losartan-potassium has been researched along with Obesity* in 32 studies
1 review(s) available for losartan-potassium and Obesity
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Erythropoietin and Nonhematopoietic Effects.
Erythropoietin (EPO) is the main regulator of red blood cell production. Since the 1990s, EPO has been used for the treatment of anemia associated with end-stage renal failure and chemotherapy. The erythropoietin receptors were found on other organs such as the brain, spinal cord, heart and skin. In addition, it has been shown that many tissues produce and locally release EPO in response to hypoxic, biochemical and physical stress. In cellular, animal and clinical studies, EPO protects tissues from ischemia and reperfusion injury, has antiapoptotic effects and improves regeneration after injury. In this article, we mainly review the nonhematopoietic effects and new possible clinical indications for EPO. Topics: Animals; Cardiovascular Diseases; Cognition; Diabetes Mellitus; Erythropoietin; Humans; Kidney; Memory; Neovascularization, Physiologic; Neurodegenerative Diseases; Neuroprotective Agents; Obesity; Retina | 2017 |
1 trial(s) available for losartan-potassium and Obesity
30 other study(ies) available for losartan-potassium and Obesity
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Erythropoietin reduces fat mass in female mice lacking estrogen receptor alpha.
Erythropoietin (EPO), the cytokine required for erythropoiesis, contributes to metabolic regulation of fat mass and glycemic control. EPO treatment in mice on high-fat diets (HFD) improved glucose tolerance and decreased body weight gain via reduced fat mass in males and ovariectomized females. The decreased fat accumulation with EPO treatment during HFD in ovariectomized females was abrogated with estradiol supplementation, providing evidence for estrogen-related gender-specific EPO action in metabolic regulation. In this study, we examined the cross-talk between estrogen mediated through estrogen receptor α (ERα) and EPO for the regulation of glucose metabolism and fat mass accumulation.. Wild-type (WT) mice and mouse models with ERα knockout (ERα-/-) and targeted deletion of ERα in adipose tissue (ERα. ERα-/- mice on HFD exhibited increased fat mass and glucose intolerance. EPO treatment on HFD reduced fat accumulation in male WT and ERα-/- mice and female ERα-/- mice but not female WT mice. EPO reduced HFD increase in adipocyte size in WT mice but not in mice with deletion of ERα independent of EPO-stimulated reduction in fat mass. EPO treatment also improved glucose and insulin tolerance significantly greater in female ERα-/- mice and female ERα. This study clearly identified the role of estrogen signaling in modifying EPO regulation of glucose metabolism and the sex-differential EPO effect on fat mass regulation. Cross-talk between EPO and estrogen was implicated for metabolic homeostasis and regulation of body mass in female mice. Topics: 3T3-L1 Cells; Adipocytes, White; Adipose Tissue; Adipose Tissue, White; Animals; Body Mass Index; Diet, High-Fat; Erythropoietin; Estrogen Receptor alpha; Estrogens; Female; Glucose; Glucose Intolerance; Homeostasis; Male; Mice; Mice, Knockout; Obesity; Uncoupling Protein 1 | 2021 |
Is the erythropoietin-erythroferrone-hepcidin axis intact in human neonates?
In a two-part process, we assessed elements of the principal hormonal pathway regulating iron homeostasis in human neonates. Part 1: Quantifying erythropoietin (Epo), erythroferrone (ERFE), hepcidin, and relevant serum and erythrocytic iron-related metrics in umbilical cord blood from term (n = 13) and preterm (n = 10) neonates, and from neonates born to mothers with diabetes and obesity (n = 13); Part 2: Quantifying serum Epo, ERFE, and hepcidin before and following darbepoetin administration. Part 1: We measured Epo, ERFE and hepcidin in all cord blood samples. Epo and ERFE levels did not differ between the three groups. Preterm neonates had the lowest hepcidin levels, while neonates born to diabetic women with a very high BMI had the lowest ferritin and RET-He levels. Part 2: Following darbepoetin dosing, ERFE levels generally increased (p < 0.05) and hepcidin levels generally fell (p < 0.05). Our observations suggest that the Epo/ERFE/hepcidin axis is intact in the newborn period. Topics: Erythropoietin; Female; Fetal Blood; Hepcidins; Humans; Infant, Newborn; Infant, Premature; Male; Obesity; Peptide Hormones; Pregnancy; Pregnancy Complications; Pregnancy in Diabetics; Premature Birth; Signal Transduction | 2021 |
Regulation of muscle and metabolic physiology by hypothalamic erythropoietin independently of its peripheral action.
The glycoprotein hormone erythropoietin (EPO) is required for erythropoiesis, and the kidney is the primary site of adult EPO synthesis. Limited evidence has suggested that EPO could be detectable in the brain under certain conditions, but it remains unknown if the brain might have its own EPO system for biological functions that are independent of peripheral EPO production and action. We performed this study to address this question using mice under normal conditions versus pathophysiological conditions including aging and dietary obesity.. EPO expression was measured in different brain regions as well as in the cerebrospinal fluid. Hypothalamic ventricular EPO was administered to physiologically examine possible therapeutic effects on the conditions of aging and dietary obesity. Body weight, body composition, insulin tolerance, and glucose tolerance were measured to assess the central effects of EPO on metabolic physiology, and muscle strength and histology were analyzed to assess the central effects of EPO on muscle function. In addition, β2-adrenergic receptor knockout bone marrow transplant was employed to determine the potential role of bone marrow in linking the brain to some of these peripheral functions.. This study revealed that EPO is expressed in the ventromedial hypothalamus in addition to a few other brain regions and is present in the cerebrospinal fluid. Unlike blood EPO concentration, which increased with aging and dietary obesity, hypothalamic EPO decreased in these disease conditions. Therapeutically, aged mice were chronically treated with EPO in the hypothalamic ventricle, showing an increase in lean mass, while body weight and fat mass decreased as a result of a moderate reduction of food intake. Both muscle and metabolic functions were improved by this central treatment, and mechanistically, adrenergic signals to the bone marrow played a role in conveying hypothalamic EPO to these peripheral actions. Dietary obesity was also studied, showing that hypothalamic EPO treatment caused a reduction in food intake and obesity, leading to improved metabolic functions related to decreased fat as well as increased lean mass.. Hypothalamic EPO plays a role in the central regulation of muscle and metabolic physiology, while its decline contributes to aging and obesity physiology in a manner that is independent of peripheral EPO. Topics: Animals; Diet, High-Fat; Erythropoietin; Glucose Tolerance Test; Hypothalamus; Male; Mice; Mice, Inbred C57BL; Muscles; Obesity | 2020 |
Erythropoietin-Induced Changes in Bone and Bone Marrow in Mouse Models of Diet-Induced Obesity.
Obesity remodels bone and increases bone marrow adipocytes (BMAT), which negatively regulate hematopoiesis and bone. Reduced BMAT could restore altered hematopoiesis and bone features. We analyzed the potential of erythropoietin (EPO), the cytokine required for erythropoiesis, to inhibit BMAT in C57BL6/J mice fed four weeks of a high-fat diet (HFD). Acute EPO administration markedly decreased BMAT in regular chow diet (RCD) and HFD-fed mice, without affecting whole body fat mass. Micro-CT analysis showed EPO reduced trabecular bone in RCD- and HFD-fed mice, but EPO-treated HFD-fed mice maintained cortical bone mineral density and cortical bone volume, which was reduced on RCD. Despite achieving similar increased hematocrits with BMAT loss in RCD- and HFD-fed mice treated with EPO, decreased bone marrow cellularity was only observed in RCD-fed mice concomitant with an increasing percentage of bone marrow erythroid cells. In contrast, in HFD-fed mice, EPO increased endothelial cells and stromal progenitors with a trend toward the normalization of marrow homeostasis. EPO administration increased c-terminal FGF23 and intact serum FGF23 only in HFD-fed mice. These data demonstrate the distinct EPO responses of bone and marrow in normal and obese states, accompanying EPO-induced loss of BMAT. Topics: Adipose Tissue; Animals; Bone and Bones; Bone Marrow; Cancellous Bone; Diet, High-Fat; Disease Models, Animal; Erythropoietin; Female; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Mice, Inbred C57BL; Obesity; Osteoblasts; Osteoclasts; Osteocytes; Periosteum | 2020 |
Erythropoietin suppresses hepatic steatosis and obesity by inhibiting endoplasmic reticulum stress and upregulating fibroblast growth factor 21.
Erythropoietin (EPO), known primarily for its role in erythropoiesis, was recently reported to play a beneficial role in regulating lipid metabolism; however, the underlying mechanism through which EPO decreases hepatic lipid accumulation requires further investigation. Endoplasmic reticulum (ER) stress may contribute to the progression of hepatic steatosis. The present study investigated the effects of EPO on regulating ER stress in fatty liver. It was demonstrated that EPO inhibited hepatic ER stress and steatosis in vivo and in vitro. Interestingly, these beneficial effects were abrogated in liver‑specific sirtuin 1 (SIRT1)‑knockout mice compared with wild‑type littermates. In addition, in palmitate‑treated hepatocytes, small interfering RNA‑mediated SIRT1 silencing suppressed the effects of EPO on lipid‑induced ER stress. Additionally, EPO stimulated hepatic fibroblast growth factor 21 (FGF21) expression and secretion in a SIRT1‑dependent manner in mice. Furthermore, the sensitivity of hepatocytes from obese mice to FGF21 was restored following treatment with EPO. Collectively, the results of the present study revealed a new mechanism underlying the regulation of hepatic ER stress and FGF21 expression induced by EPO; thus, EPO may be considered as a potential therapeutic agent for the treatment of fatty liver and obesity. Topics: Animals; Cells, Cultured; Endoplasmic Reticulum Stress; Erythropoietin; Fatty Liver; Fibroblast Growth Factors; Male; Mice, Inbred C57BL; Obesity; Up-Regulation | 2019 |
Predictors of anemia and iron status at birth in neonates born to women carrying multiple fetuses.
Iron (Fe) status of neonates born to women carrying multiple fetuses might be compromised as a consequence of the high prevalence of maternal Fe deficiency and anemia coupled with an increased risk of preterm birth. This study aimed to characterize and identify determinants of anemia in this neonatal population.. Umbilical cord blood obtained from 183 neonates was utilized to assess hemoglobin (Hb), ferritin (SF), soluble transferrin receptor (sTfR), hepcidin, serum Fe, erythropoietin, folate, vitamin B-12, C-reactive protein, and interleukin-6. Associations with maternal Fe status were explored.. Cord Hb or SF did not change significantly as a function of gestational age at birth (25-38 wks). Neonates born to women who were obese prior to pregnancy or smoked cigarettes during pregnancy had a 4-5-fold greater odds of anemia at birth. Cord sTfR was the strongest indicator of cord Hb (P < 0.0001), and it was significantly associated with maternal sTfR at mid-gestation (P = 0.01) and delivery (P = 0.002). Cord Fe indicators were significantly associated with cord hepcidin, but not maternal hepcidin.. Screening for Fe status in neonates born to women carrying multiple fetuses is warranted, especially for those born to smokers or to women who are obese at entry into pregnancy. Topics: Adult; Anemia; Anemia, Iron-Deficiency; C-Reactive Protein; Cohort Studies; Erythropoietin; Female; Ferritins; Fetal Blood; Folic Acid; Hemoglobins; Hepcidins; Humans; Infant, Newborn; Infant, Newborn, Diseases; Infant, Premature; Infant, Premature, Diseases; Interleukin-6; Iron; Obesity; Pregnancy; Pregnancy Complications; Pregnancy, Multiple; Premature Birth; Receptors, Transferrin; Smoking; Tobacco Use Disorder; Vitamin B 12; Young Adult | 2018 |
[Effect of EPO on PRDM16, FGF21 expression and STAT phosphorylation of brown adipose tissue in HFD mice].
To investigate the effect of erythropoietin (EPO) on blood glucoseand plasma insulin level, index of insulin resistance (HOMA-IR), introperitoneal glucose tolerance test (IPGTT), the mRNA and protein level of PR domain-containing 16 (PRDM16), phosphorylated signal transducer and activator of transcription 3 (p-STAT3), fibroblast growth factor 21 (FGF21) of brown adipose tissue (BAT) in mice fed with high fat diet (HFD) in order to provide clues for the mechanism of obesity and complication.. Twenty C57BL/6J male mice fed with HFD were randomly divided into control group (HFD-Con) and EPO group (HFD-EPO), mice in the two groups were injected intraperitoneally normal saline and EPO (200 IU/kg) res pectively, 3 times per week for consecutive 4 weeks.Then the body weight, blood glucose, plasma insulin level, HOMA-IR and IPGTT were detected.The mRNA and protein level of PRDM16, FGF21, p-STAT3/STAT3 in brown adipose tissue were detected by real-time quantitative RT-PCR and Western blot respectively.. After intraperitoneal injection of EPO for 4 weeks, the body weight of the mice in HFD-EPO and HFD-Con groups was (26.65±0.85) g and (31.50±1.6 0) g respectively.The blood glucose of the mice in HFD-EPO group[(62.79±8.09) mg/dl]was significantly decreased compared with that in HFD-Con group[(91.06±9.86) mg/dl].The plasmainsulin level in HFD-EPO group[(10.56±1.06)μU/ml]was significantly decreased compared with that in HFD-Con group[(13.2±1.1)μU/ml,. EPO could promote differentiation of brown adipose tissue by increase in the express ion of PRDM16, and decrease the blood glucose level, ameliorate glucose metabolism in obses mice. Topics: Adipose Tissue, Brown; Animals; Diet, High-Fat; DNA-Binding Proteins; Erythropoietin; Fibroblast Growth Factors; Insulin Resistance; Male; Mice; Mice, Inbred C57BL; Obesity; Phosphorylation; STAT Transcription Factors; Transcription Factors | 2018 |
Cord blood erythropoietin and cord blood nucleated red blood cells for prediction of adverse neonatal outcome associated with maternal obesity in term pregnancy: prospective cohort study.
To determine the adverse pregnancy outcomes associated with maternal pre-pregnancy overweight and obesity and we measure cord blood erythropoietin and NRBC count as indices of hypoxia and predictors of neonatal outcome.. This prospective cohort study was done in Minia University Hospital, carried out from May 2015 to April 2016. Two hundred and seventy full-term neonates born to mothers of various body mass indices were included. Excluded were neonates with major factors known to be associated with a potential increase in fetal erythropoiesis. Pre-pregnancy maternal BMI was calculated from maternally reported weight and height. Cord blood erythropoietin and nucleated red blood cells were measured.. There is a significant increase of various adverse pregnancy outcomes as cesarean section. Postpartum hemorrhage and macrosomia with the increase of maternal pre-pregnancy BMI. Significant positive correlations between cord blood erythropoietin and nucleated red blood cells with maternal BMI.. The increase in the maternal pre-pregnancy BMI is associated with poor pregnancy outcomes. Cord blood erythropoietin and nucleated red blood cells can predict the poor neonatal outcome. Topics: Adult; Body Mass Index; Case-Control Studies; Cesarean Section; Erythroblasts; Erythropoietin; Female; Fetal Blood; Humans; Infant, Newborn; Middle Aged; Obesity; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Prospective Studies; ROC Curve | 2017 |
Erythropoietin (EPO) ameliorates obesity and glucose homeostasis by promoting thermogenesis and endocrine function of classical brown adipose tissue (BAT) in diet-induced obese mice.
Erythropoietin (EPO), clinically used as a hematopoietic drug, has received much attention due to its nonhematopoietic effects. EPO reportedly has beneficial effects on obesity and diabetes mellitus. We investigated whether interscapular brown adipose tissue (iBAT: main part of classical BAT) could play a role in EPO's anti-obesity and anti-diabetic effects in diet-induced obese mice. Four-week-old male C57BL/6J mice were fed a high-fat diet (HFD-Con), and half were additionally given an intraperitoneal injection of recombinant human EPO (200 IU/kg) (HFD-EPO) thrice a week for four weeks. At 8 weeks, EPO-injected mice showed significantly reduced body weight with reduced epididymal and subcutaneous white fat mass and unchanged caloric intake and locomotor activity. HOMA-IR (insulin resistance index) and glucose levels during intraperitoneal glucose tolerance test (IPGTT) were significantly lower in HFD-EPO mice than in HFD-Con mice. EPO-injected mice also showed increased oxygen consumption, indicative of metabolic rate, and skin temperature around iBAT tissue masses. EPO significantly upregulated the PRD1-BF1-RIZ1 homologous domain containing 16 (PRDM16), a transcriptional factor with a crucial role in brown adipocyte differentiation. EPO significantly increased phosphorylated signal transducer and activator of transcription 3 (STAT3), which is downstream of erythropoietin receptor (EpoR) and known to stabilize PRDM16. EPO's suppression of myocyte enhancer factor 2c (Mef2c) and microRNA-133a (miR-133a) via β3-adrenergic receptor caused PRDM16 upregulation. EPO-mediated enhancement of EpoR/STAT3 and β-adrenergic receptor/Mef2c/miR-133 pathways dramatically increases total uncoupling protein 1 (UCP1), an essential enzyme for BAT thermogenesis. Furthermore, EPO activated BAT's endocrine functions. EPO facilitated fibroblast growth factor 21 (FGF21) production and excretion in iBAT, associated with reduction of liver gluconeogenesis-related genes. Thus, EPO's improvement of obesity and glucose homeostasis can be attributed to increased iBAT thermogenic capacity and activation of BAT's endocrine functions. Topics: Adipocytes; Adipose Tissue, Brown; Adipose Tissue, White; Animals; Anti-Obesity Agents; Diet, High-Fat; DNA-Binding Proteins; Energy Metabolism; Erythropoietin; Fibroblast Growth Factors; Glucose Intolerance; Glucose Tolerance Test; Insulin Resistance; Male; Mice, Inbred C57BL; Obesity; Thermogenesis; Transcription Factors | 2017 |
Differentiating the Influences of Aging and Adiposity on Brain Weights, Levels of Serum and Brain Cytokines, Gastrointestinal Hormones, and Amyloid Precursor Protein.
Aging and obesity exert important effects on disease. Differentiating these effects is difficult, however, because weight gain often accompanies aging. Here, we used a nested design of aged, calorically restricted, and refed rats to measure changes in brain and blood levels of cytokines and gastrointestinal hormones, brain amyloid precursor protein levels, and brain and body weights. By comparing groups and using path analysis, we found divergent influences of chronological aging versus body weight, our main findings being (i) changes in whole brain weight and serum macrophage colony-stimulating factor levels correlated better with body weight than with chronological aging, (ii) a decrease in brain cytokines and brain plasminogen activator inhibitor levels correlated better with chronological aging than with body weight, (iii) serum erythropoietin levels were influenced by both body weight and aging, (iv) serum plasminogen activator inhibitor, serum cytokines, and brain tumor necrosis factor were not influenced by aging or body weight, and (v) brain amyloid precursor protein more closely related to body weight and serum levels of gastrointestinal hormones than to brain weight, chronological aging, or cytokines. These findings show that although aging and body weight interact, their influences are distinct not only among various cytokines and hormones but also between the central nervous system and the peripheral tissue compartments. Topics: Adipose Tissue; Aging; Amyloid beta-Protein Precursor; Animals; Body Weight; Brain; Erythropoietin; Gastrointestinal Hormones; Leptin; Macrophage Colony-Stimulating Factor; Male; Obesity; Organ Size; Plasminogen Inactivators; Rats; Statistics as Topic; Tumor Necrosis Factor-alpha | 2016 |
Non-hematopoietic effects of endogenous erythropoietin on lean mass and body weight regulation.
To investigate the concurrent relationships between human plasma erythropoietin concentrations and energy expenditure (EE), body composition, plasma leptin concentrations, and associations with weight change.. Plasma to measure erythropoietin and leptin; data for body composition; 24-h EE measured in a whole-room calorimeter; and 75 g oral glucose tolerance testing were available from 109 full-heritage Pima Indians (55% male) from a larger study designed to understand the causes of obesity. Seventy-nine subjects had data for weight at a later visit (mean follow-up = 4.3 ± 1.9 years) to calculate percent weight change per year.. Erythropoietin, adjusted for covariates, correlated with 24-h EE (r = 0.26, P = 0.007), sleeping EE (r = 0.29, P = 0.003), fat-free mass (r = 0.19, P = 0.05), and fat mass (r = 0.27, P = 0.005), but not insulin or glucose measures. The association of erythropoietin with 24-h EE was fully mediated by fat-free mass. Erythropoietin associated with leptin in women (ρ = 0.36, P = 0.01), but not in men (P = 0.9), independently from fat mass. The association of erythropoietin with percent weight change per year was in opposing directions (interaction: P = 0.002) in males (r = -0.35, P = 0.02) versus females (r = 0.37, P = 0.02).. Non-hematopoietic endogenous erythropoietin action may be involved in body weight regulation in opposing directions in men and women, i.e., weight loss in men and weight gain in women. Topics: Adolescent; Adult; Body Composition; Body Weight; Energy Metabolism; Erythropoietin; Female; Glucose Tolerance Test; Humans; Indians, North American; Insulin; Leptin; Male; Middle Aged; Obesity; Sex Factors; Young Adult | 2016 |
Longitudinal Analysis of the Interaction Between Obesity and Pregnancy on Iron Homeostasis: Role of Hepcidin.
When pregnancy occurs in obese women, two opposite mechanisms for iron homeostasis concur: increased need for available iron to support erythropoiesis and decreased iron mobilization from diets and stores due to obesity-related inflammation linked to overexpressed hepcidin. Few studies have examined the role of hepcidin on maternal iron homeostasis in the context of obese pregnancy. The aim of the study was to evaluate the combined effect of maternal obesity and pregnancy on hepcidin and maternal iron status while accounting for inflammation and iron supplementation.. We conducted a secondary analysis of a cohort of pregnant women recruited from a referral obstetric hospital in Mexico City. Circulating biomarkers of iron status (hepcidin, ferritin [SF], transferrin receptor [sTfR], erythropoietin [EPO]), and inflammation (C-reactive protein [CRP], tumor necrosis factor-[TNF]α, and interleukin-[IL]6) were determined monthly throughout pregnancy. Repeated measures ANOVA and logistic regression models were used for statistics.. Twenty-three obese (Ob) and 25 lean (Lc) women were studied. SF and hepcidin declined, and EPO and sTfR increased throughout pregnancy in both groups. sTfR increased more in Ob than in Lc (p = 0.024). The smallest hepcidin decline occurred in iron-supplemented Ob women compared to non-supplemented Lc women (p = 0.022). The risk for iron deficiency at the end of pregnancy was higher for Ob than for Lc (OR = 4.45, 95% CI = 2.07-9.58) after adjusting for iron supplementation and hepcidin concentration.. Pre-gestational obesity increases the risk of maternal iron deficiency despite iron supplementation. Overexpressed hepcidin appears to be a potential mechanism. Topics: Adult; Biomarkers; C-Reactive Protein; Dietary Supplements; Erythropoietin; Female; Ferritins; Hepcidins; Homeostasis; Humans; Iron; Iron Deficiencies; Iron, Dietary; Mexico; Obesity; Pregnancy; Pregnancy Complications; Receptors, Transferrin | 2016 |
Nonerythropoietic Erythropoietin-Derived Peptide Suppresses Adipogenesis, Inflammation, Obesity and Insulin Resistance.
Erythropoietin (EPO) has been identified as being crucial for obesity modulation; however, its erythropoietic activity may limit its clinical application. EPO-derived Helix B-surface peptide (pHBSP) is nonerythrogenic but has been reported to retain other functions of EPO. The current study aimed to evaluate the effects and potential mechanisms of pHBSP in obesity modulation. We found that pHBSP suppressed adipogenesis, adipokine expression and peroxisome proliferator-activated receptor γ (PPARγ) levels during 3T3-L1 preadipocyte maturation through the EPO receptor (EPOR). In addition, also through EPOR, pHBSP attenuated macrophage inflammatory activation and promoted PPARγ expression. Furthermore, PPARγ deficiency partly ablated the anti-inflammatory activity of pHBSP in macrophages. Correspondingly, pHBSP administration to high-fat diet (HFD)-fed mice significantly improved obesity, insulin resistance (IR) and adipose tissue inflammation without stimulating hematopoiesis. Therefore, pHBSP can significantly protect against obesity and IR partly by inhibiting adipogenesis and inflammation. These findings have therapeutic implications for metabolic disorders, such as obesity and diabetes. Topics: 3T3-L1 Cells; Adipogenesis; Adipokines; Animals; Biomarkers; Cytokines; Diet, High-Fat; Erythropoietin; Gene Expression Regulation; Hematopoiesis; Inflammation; Inflammation Mediators; Insulin Resistance; Macrophages; Mice; Obesity; Peptides; PPAR gamma | 2015 |
Erythropoietin signaling: a novel regulator of white adipose tissue inflammation during diet-induced obesity.
Obesity-induced white adipose tissue (WAT) inflammation and insulin resistance are associated with macrophage (Mф) infiltration and phenotypic shift from "anti-inflammatory" M2-like to predominantly "proinflammatory" M1-like cells. Erythropoietin (EPO), a glycoprotein hormone indispensable for erythropoiesis, has biological activities that extend to nonerythroid tissues, including antiapoptotic and anti-inflammatory effects. Using comprehensive in vivo and in vitro analyses in mice, EPO treatment inhibited WAT inflammation, normalized insulin sensitivity, and reduced glucose intolerance. We investigated EPO receptor (EPO-R) expression in WAT and characterized the role of its signaling during obesity-induced inflammation. Remarkably, and prior to any detectable changes in body weight or composition, EPO treatment reduced M1-like Mф and increased M2-like Mф in WAT, while decreasing inflammatory monocytes. These anti-inflammatory effects were found to be driven, at least in part, by direct EPO-R response in Mф via Stat3 activation, where EPO effects on M2 but not M1 Mф required interleukin-4 receptor/Stat6. Using obese ∆EpoR mice with EPO-R restricted to erythroid cells, we demonstrated an anti-inflammatory role for endogenous EPO. Collectively, our findings identify EPO-R signaling as a novel regulator of WAT inflammation, extending its nonerythroid activity to encompass effects on both Mф infiltration and subset composition in WAT. Topics: Adipose Tissue, White; Animals; Cells, Cultured; Diet, High-Fat; Erythropoietin; Inflammation; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Obesity; Panniculitis; Receptors, Erythropoietin; Signal Transduction | 2014 |
Beyond erythropoiesis: emerging metabolic roles of erythropoietin.
Topics: Adipose Tissue, White; Animals; Erythropoietin; Inflammation; Male; Obesity; Panniculitis | 2014 |
PPARα and Sirt1 mediate erythropoietin action in increasing metabolic activity and browning of white adipocytes to protect against obesity and metabolic disorders.
Erythropoietin (EPO) has shown beneficial effects in the regulation of obesity and metabolic syndrome; however, the detailed mechanism is still largely unknown. Here, we created mice with adipocyte-specific deletion of EPO receptor. These mice exhibited obesity and decreased glucose tolerance and insulin sensitivity, especially when fed a high-fat diet. Moreover, EPO increased oxidative metabolism, fatty acid oxidation, and key metabolic genes in adipocytes and in white adipose tissue from diet-induced obese wild-type mice. Increased metabolic activity by EPO is associated with induction of brown fat-like features in white adipocytes, as demonstrated by increases in brown fat gene expression, mitochondrial content, and uncoupled respiration. Peroxisome proliferator-activated receptor (PPAR)α was found to mediate EPO activity because a PPARα antagonist impaired EPO-mediated induction of brown fat-like gene expression and uncoupled respiration. PPARα also cooperates with Sirt1 activated by EPO through modulating the NAD+ level to regulate metabolic activity. PPARα targets, including PPARγ coactivator 1α, uncoupling protein 1, and carnitine palmitoyltransferase 1α, were increased by EPO but impaired by Sirt1 knockdown. Sirt1 knockdown also attenuated adipose response to EPO. Collectively, EPO, as a novel regulator of adipose energy homeostasis via these metabolism coregulators, provides a potential therapeutic strategy to protect against obesity and metabolic disorders. Topics: 3T3-L1 Cells; Adipocytes, White; Animals; Carnitine O-Palmitoyltransferase; Diet, High-Fat; Erythropoietin; Ion Channels; Lipid Metabolism; Metabolic Diseases; Mice; Mice, Knockout; Mitochondria; Mitochondrial Proteins; Obesity; Oxidation-Reduction; Oxygen Consumption; PPAR alpha; Receptors, Erythropoietin; Sirtuin 1; Uncoupling Protein 1 | 2013 |
Comparison of serum prohepcidin and iron metabolism parameters in obese and non-obese elderly individuals.
Current knowledge indicates that there is a close connection between being overweight, obesity and iron metabolism disorders,but the underlying mechanism is unclear. Hepcidin could be a major contributor to poor iron status observed in the obese population.. The study was performed in 58 obese elderly individuals (F/M 34/24) aged 65-91 (78.92 ± 8.32) years. The controlgroup consisted of 15 non-obese elderly volunteers, age- and sex-matched. Based on the WHO definition, 36 (62%) obese individualswere diagnosed with normo- or microcytic anaemia. The following parameters were determined: prohepcidin, haemoglobin, serum iron,erythropoietin, ferritin and C-reactive protein (CRP).. Prohepcidin concentrations were significantly increased in obese elderly individuals without anaemia compared to obese andanaemic (p < 0.01) as well as non-obese volunteers (p < 0.01). In obese individuals with anaemia there was a decrease in serum iron,concomitant with increased levels of erythropoietin and CRP compared to two other groups. Ferritin concentration was increased inobese people (with and without anaemia) compared to the non-obese group. Serum prohepcidin levels were positively correlated withfat mass percentage in obese individuals without and with anaemia (r = 0.32; p = 0.02).. Results of this preliminary study suggest that body fat content does have an impact on prohepcidin concentration, andthereby on iron homeostasis. Topics: Adult; Aged; Aged, 80 and over; Anemia, Iron-Deficiency; Biomarkers; C-Reactive Protein; Erythropoietin; Female; Ferritins; Hepcidins; Humans; Male; Middle Aged; Obesity; Risk Factors; Serum Albumin | 2013 |
UK Renal Registry 16th annual report: chapter 13 clinical, haematological and biochemical parameters in patients receiving renal replacement therapy in paediatric centres in the uk in 2012: national and centre-specific analyses.
The British Association for Paediatric Nephrology Registry (BAPN) was established to analyse data related to renal replacement therapy (RRT) in children. The registry receives data from the 13 paediatric nephrology centres in the UK. This chapter aims to provide centre specific data so that individual centres can reflect on the contribution that their data makes to the national picture and to determine the extent to which their patient parameters meet nationally agreed audit standards for the management of children with established renal failure (ERF).. Data returns included a mixture of electronic (92%) and paper (8%) returns. Data were analysed to calculate summary statistics and where applicable the percentage achieving an audit standard. The standards used were those set out by the Renal Association and the National Institute for Health and Clinical Excellence.. Anthropometric data confirmed that children receiving RRT were short compared to healthy peers. Amongst patients with a height of <2SD between 2001 and 2012, 29.2%were receiving growth hormone if they were on dialysis compared to 11.9% if they had a functioning transplant. Prevalence rates of overweight and obese status in children with ERF remain concerningly high. Blood pressure control remained challenging with wide inter-centre variation although this was significantly better in children with a functioning transplant. Over a quarter of haemodialysis patients and 17.3% of peritoneal dialysis patients were anaemic, compared to only 8.3% of transplanted patients. ESA use in the dialysis population exceeded 90% amongst anaemic patients. The control of renal bone disease remained challenging.. Optimising growth and reducing prevalent excess weight in children on RRT remains challenging. The likelihood of complete electronic reporting in the near future with plans for quarterly reporting in the format of the recently finalised NEW paediatric dataset will hopefully improve quality of data and their reporting, allowing improvements in patient care. Topics: Adolescent; Anemia; Annual Reports as Topic; Bicarbonates; Blood Pressure; Body Height; Body Mass Index; Calcium; Catchment Area, Health; Child; Child, Preschool; Cross-Sectional Studies; Erythropoietin; Glomerular Filtration Rate; Growth Hormone; Guideline Adherence; Hematinics; Hemoglobins; Humans; Infant; Infant, Newborn; Kidney Failure, Chronic; Kidney Transplantation; Longitudinal Studies; Obesity; Parathyroid Hormone; Phosphates; Practice Guidelines as Topic; Prevalence; Registries; Renal Dialysis; United Kingdom | 2013 |
Erythropoietin inhibits gluconeogenesis and inflammation in the liver and improves glucose intolerance in high-fat diet-fed mice.
Erythropoietin (EPO) has multiple biological functions, including the modulation of glucose metabolism. However, the mechanisms underlying the action of EPO are still obscure. This study is aimed at investigating the potential mechanisms by which EPO improves glucose tolerance in an animal model of type 2 diabetes. Male C57BL/6 mice were fed with high-fat diet (HFD) for 12 weeks and then treated with EPO (HFD-EPO) or vehicle saline (HFD-Con) for two week. The levels of fasting blood glucose, serum insulin and glucose tolerance were measured and the relative levels of insulin-related phosphatidylinositol 3-kinase (PI3K)/Akt, insulin receptor (IR) and IR substrate 1 (IRS1) phosphorylation were determined. The levels of phosphoenolpyruvate carboxykinase (PEPCK), glucose-6- phosphatase (G6Pase), toll like receptor 4 (TLR4), tumor necrosis factor (TNF)-α and IL-6 expression and nuclear factor-κB (NF-κB) and c-Jun N-terminal kinase (JNK), extracellular-signal-regulated kinase (ERK) and p38 MAPK activation in the liver were examined. EPO treatment significantly reduced the body weights and the levels of fasting blood glucose and serum insulin and improved the HFD-induced glucose intolerance in mice. EPO treatment significantly enhanced the levels of Akt, but not IR and IRS1, phosphorylation, accompanied by inhibiting the PEPCK and G6Pase expression in the liver. Furthermore, EPO treatment mitigated the HFD-induced inflammatory TNF-α and IL-6 production, TLR4 expression, NF-κB and JNK, but not ERK and p38 MAPK, phosphorylation in the liver. Therefore, our data indicated that EPO treatment improved glucose intolerance by inhibiting gluconeogenesis and inflammation in the livers of HFD-fed mice. Topics: Animals; Blood Glucose; Body Weight; Diet, High-Fat; Erythropoietin; Fasting; Feeding Behavior; Gene Expression Regulation; Gluconeogenesis; Glucose Intolerance; Glucose Tolerance Test; Glucose-6-Phosphatase; Humans; Inflammation; Insulin; Insulin Receptor Substrate Proteins; Liver; Mice; Mice, Inbred C57BL; Obesity; Phosphoenolpyruvate Carboxykinase (ATP); Proto-Oncogene Proteins c-akt; Receptor, Insulin; Receptors, Erythropoietin; RNA, Messenger; Signal Transduction | 2013 |
Erythropoietin as additive of HTK preservation solution in cold ischemia/reperfusion injury of steatotic livers.
Organ shortage in liver transplantation has justified usage of marginal donor livers to expand the donor organ pool. The particular susceptibility of steatotic livers to I/R injury necessitates optimal preservation conditions in order to minimize preservation-reperfusion injury for successful transplantation.. The effect of erythropoietin (EPO) as additive to HTK preservation solution was studied in a mouse model. Lean and steatotic livers were harvested, stored for 24 h in 4°C HTK solution containing either EPO or saline and reperfused for 2 h with 37°C Krebs-Henseleit buffer. Livers without cold storage served as sham controls.. Flushing of livers upon cold storage revealed a transaminase release, which was 2- to 10-fold higher in steatotic versus lean livers. EPO was effective in reducing the enzyme release to 50% in steatotic but not in lean livers. EPO prevented cold storage-induced denudation of the endothelial lining in steatotic livers, but aggravated it in lean livers. During reperfusion, steatotic livers presented with lower oxygen consumption and higher enzyme release than lean livers. In all livers, parameters of reperfusion injury remained unaffected by EPO. Expression of UCP2 was found markedly higher in steatotic livers. After I/R, steatotic livers revealed a significant drop of UCP2, whereas expression in lean livers was only slightly affected. EPO diminished Erk phosphorylation to almost the same extent in both mouse strains.. Fortification of the preservation solution by EPO ameliorates cold ischemic injury of steatotic livers and may thus be considered for use as an adjunctive agent to increase the success of transplanting steatotic livers. Topics: Animals; Cold Temperature; Disease Models, Animal; Erythropoietin; Fatty Liver; Female; Glucose; Ion Channels; Liver; Liver Transplantation; Male; Mannitol; Mice; Mice, Inbred Strains; Mice, Obese; Mitochondrial Proteins; Mitogen-Activated Protein Kinase Kinases; Obesity; Organ Preservation Solutions; Potassium Chloride; Procaine; Receptors, Erythropoietin; Reperfusion Injury; Signal Transduction; Thinness; Uncoupling Protein 2 | 2012 |
The effects of erythropoietin dose titration during high-fat diet-induced obesity.
Erythropoietin (Epo) is a pleotropic cytokine with several nonhematopoietic tissue effects. High-dose Epo treatment-mediated effects on body weight, fat mass and glucose tolerance have recently been reported, thus extending its pleotropic effects to fat and glucose metabolism. However, the exact dose range of Epo treatment required for such effects remains unidentified to date. We investigated Epo dosage effect (up to 1000 U/kg) on hematocrit, body weight, body composition, glucose metabolism, food intake, and physical activity, during high-fat diet-induced obesity. We report that Epo doses (1000, 600, 300, and 150 U/kg) significantly reduced body weight gain and fat mass, while, only Epo doses of 300 U/kg and higher significantly affected glucose tolerance. None of the tested Epo doses showed any detectable effects on food intake, and only 1000 U/kg dose significantly increased physical activity, suggesting that these parameters may only be partially responsible for the metabolic effects of Epo treatment. Topics: Adiposity; Animals; Diet; Dietary Fats; Dose-Response Relationship, Drug; Epoetin Alfa; Erythropoietin; Feeding Behavior; Glucose; Hematocrit; Humans; Male; Mice; Mice, Inbred C57BL; Motor Activity; Obesity; Recombinant Proteins; Weight Gain | 2011 |
A novel EPO receptor agonist improves glucose tolerance via glucose uptake in skeletal muscle in a mouse model of diabetes.
Patients treated with recombinant human Epo demonstrate an improvement in insulin sensitivity. We aimed to investigate whether CNTO 530, a novel Epo receptor agonist, could affect glucose tolerance and insulin sensitivity. A single administration of CNTO 530 significantly and dose-dependently reduced the area under the curve in a glucose tolerance test in diet-induced obese and diabetic mice after 14, 21, and 28 days. HOMA analysis suggested an improvement in insulin sensitivity, and this effect was confirmed by a hyperinsulinemic-euglycemic clamp. Uptake of (14)C-2-deoxy-D-glucose indicated that animals dosed with CNTO 530 transported more glucose into skeletal muscle and heart relative to control animals. In conclusion, CNTO530 has a profound effect on glucose tolerance in insulin-resistant rodents likely because of improving peripheral insulin sensitivity. This effect was observed with epoetin-α and darbepoetin-α, suggesting this is a class effect, but the effect with these compounds relative to CNTO530 was decreased in duration and magnitude. Topics: Animals; Darbepoetin alfa; Diabetes Mellitus, Experimental; Dietary Fats; Disease Models, Animal; Dose-Response Relationship, Drug; Epoetin Alfa; Erythropoietin; Glucose; Glucose Clamp Technique; Glucose Tolerance Test; Insulin Resistance; Male; Mice; Mice, Inbred C57BL; Muscle, Skeletal; Obesity; Receptors, Erythropoietin; Recombinant Fusion Proteins; Recombinant Proteins; Time Factors | 2011 |
Disrupted erythropoietin signalling promotes obesity and alters hypothalamus proopiomelanocortin production.
Although erythropoietin (Epo) is the cytokine known to regulate erythropoiesis, erythropoietin receptor (EpoR) expression and associated activity beyond haematopoietic tissue remain uncertain. Here we show that mice with EpoR expression restricted to haematopoietic tissues (Tg) develop obesity and insulin resistance. Tg-mice exhibit a decrease in energy expenditure and an increase in white fat mass and adipocyte number. Conversely, Epo treatment of wild-type (WT)-mice increases energy expenditure and reduces food intake and fat mass accumulation but shows no effect in body weight of Tg-mice. EpoR is expressed at a high level in white adipose tissue and in the proopiomelanocortin (POMC) neurons of the hypothalamus. Although Epo treatment in WT-mice induces the expression of the polypeptide hormone precursor, POMC, mice lacking EpoR show reduced levels of POMC in the hypothalamus. This study provides the first evidence that mice lacking EpoR in non-haematopoietic tissue become obese and insulin resistant with loss of Epo regulation of energy homeostasis. Topics: Animals; Blotting, Western; Erythropoietin; Female; Hypothalamus; Immunohistochemistry; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Obesity; Pro-Opiomelanocortin; Receptors, Erythropoietin; Reverse Transcriptase Polymerase Chain Reaction | 2011 |
[The importance of starting regular haemodialysis through a native arteriovenous venous fistula].
Topics: Aged; Aged, 80 and over; Anemia; Arteriovenous Shunt, Surgical; Catheterization; Comorbidity; Diabetic Nephropathies; Erythropoietin; Female; Humans; Kidney Failure, Chronic; Length of Stay; Male; Middle Aged; Obesity; Renal Dialysis; Retrospective Studies | 2009 |
Erythropoietin over-expression protects against diet-induced obesity in mice through increased fat oxidation in muscles.
Erythropoietin can be over-expressed in skeletal muscles by gene electrotransfer, resulting in 100-fold increase in serum EPO and significant increases in haemoglobin levels. Earlier studies have suggested that EPO improves several metabolic parameters when administered to chronically ill kidney patients. Thus we applied the EPO over-expression model to investigate the metabolic effect of EPO in vivo.At 12 weeks, EPO expression resulted in a 23% weight reduction (P<0.01) in EPO transfected obese mice; thus the mice weighed 21.9+/-0.8 g (control, normal diet,) 21.9+/-1.4 g (EPO, normal diet), 35.3+/-3.3 g (control, high-fat diet) and 28.8+/-2.6 g (EPO, high-fat diet). Correspondingly, DXA scanning revealed that this was due to a 28% reduction in adipose tissue mass.The decrease in adipose tissue mass was accompanied by a complete normalisation of fasting insulin levels and glucose tolerance in the high-fat fed mice. EPO expression also induced a 14% increase in muscle volume and a 25% increase in vascularisation of the EPO transfected muscle. Muscle force and stamina were not affected by EPO expression. PCR array analysis revealed that genes involved in lipid metabolism, thermogenesis and inflammation were increased in muscles in response to EPO expression, while genes involved in glucose metabolism were down-regulated. In addition, muscular fat oxidation was increased 1.8-fold in both the EPO transfected and contralateral muscles.In conclusion, we have shown that EPO when expressed in supra-physiological levels has substantial metabolic effects including protection against diet-induced obesity and normalisation of glucose sensitivity associated with a shift to increased fat metabolism in the muscles. Topics: Adipose Tissue; Animals; Erythropoietin; Female; Gene Expression Regulation; Glucose; Glucose Tolerance Test; Inflammation; Lipid Metabolism; Mice; Mice, Inbred C57BL; Models, Biological; Muscles; Obesity; Oxygen | 2009 |
Erythrocytosis in a patient on hemodialysis for thirteen years.
Most hemodialysis patients exhibit renal anemia mainly due to erythropoietin deficiency as a result of impaired erythropoetin production in the kidney. However, erythrocytosis in patients with renal failure requiring hemodialysis is extremely rare. We report the development of erythrocytosis in a patient with a polycystic kidney disease on hemodialysis for 13 years. She had erythrocytosis with increased serum erythropoietin levels despite severe secondary hyperparathyroidism, which is known to depress erythrocytosis. Since neither renal disease (renal cell carcinoma) nor extrarenal diseases (hypoxia, hepatoma, cerebellar diseases) linked with erythropoietin production could be proven, this case might be one with inappropriate idiopathic erythropoietin production after 13 years of hemodialysis, the longest duration of dialysis in the literature before erythrocytosis was observed. Topics: Erythropoietin; Female; Humans; Kidney Failure, Chronic; Middle Aged; Obesity; Polycystic Kidney Diseases; Polycythemia; Renal Dialysis; Time Factors | 2006 |
Quality of life in chronic kidney disease (CKD): a cross-sectional analysis in the Renal Research Institute-CKD study.
Health-related quality of life (QOL) is an important measure of how disease affects patients' lives. Dialysis patients have decreased QOL relative to healthy controls. Little is known about QOL in patients with chronic kidney disease (CKD) before renal replacement therapy.. The Medical Outcomes Study Short Form-36 (SF-36), a standard QOL instrument, was used to evaluate 634 patients (mean glomerular filtration rate [GFR], 23.6 +/- 9.6 mL/min/1.73 m2 [0.39 +/- 0.16 mL/s/1.73 m2]) enrolled in a 4-center, prospective, observational study of CKD. SF-36 scores in these patients were compared with those in a prevalent cohort of hemodialysis (HD) patients and healthy controls (both from historical data). QOL data also were analyzed for correlations with GFR and albumin and hemoglobin levels in multivariable analyses.. Patients with CKD had higher SF-36 scores than a large cohort of HD patients (P < 0.0001 for 8 scales and 2 summary scales), but lower scores than those reported for the US adult population (P < 0.0001 for 7 of 8 scales and 1 of 2 summary scales). Patients with CKD stage 4 had lower QOL scores than patients with CKD stage 5, although differences were not significant. Hemoglobin level was associated positively with higher mental and physical QOL scores (P < 0.05) in all individual and component scales except Pain.. SF-36 scores were higher in this CKD cohort compared with HD patients, but lower than in healthy controls. GFR was not significantly associated with QOL. Hemoglobin level predicted both physical and mental domains of the SF-36. Longitudinal studies are needed to define at-risk periods for decreases in QOL during progression of CKD. Topics: Aged; Anemia; Black or African American; Cardiovascular Diseases; Cohort Studies; Comorbidity; Cross-Sectional Studies; Diabetes Complications; Erythropoietin; Female; Glomerular Filtration Rate; Hemoglobins; Humans; Kidney Diseases; Male; Middle Aged; Obesity; Prospective Studies; Quality of Life; Renal Dialysis; Serum Albumin; Socioeconomic Factors; Surveys and Questionnaires; United States; White People | 2005 |
Serum levels of vascular endothelial growth factor are elevated in patients with obstructive sleep apnea and severe nighttime hypoxia.
Obstructive sleep apnea (OSA) is associated with increased cardiovascular morbidity and mortality; however, some patients with OSA do not develop cardiovascular disease even in the presence of severe nocturnal oxygen desaturations. Vascular endothelial growth factor (VEGF) is a hypoxia-sensitive glycoprotein stimulating neoangiogenesis. We hypothesized that VEGF production is increased in OSA because of repetitive nocturnal hypoxia. Three different groups were investigated: 10 OSA patients with severe nighttime hypoxia (Group A), 10 OSA patients with moderate hypoxia (Group B), and 10 healthy volunteers (Group C). Serum levels of VEGF were measured by ELISA from peripheral venous blood samples obtained at 7 AM. Group A had significantly (p < 0.01) increased VEGF serum levels when compared with Group B and Group C (mean +/- SEM: 410 +/- 77 pg/ml versus 224 +/- 38 pg/ml and 245 +/- 61 pg/ml). The degree of nocturnal oxygen desaturation in OSA significantly correlated with the VEGF concentrations (r = 0.67, p < 0.01). In conclusion, serum levels of VEGF are elevated in severely hypoxic patients with OSA and are related to the degree of nocturnal oxygen desaturation. This might constitute an adaptive mechanism to counterbalance the emergence of OSA-related cardiovascular disease. Topics: Adaptation, Physiological; Analysis of Variance; Case-Control Studies; DNA-Binding Proteins; Endothelial Growth Factors; Enzyme-Linked Immunosorbent Assay; Erythropoietin; Female; Forced Expiratory Volume; Humans; Hypoxia; Hypoxia-Inducible Factor 1; Hypoxia-Inducible Factor 1, alpha Subunit; Logistic Models; Lymphokines; Male; Nuclear Proteins; Obesity; Oximetry; Oxygen; Polysomnography; Recurrence; Severity of Illness Index; Sleep Apnea, Obstructive; Transcription Factors; Up-Regulation; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors; Vital Capacity | 2002 |
Erythropoietin response in subjects with obstructive sleep apnea.
We measured nocturnal plasma erythropoietin concentration (EPO) in eight subjects with obstructive sleep apnea syndrome (OSAS) and eight healthy overweight subjects while they were undergoing nocturnal polysomnography. We also measured EPO (radioimmunoassay) after 120 min of exposure to 10.5% O2. The subjects with OSAS had a respiratory disturbance index (RDI) of 50.8 +/- 41.9 and a maximal O2 desaturation of 65 +/- 13.3%, and they spent 104.5 +/- 89.3 min out of a total sleep time of 356 +/- 54 min below 90% oxygen saturation (T90). Nocturnal EPO concentrations were normal and did not differ between the two groups. We found no correlation between the T90, T80, or RDI and either the mean or maximal EPO concentrations. After the exposure to 10.5% oxygen, during which oxygen saturations were between 80 and 85%, the healthy subjects and those with OSAS developed increases in EPO of 34 and 49%, respectively, 240 min after the initiation of exposure (p < 0.05). We conclude that the nocturnal hypoxemia occurring in these subjects with OSAS may not have been sufficiently severe to stimulate an increased EPO production. The lack of EPO response was not due to down-regulation of EPO production. Topics: Adaptation, Physiological; Adult; Case-Control Studies; Down-Regulation; Erythropoietin; Female; Humans; Hypoxia; Male; Obesity; Polysomnography; Radioimmunoassay; Sleep Apnea Syndromes; Time Factors | 1995 |
Postural hypoxemia and erythrocytosis.
Topics: Adult; Aged; Altitude; Arteries; Blood Gas Analysis; Blood Pressure; Body Weight; Bone Marrow Cells; Carbon Dioxide; Colorado; Culture Techniques; Erythropoietin; Female; Hematocrit; Humans; Hydrogen-Ion Concentration; Hypertension; Hypoxia; Male; Middle Aged; Obesity; Oxygen; Oxygen Inhalation Therapy; Partial Pressure; Polycythemia; Posture; Respiratory Function Tests | 1968 |