engl J Med. 1996; 334: 292-295Crossref PubMed Scopus (5306) Google Scholar However, leptin sensitivity may be restored when plasma leptin is reduced, for instance, after weight loss.20.Auwerx J. Staels B. Leptin.Lancet. 1998; 351: 737-742Abstract Full Text Full Text PDF PubMed Scopus (509) Google Scholar Leptin has effects well beyond the regulation of energy balance. The discovery of Ob-Rb receptors in peripheral tissues such as T cells21.Lord G.M. Matarese G. Howard J.K. et al.Leptin modulates the T-cell immune response and reverses starvation-induced immunosuppression.Nature. 1998; 394: 897-901Crossref PubMed Scopus (1760) Google Scholar and vascular endothelial cells22.Bouloumié A. Marumo T. Lafontan M. Busse R. Leptin induces oxidative stress in human endothelial cells.FASEB J. 1999; 13: 1231-1238Crossref PubMed Scopus (592) Google Scholar has indeed ascribed to leptin a status of pleiotropic adipokine. In particular, leptin has distinct pathophysiological effects on the cardiovascular system, which may be important in hyperleptinemic states such as in PD, in light of the high cardiovascular mortality of these patients. Leptin-induced cardiovascular actions have been summarized in two recent reviews.23.Correia M.L. Haynes W.G. Leptin, obesity and cardiovascular disease.Curr Opin Nephrol Hypertens. 2004; 13: 215-223Crossref PubMed Scopus (135) Google Scholar,24.Ren J. Leptin and hyperleptinaemia—from friend to foe for cardiovascular function.J Endocrinol. 2004; 181: 1-10Crossref PubMed Scopus (249) Google Scholar Experimental and clinically relevant data are detailed in the following paragraph. Leptin injected acutely in mice activates sympathetic outflow via both central and peripheral mechanisms.25.Satoh N. Ogawa Y. Katsuura G. et al.Sympathetic activation of leptin via the ventromedial hypothalamus: leptin-induced increase in catecholamine secretion.Diabetes. 1999; 48: 1787-1793Crossref PubMed Scopus (188) Google Scholar Chronic intravenous infusion of leptin over 1 week increases blood pressure and heart rate in conjunction with overt weight loss,26.Shek E.W. Brands M.W. Hall J.E. Chronic leptin infusion increases arterial pressure.Hypertension. 1998; 31: 409-414Crossref PubMed Scopus (630) Google Scholar indicating that leptin per se induces a sympathetic effect independent of fat mass accumulation. The above experimental findings are supported by epidemiological evidence that leptin and arterial pressure are correlated, although modestly, even after adjustment for adiposity.27.Agata J. Matsuda A. Takada M. et al.High plasma immunoreactive leptin level in essential hypertension.Am J Hypertens. 1997; 10: 1171-1174Crossref PubMed Scopus (232) Google Scholar An independent association between leptin levels and heart rate was found in heart transplant recipients with sympathetic denervation,28.Winnicki M. Phillips B.G. Accurso V. et al.Independent association between plasma leptin levels and heart rate in heart transplant recipients.Circulation. 2001; 104: 384-386Crossref PubMed Scopus (41) Google Scholar suggesting a direct effect of leptin on heart rate, presumably through cardiac leptin receptors. Angiotensin II has been shown to increase leptin synthesis in cultured adipocytes29.Kim S. Whelan J. Claycombe K. et al.Angiotensin II increases leptin secretion by 3T3-L1 and human adipocytes via a prostaglandin-independent mechanism.J Nutr. 2002; 132: 1135-1140PubMed Google Scholar and in rats in vivo,30.Cassis L.A. English V.L. Bharadwaj K. Boustany C.M. Differential effects of local versus systemic angiotensin II in the regulation of leptin release from adipocytes.Endocrinology. 2004; 145: 169-174Crossref PubMed Scopus (63) Google Scholar which suggests that angiotensin II and leptin could synergically interact to promote hypertension. Leptin directly acts on the vasculature. In vitro experiments have shown that leptin induces proliferation of rat vascular smooth muscle cells,31.Oda A. Taniguchi T. Yokoyama M. Leptin stimulates rat aortic smooth muscle cell proliferation and migration.Kobe J Med Sci. 2001; 47: 141-150PubMed Google Scholar osteogenic transformation of cultured vascular cells prone to develop calcified lesions,32.Parhami F. Tintut Y. Ballard A. et al.Leptin enhances the calcification of vascular cells: artery wall as a target of leptin.Circ Res. 2001; 88: 954-960Crossref PubMed Scopus (288) Google Scholar regeneration of endothelial cells after intimal injury,33.Stephenson K. Tunstead J. Tsai A. et al.Neointimal formation after endovascular arterial injury is markedly attenuated in db/db mice.Arterioscler Thromb Vasc Biol. 2003; 23: 2027-2033Crossref PubMed Scopus (63) Google Scholar and stimulation of oxidative stress.22.Bouloumié A. Marumo T. Lafontan M. Busse R. Leptin induces oxidative stress in human endothelial cells.FASEB J. 1999; 13: 1231-1238Crossref PubMed Scopus (592) Google ScholarIn vivo, leptin may exert a direct vasodilatory action through nitric oxide-dependent and independent effects. However, the sympathetically mediated pressor effect of leptin predominates over its vasodilatory effect.23.Correia M.L. Haynes W.G. Leptin, obesity and cardiovascular disease.Curr Opin Nephrol Hypertens. 2004; 13: 215-223Crossref PubMed Scopus (135) Google Scholar Leptin is a pro-coagulant factor. In ob/ob mice, thrombi from arterial lesions are unstable compared with those in littermate controls, and leptin replacement normalizes thrombi formation.34.Konstantinides S. Schafer K. Koschnick S. Loskutoff D.J. Leptin-dependent platelet aggregation and arterial thrombosis suggests a mechanism for atherothrombotic disease in obesity.J Clin Invest. 2001; 8: 1533-1540Crossref Scopus (326) Google Scholar Leptin may also modulate fibrinolysis since plasma leptin was significantly associated with decreased plasminogen activator inhibitor-1 activity even after adjustments for adiposity and age.35.Soderberg S. Olsson T. Eliasson M. et al.Plasma leptin levels are associated with abnormal fibrinolysis in men and postmenopausal women.J Intern Med. 1999; 245: 533-543Crossref PubMed Scopus (83) Google Scholar Along with the above experimental data, there is increasing epidemiological evidence linking leptin and cardiovascular markers and/or clinical end points. Leptin was independently associated with decreased arterial distensibility in healthy adolescents within a wide range of body mass indexes.36.Singhal A. Farooqi I.S. Cole T.J. et al.Influence of leptin on arterial distensibility: a novel link between obesity and cardiovascular disease?.Circulation. 2002; 106: 1919-1924Crossref PubMed Scopus (328) Google Scholar In hypertensive men, myocardial wall thickness was associated with high plasma leptin, independently of body composition and blood pressure.37.Paolisso G. Tagliamonte M.R. Galderisi M. et al.Plasma leptin is associated with myocardial thickness in hypertensive insulin-resistant men.Hypertension. 1999; 34: 1047-1052Crossref PubMed Scopus (142) Google Scholar Leptin was independently associated with coronary calcification in a cohort of type II diabetic patients.38.Reilly M.P. Iqbal N. Shutta M. et al.Plasma leptin levels are associated with coronary atherosclerosis in type 2 diabetes.J Clin Endocrinol Metab. 2004; 89: 3872-3878Crossref PubMed Scopus (173) Google Scholar Leptin also has been associated with myocardial infarction and stroke.39.Soderberg S. Ahren B. Jansson J.H. et al.Leptin is associated with increased risk of myocardial infarction.J Intern Med. 1999; 246: 409-418Crossref PubMed Scopus (318) Google Scholar,40.Soderberg S. Stegmayr B. Ahlbeck-Glader C. et al.High leptin levels are associated with stroke.Cerebrovasc Dis. 2003; 15: 63-69Crossref PubMed Scopus (85) Google Scholar Finally, in the prospective West of Scotland Coronary Prevention Study (WOSCOPS), leptin independently increased the relative risk for a first myocardial infarction.41.Wallace A.M. McMahon A.D. Packard C.J. et al.Plasma leptin and the risk of cardiovascular disease in the west of Scotland coronary prevention study (WOSCOPS).Circulation. 2001; 104: 3052-3056Crossref PubMed Scopus (716) Google Scholar Adiponectin is a 30-kDa adipocyte complement-related protein encoded by the adipose most abundant gene transcript 1 (apM1), which has distinct insulin-sensitizing effects.42.Lihn A.S. Pedersen S.B. Richelsen B. Adiponectin: action, regulation and association to insulin sensitivity.Obes Rev. 2005; 6: 13-21Crossref PubMed Scopus (487) Google Scholar Adiponectin circulates in human plasma as a hexamer of relatively low molecular weight, and as a larger multimeric structure of high molecular weight (HMW) at high concentrations ranging from 0.5 to 20 μg ml−1 that is 0.01% of the total plasma protein pool.42.Lihn A.S. Pedersen S.B. Richelsen B. Adiponectin: action, regulation and association to insulin sensitivity.Obes Rev. 2005; 6: 13-21Crossref PubMed Scopus (487) Google Scholar It is thought that the HMW adiponectin complex is the active form of this protein, and that the ratio HMW/total adiponectin (HMW+low molecular weight) is more accurate than total adiponectin in predicting insulin sensitivity.43.Pajvani U.B. Hawkins M. Combs T.P. et al.Complex distribution, not absolute amount of adiponectin, correlates with thiazolidinedione-mediated improvement in insulin sensitivity.J Biol Chem. 2003; 279: 12152-12162Crossref PubMed Scopus (982) Google Scholar In contrast to most adipose tissue-derived proteins such as leptin, plasma adiponectin has a paradoxical negative correlation with fat mass.9.Arita Y. Kihara S. Ouchi N. et al.Paradoxical decrease of an adipose-specific protein, adiponectin, in obesity.Biochem Biophys Res Commun. 1999; 257: 79-83Crossref PubMed Scopus (3923) Google Scholar Adiponectin release is significantly lower from omental than subcutaneous adipose tissue (Johnson J et al. Obes Res 2003; 11: A34; abstract), which is consistent with the higher cardiovascular risk observed in men and in clinical situations in which truncal (that is, visceral) obesity is predominant. The insulin-sensitizing effects of adiponectin are mediated through adiponectin receptors 1 and 2, which are primarily expressed in skeletal muscle and in the liver, respectively. Receptors are indeed markedly expressed in pancreatic β-cells,44.Kharroubi I. Rasschaert J. Eizirik D.L. Cnop M. Expression of adiponectin receptors in pancreatic beta cells.Biochem Biophys Res Commun. 2003; 312: 1118-1122Crossref PubMed Scopus (222) Google Scholar macrophages, atherosclerotic lesions45.Chinetti G. Zawadski C. Fruchart J.C. Staels B. Expression of adiponectin receptors in human macrophages and regulation by agonists of the nuclear receptors PPARalpha, PPARgamma and LXR.Biochem Biophys Res Commun. 2004; 314: 151-158Crossref PubMed Scopus (239) Google Scholar and the brain,46.Qi Y. Takahashi N. Hileman S.M. et al.Adiponectin acts in the brain to decrease body weight.Nat Med. 2004; 10: 524-529Crossref PubMed Scopus (647) Google Scholar reflecting pleiotropic actions of adiponectin, such as for leptin. Beyond its primary insulin-sensitizing effect, the interest in adiponectin derives from its potential protective role for the cardiovascular system. Adiponectin inhibits endothelial cell production of adhesion molecules in vitro, thus suppressing the attachment of monocytes, an early event occurring in the atherosclerotic process.4.Ouchi N. Kihara S. Arita Y. et al.Novel modulator for endothelial adhesion molecules. Adipocyte-derived plasma protein adiponectin.Circulation. 1999; 100: 2473-2476Crossref PubMed Scopus (1895) Google Scholar In addition, adiponectin has direct anti-inflammatory actions, since it reduces the production and activity of tumor necrosis factor-α;47.Masaki T. Chiba S. Tatsukawa H. et al.Adiponectin protects LPS-induced liver injury through modulation of TNF-alpha in KK-ay obese mice.Hepatology. 2004; 40: 177-184Crossref PubMed Scopus (351) Google Scholar conversely, tumor necrosis factor-α downregulates adiponectin production.48.Kappes A. Loffler G. Influences of ionomycin, dibutyryl-cycloAMP and tumor necrosis factor alpha on intracellular amount and secretion of apM1 in differentiating primary human preadipocytes.Horm Metab Res. 2000; 32: 548-554Crossref PubMed Scopus (171) Google Scholar Neointimal thickening of damaged arteries was exacerbated in adiponectin-deficient mice and was inhibited by exogenous adiponectin,49.Matsuda M. Shimomura I. Sata M. et al.Role of adiponectin in preventing vascular stenosis. The missing link of adipo-vascular axis.J Biol Chem. 2002; 277: 37487-37491Crossref PubMed Scopus (710) Google Scholar suggesting that adiponectin may play a role in the intimal proliferation observed after angioplasty. In line with experimental data, low plasma adiponectin concentrations have been reported in patients with coronary artery disease,50.Kumada M. Kihara S. Sumitsuji S. et al.Association of hypoadiponectinaemia with coronary artery disease in men.Arterioscler Thromb Vasc Biol. 2003; 23: 85-89Crossref PubMed Scopus (1230) Google Scholar obesity,9.Arita Y. Kihara S. Ouchi N. et al.Paradoxical decrease of an adipose-specific protein, adiponectin, in obesity.Biochem Biophys Res Commun. 1999; 257: 79-83Crossref PubMed Scopus (3923) Google Scholar essential hypertension,51.Adamczak M. Wiecek A. Funahashi T. et al.Decreased plasma adiponectin concentration in patients with essential hypertension.Am J Hypertens. 2003; 16: 72-75Crossref PubMed Scopus (355) Google Scholar and type II diabetes mellitus.52.Hotta K. Funahashi T. Arita Y. et al.Plasma concentrations of a novel, adipose-specific protein, adiponectin, in type 2 diabetic patients.Arterioscler Thromb Vasc Biol. 2000; 20: 1595-1599Crossref PubMed Scopus (2634) Google Scholar Furthermore, low levels of adiponectin were found to predict later development of type II diabetes,53.Spranger J. Kroke A. Moehlig M. et al.Adiponectin and protection against type 2 diabetes mellitus.Lancet. 2003; 361: 226-228Abstract Full Text Full Text PDF PubMed Scopus (897) Google Scholar myocardial infarction,54.Pischon T. Girman C.J. Hotamisligil G.S. et al.Plasma adiponectin levels and risk of myocardial infarction in men.JAMA. 2004; 291: 1730-1737Crossref PubMed Scopus (1471) Google Scholar and coronary heart disease.55.Frystic J. Berne C. Berglund L. et al.Serum adiponectin is a predictor of coronary heart disease: a population-based 10-year follow-up study in elderly men.J Clin Endocrinol Metab. 2007; 92: 571-576Crossref PubMed Scopus (172) Google Scholar As shown above, there is clear biological evidence that leptin and adiponectin have opposite effects on the cardiovascular system, including directly on blood vessels. Clinical studies linking adipokines and outcome are not overwhelming, but the evidence we have so far indicates that both hyperleptinemia and hypoadiponectinemia are associated with a worse cardiovascular outcome. In line with this view, it was reported that the leptin/adiponectin ratio is correlated with pulse wave velocity to a greater extent than plasma leptin and adiponectin alone.56.Satoh N. Naruse M. Usui T. et al.Leptin-to-adiponectin ratio as a potential atherogenic index in obese type 2 diabetic patients.Diabetes Care. 2004; 27: 2488-2490Crossref PubMed Scopus (176) Google Scholar Another recent study showed that the leptin/adiponectin ratio could serve as a clinical marker for atherosclerosis in type II diabetic subjects, as it was a strong indicator of increased carotid intima-media thickness.57.Kotani K. Sakane N. Saiga K. Kurozawa Y. Leptin: adiponectin ratio as an atherogenic index in patients with type 2 diabetes: relationship of the index to carotid intima-media thickness.Diabetologia. 2005; 48: 2684-2686Crossref PubMed Scopus (85) Google Scholar Although further epidemiological evidence is needed to consolidate the notion of leptin/adiponectin ratio, these preliminary observations suggest that patients exhibiting a high plasma ratio may be prone to cardiovascular events. Plasma leptin levels in patients treated by PD are considerably higher than those observed in hemodialysis patients and in patients with chronic renal failure under conservative treatment.15.Pérez Fontán M. Rodríguez-Carmona A. Cordido F. García-Buela J. Hyperleptinemia in uremic patients undergoing conservative management, peritoneal dialysis and hemodialysis: a comparative analysis.Am J Kidney Dis. 1999; 34: 824-831Abstract Full Text Full Text PDF PubMed Scopus (75) Google Scholar PD-associated hyperleptinemia is out of proportion to fat accumulation observed under this treatment and reaches a 5- to 20-fold increment vs controls.15.Pérez Fontán M. Rodríguez-Carmona A. Cordido F. García-Buela J. Hyperleptinemia in uremic patients undergoing conservative management, peritoneal dialysis and hemodialysis: a comparative analysis.Am J Kidney Dis. 1999; 34: 824-831Abstract Full Text Full Text PDF PubMed Scopus (75) Google Scholar Furthermore, plasma leptin is already elevated a few days after PD treatment is started,58.Kim D.J. Oh D.J. Kim B. et al.The effect of continuous ambulatory peritoneal dialysis on change in serum leptin.Perit Dial Int. 1999; 19: S172-S175PubMed Google Scholar which suggests that specific factors associated with the PD procedure itself may stimulate leptin production in these patients. Compared to leptin, plasma adiponectin is only modestly increased in PD patients, by about two- to threefold vs controls.6.Huang J.W. Yen C.J. Chiang H.W. et al.Adiponectin in peritoneal dialysis patients: a comparison with hemodialysis patients and subjects with normal renal function" @default.
• W2081730949 created "2016-06-24" @default.
• W2081730949 creator A5024841234 @default.
• W2081730949 creator A5047911273 @default.
• W2081730949 creator A5070800289 @default.
• W2081730949 creator A5084492517 @default.
• W2081730949 date "2008-04-01" @default.
• W2081730949 modified "2023-10-02" @default.
• W2081730949 title "The leptin/adiponectin ratio: Potential implications for peritoneal dialysis" @default.
• W2081730949 cites W1515160531 @default.
• W2081730949 cites W1590709474 @default.
• W2081730949 cites W1631449371 @default.
• W2081730949 cites W1893788133 @default.
• W2081730949 cites W1898391394 @default.
• W2081730949 cites W1964056978 @default.
• W2081730949 cites W1968284284 @default.
• W2081730949 cites W1968893131 @default.
• W2081730949 cites W1969529626 @default.
• W2081730949 cites W1970022980 @default.
• W2081730949 cites W1970374778 @default.
• W2081730949 cites W1973573989 @default.
• W2081730949 cites W1975898092 @default.
• W2081730949 cites W1981261500 @default.
• W2081730949 cites W1981293033 @default.
• W2081730949 cites W1986423701 @default.
• W2081730949 cites W1989328736 @default.
• W2081730949 cites W1990372606 @default.
• W2081730949 cites W1992609506 @default.
• W2081730949 cites W1993203791 @default.
• W2081730949 cites W1994961575 @default.
• W2081730949 cites W1996713062 @default.
• W2081730949 cites W1998238961 @default.
• W2081730949 cites W2011823591 @default.
• W2081730949 cites W2014093920 @default.
• W2081730949 cites W2022430938 @default.
• W2081730949 cites W2033531913 @default.
• W2081730949 cites W2039680101 @default.
• W2081730949 cites W2044277849 @default.
• W2081730949 cites W2051051060 @default.
• W2081730949 cites W2053111130 @default.
• W2081730949 cites W2059393016 @default.
• W2081730949 cites W2059748176 @default.
• W2081730949 cites W2067106268 @default.
• W2081730949 cites W2068768095 @default.
• W2081730949 cites W2069038722 @default.
• W2081730949 cites W2081393100 @default.
• W2081730949 cites W2085797760 @default.
• W2081730949 cites W2093231293 @default.
• W2081730949 cites W2095726149 @default.
• W2081730949 cites W2096387826 @default.
• W2081730949 cites W2096478205 @default.
• W2081730949 cites W2097794068 @default.
• W2081730949 cites W2097827059 @default.
• W2081730949 cites W2104053160 @default.
• W2081730949 cites W2107748973 @default.
• W2081730949 cites W2108931588 @default.
• W2081730949 cites W2114343773 @default.
• W2081730949 cites W2115560611 @default.
• W2081730949 cites W2117260572 @default.
• W2081730949 cites W2120294419 @default.
• W2081730949 cites W2123747735 @default.
• W2081730949 cites W2124588973 @default.
• W2081730949 cites W2126412697 @default.
• W2081730949 cites W2127610524 @default.
• W2081730949 cites W2131541226 @default.
• W2081730949 cites W2134524309 @default.
• W2081730949 cites W2134892922 @default.
• W2081730949 cites W2138750223 @default.
• W2081730949 cites W2141600407 @default.
• W2081730949 cites W2143158403 @default.
• W2081730949 cites W2147721510 @default.
• W2081730949 cites W2149252002 @default.
• W2081730949 cites W2155544733 @default.
• W2081730949 cites W2156107157 @default.
• W2081730949 cites W2156783437 @default.
• W2081730949 cites W2168105134 @default.
• W2081730949 cites W2168761911 @default.
• W2081730949 cites W2334337188 @default.
• W2081730949 cites W4245866536 @default.
• W2081730949 doi "https://doi.org/10.1038/sj.ki.5002611" @default.
• W2081730949 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18379533" @default.
• W2081730949 hasPublicationYear "2008" @default.
• W2081730949 type Work @default.
• W2081730949 sameAs 2081730949 @default.
• W2081730949 citedByCount "44" @default.
• W2081730949 countsByYear W20817309492012 @default.
• W2081730949 countsByYear W20817309492013 @default.
• W2081730949 countsByYear W20817309492014 @default.
• W2081730949 countsByYear W20817309492015 @default.
• W2081730949 countsByYear W20817309492016 @default.
• W2081730949 countsByYear W20817309492017 @default.
• W2081730949 countsByYear W20817309492018 @default.
• W2081730949 countsByYear W20817309492019 @default.
• W2081730949 countsByYear W20817309492021 @default.
• W2081730949 crossrefType "journal-article" @default.
• W2081730949 hasAuthorship W2081730949A5024841234 @default.
• W2081730949 hasAuthorship W2081730949A5047911273 @default.
• W2081730949 hasAuthorship W2081730949A5070800289 @default.

• next