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pubmed: 0013-7227

High Glucose Potentiates Collagen Synthesis and Bone Morphogenetic Protein-2-Induced Early Osteoblast Gene Expression in Rat Spinal Ligament Cells.
Li H, Jiang LS, Dai LY Related Articles High Glucose Potentiates Collagen Synthesis and Bone Morphogenetic Protein-2-Induced Early Osteoblast Gene Expression in Rat Spinal Ligament Cells. Endocrinology. 2009 Nov 13; Authors: Li H, Jiang LS, Dai LY Type 2 diabetes mellitus (T2DM) is an independent risk factor for ossification of the posterior longitudinal ligament, but the mechanism is unclear. We isolated cells from rat cervical spine ligaments and studied the effects of high glucose on expression of osteoblast genes to provide insight into molecular mechanism. Using these cells, high glucose stimulated the synthesis of type I collagen and significantly potentiated expression of early osteoblast genes (Runx2; alkaline phosphatase, ALP; and osteopontin, OP) induced by bone morphogenetic protein-2 (BMP-2). Notably, these effects of high glucose were fully mimicked and augmented by H2O2, although blocked by the reactive oxygen species inhibitor N-acetyl cysteine. Furthermore, exposure of these cells to high glucose significantly suppressed the phosphorylation of p38MAPK while enhancing the phosphorylation of protein kinase C (PKC) in the cells. Consistent with these observations, an inhibitor of p38 augmented the potentiation of high glucose on BMP-2-induced early osteogenic gene expression, whereas the PKC inhibitor repressed the effect of high glucose on type I collagen synthesis of the cells. In conclusion, high glucose, via production of reactive oxygen species, subsequent activation of PKC, and inhibition of p38, enhances type I collagen synthesis and expression of early osteogenesis genes induced by BMP-2 in rat spinal ligament cells. Hyperglycemia may play an important role in the onset or progression of ossification of the posterior longitudinal ligament by promoting the responsiveness of ligament cells to osteogenic differentiation. PMID: 19915165 [PubMed - as supplied by publisher]
Meal-Anticipatory Glucagon-Like Peptide-1 Secretion in Rats.
Vahl TP, Drazen DL, Seeley RJ, D'Alessio DA, Woods SC Related Articles Meal-Anticipatory Glucagon-Like Peptide-1 Secretion in Rats. Endocrinology. 2009 Nov 13; Authors: Vahl TP, Drazen DL, Seeley RJ, D'Alessio DA, Woods SC Animals anticipating a meal initiate a series of responses enabling them to better cope with the meal's metabolic impact. These responses, such as cephalic insulin, occur prior to the onset of ingestion and are especially evident in animals maintained on a meal-feeding schedule with limited but predictable access to food each day. We tested the hypothesis that meal-fed rats secrete the incretin hormone glucagon-like peptide-1 (GLP-1) cephalically when anticipating a large meal. Male Long-Evans rats were fed ad libitum (controls) or adapted to a schedule on which food was available for the same 4-h period each day (meal fed animals). Plasma GLP-1 increased in meal-fed rats over an interval from 75 to 60 min prior to feeding time, from a baseline of 10 to around 40 pM, and then returned to baseline prior to food presentation. Controls had steady plasma GLP-1 levels (10-15 pM) over the same span. Meal-fed rats also secreted cephalic insulin starting around 15 min prior to food presentation. Administration of the selective GLP-1 receptor antagonist exendin-4[desHis-1,Glu-9] prior to the premeal spike of GLP-1 caused meal-fed rats to eat significantly less food than normal, whereas administration of the antagonist after the GLP-1 spike but prior to food presentation resulted in a significant increase in food consumption. These findings document for the first time a cephalic increase of plasma GLP-1 and suggest that it functions to facilitate consumption of a large meal. PMID: 19915164 [PubMed - as supplied by publisher]
1{alpha},25-Dihydroxyvitamin D3 and Its TX527 Analog Inhibit the Growth of Endothelial Cells Transformed by Kaposi Sarcoma-Associated Herpes Virus G Protein-Coupled Receptor in Vitro and in Vivo.
Gonzalez-Pardo V, Martin D, Gutkind JS, Verstuyf A, Bouillon R, Russo de Boland A, Boland RL Related Articles 1{alpha},25-Dihydroxyvitamin D3 and Its TX527 Analog Inhibit the Growth of Endothelial Cells Transformed by Kaposi Sarcoma-Associated Herpes Virus G Protein-Coupled Receptor in Vitro and in Vivo. Endocrinology. 2009 Nov 13; Authors: Gonzalez-Pardo V, Martin D, Gutkind JS, Verstuyf A, Bouillon R, Russo de Boland A, Boland RL The Kaposi sarcoma-associated herpes virus-G protein-coupled receptor is a key molecule in the pathogenesis of Kaposi sarcoma, playing a central role in promoting vascular endothelial growth factor-driven angiogenesis and spindle cell proliferation. We studied the effects of 1alpha,25-dihydroxyvitamin D3 [1alpha,25(OH)2D3] and the analog TX527 on the proliferation of endothelial cells (SVECs) and SVECs transformed by the viral G protein-coupled receptor (SVEC-vGPCR). 1alpha,25(OH)2D3 and TX527 decreased SVEC-vGPCR and SVEC numbers, the response being time dependent and similar in both cell lines. Vitamin D receptor (VDR) levels increased on treatment with 10 nM 1alpha,25(OH)2D3 or 1 nM TX527 in a time-dependent manner (1.5-24 h) in SVECs and SVEC-vGPCR. Basal VDR levels were increased in SVEC-vGPCR. The antiproliferative effects were accompanied by reduction in cyclin D1 and accumulation of p27 in SVECs but not SVEC-vGPCR. Induction of VDR was blocked by transfection of short hairpin RNA against VDR in SVEC-vGPCR and the antiproliferative effects of 1alpha,25(OH)2D3 and TX527 were decreased, involving the VDR genomic pathway in the hormone and analog mechanism of action. In vivo experiments showed that 1alpha,25(OH)2D3 and TX527 decreased SVEC-vGPCR tumor progression when the tumor cells were implanted in nude mice. In conclusion, we have demonstrated that 1alpha,25(OH)2D3 and its TX527 analog have antiproliferative effects on the growth of endothelial cells transformed by the vGPCR in vitro and in vivo, the vitamin D receptor being part of the inhibitory mechanism of action. PMID: 19915163 [PubMed - as supplied by publisher]
Does finger fat produce sex differences in second to fourth digit ratios?
Wallen K Related Articles Does finger fat produce sex differences in second to fourth digit ratios? Endocrinology. 2009 Nov;150(11):4819-22 Authors: Wallen K PMID: 19846613 [PubMed - indexed for MEDLINE]
In vivo characterization of high Basal signaling from the ghrelin receptor.
Petersen PS, Woldbye DP, Madsen AN, Egerod KL, Jin C, Lang M, Rasmussen M, Beck-Sickinger AG, Holst B Related Articles In vivo characterization of high Basal signaling from the ghrelin receptor. Endocrinology. 2009 Nov;150(11):4920-30 Authors: Petersen PS, Woldbye DP, Madsen AN, Egerod KL, Jin C, Lang M, Rasmussen M, Beck-Sickinger AG, Holst B The receptor for the orexigenic peptide, ghrelin, is one of the most constitutively active 7TM receptors known, as demonstrated under in vitro conditions. Change in expression of a constitutively active receptor is associated with change in signaling independent of the endogenous ligand. In the following study, we found that the expression of the ghrelin receptor in the hypothalamus was up-regulated approximately 2-fold in rats both during 48-h fasting and by streptozotocin-induced hyperphagia. In a separate experiment, to probe for the effect of the high basal signaling of the ghrelin receptor in vivo, we used intracerebroventricular administration by osmotic pumps of a peptide [D-Arg(1), D-Phe(5), D-Trp(7,9), Leu(11)]-substance P. This peptide selectively displays inverse agonism at the ghrelin receptor as compared with an inactive control peptide with just a single amino acid substitution. Food intake and body weight were significantly decreased in the group of rats treated with the inverse agonist, as compared with the groups treated with the control peptide or the vehicle. In the hypothalamus, the expression of neuropeptide Y and uncoupling protein 2 was decreased by the inverse agonist. In a hypothalamic cell line that endogenously expresses the ghrelin receptor, we observed high basal activity of the cAMP response element binding protein, an important signaling transduction pathway for appetite regulation. The activation was further increased by ghrelin administration and decreased by administration of the inverse agonist. It is suggested that the high constitutive signaling activity is important for the in vivo function of the ghrelin receptor in the control of food intake and body weight. PMID: 19819980 [PubMed - indexed for MEDLINE]
Phosphatidylinositol 3 kinase/Akt signal relay cooperates with smad in bone morphogenetic protein-2-induced colony stimulating factor-1 (CSF-1) expression and osteoclast differentiation.
Mandal CC, Ghosh Choudhury G, Ghosh-Choudhury N Related Articles Phosphatidylinositol 3 kinase/Akt signal relay cooperates with smad in bone morphogenetic protein-2-induced colony stimulating factor-1 (CSF-1) expression and osteoclast differentiation. Endocrinology. 2009 Nov;150(11):4989-98 Authors: Mandal CC, Ghosh Choudhury G, Ghosh-Choudhury N Murine spleen cells produce mature osteoclasts when cocultured with osteoblastic cells. Colony-stimulating factor (CSF)-1 is the growth factor required for differentiating the monocyte-macrophage precursor cells into preosteoclasts. Bone morphogenic protein (BMP) signaling in osteoblasts regulates bone mass in mice, suggesting a role of BMP in osteoclastogenesis along with osteoblast activity. The intracellular signal transduction cross talk regulating the osteoblastic production of CSF-1 as a mechanism of BMP-induced osteoclastogenesis is described in this report. We have recently described the involvement of Smad 1/5 in BMP-2-induced CSF-1 expression and osteoclast formation. In this study, using the pharmacological inhibitors and the adenovirus (Ad) vectors expressing dominant-negative (DN) phosphatidylinositol 3 kinase (PI3K), the PI3K-signaling inhibitor, phosphatase and tensin homolog deleted in chromosome 10 (PTEN) or DN Akt kinase in the in vitro coculture assay, we show an essential role of the lipid kinase cascade in BMP-2-mediated multinucleated osteoclast formation and CSF-1 mRNA expression, transcription, and secretion. Inhibition of PI3K/Akt signaling blocked the binding of Smads 1/5 to the CSF-1 BMP-responsive element present in the CSF-1 promoter, resulting in attenuation of Smad-dependent CSF-1 transcription. Furthermore, PI3K inhibition and DN Akt prevented association of the transcriptional coactivator, CREB (cAMP response element binding protein) binding protein (CBP), with Smads 1/5. Together, these data for the first time demonstrate that PI3K-dependent Akt activation regulates BMP-2-induced CSF-1 expression and provides a mechanism for osteoblastic cell-assisted osteoclast differentiation. PMID: 19819979 [PubMed - indexed for MEDLINE]
Residues K128, 132, and 134 in the thyroid hormone receptor-alpha are essential for receptor acetylation and activity.
Sánchez-Pacheco A, Martínez-Iglesias O, Méndez-Pertuz M, Aranda A Related Articles Residues K128, 132, and 134 in the thyroid hormone receptor-alpha are essential for receptor acetylation and activity. Endocrinology. 2009 Nov;150(11):5143-52 Authors: Sánchez-Pacheco A, Martínez-Iglesias O, Méndez-Pertuz M, Aranda A The thyroid hormone receptor (TR)-alpha is a nuclear receptor that mediates both transrepression and ligand-dependent transactivation. Here we show that TRalpha is posttranslationally modified by acetylation in response to its own ligand (T(3)). Acetylation increases binding to DNA. Using mutagenesis, we identified three conserved lysine residues in the carboxi-terminal extension (CTE) of the DNA binding domain that are targets of the cAMP-response element-binding protein acetyltransferase. Substitution of these lysines by arginines in TRalpha decreased ligand binding affinity and precluded ligand-dependent release of corepressors and recruitment of coactivators. The acetylation TRalpha mutant lost the ability to transactivate even at high T(3) concentrations and acts as a dominant-negative inhibitor of wild-type TR activity. In addition, whereas native TRalpha interferes with AP-1 function, the mutant is unable to mediate transrepression. Finally, TRalpha suppresses NIH-3T3 fibroblast transformation by the Ras oncogene both in a ligand-dependent and -independent manner, but the CTE mutant is unable to mediate ligand-dependent repression of transformation. These results reveal a key role for the CTE region on acetylation, ligand affinity, transactivation, transrepression, and antitransforming properties of TRalpha. PMID: 19819978 [PubMed - indexed for MEDLINE]
Impaired skeletal muscle beta-adrenergic activation and lipolysis are associated with whole-body insulin resistance in rats bred for low intrinsic exercise capacity.
Lessard SJ, Rivas DA, Chen ZP, van Denderen BJ, Watt MJ, Koch LG, Britton SL, Kemp BE, Hawley JA Related Articles Impaired skeletal muscle beta-adrenergic activation and lipolysis are associated with whole-body insulin resistance in rats bred for low intrinsic exercise capacity. Endocrinology. 2009 Nov;150(11):4883-91 Authors: Lessard SJ, Rivas DA, Chen ZP, van Denderen BJ, Watt MJ, Koch LG, Britton SL, Kemp BE, Hawley JA Rats selectively bred for high endurance running capacity (HCR) have higher insulin sensitivity and improved metabolic health compared with those bred for low endurance capacity (LCR). We investigated several skeletal muscle characteristics, in vitro and in vivo, that could contribute to the metabolic phenotypes observed in sedentary LCR and HCR rats. After 16 generations of selective breeding, HCR had approximately 400% higher running capacity (P < 0.001), improved insulin sensitivity (P < 0.001), and lower fasting plasma glucose and triglycerides (P < 0.05) compared with LCR. Skeletal muscle ceramide and diacylglycerol content, basal AMP-activated protein kinase (AMPK) activity, and basal lipolysis were similar between LCR and HCR. However, the stimulation of lipolysis in response to 10 mum isoproterenol was 70% higher in HCR (P = 0.004). Impaired isoproterenol sensitivity in LCR was associated with lower basal triacylglycerol lipase activity, Ser660 phosphorylation of HSL, and beta2-adrenergic receptor protein content in skeletal muscle. Expression of the orphan nuclear receptor Nur77, which is induced by beta-adrenergic signaling and is associated with insulin sensitivity, was lower in LCR (P < 0.05). Muscle protein content of Nur77 target genes, including uncoupling protein 3, fatty acid translocase/CD36, and the AMPK gamma3 subunit were also lower in LCR (P < 0.05). Our investigation associates whole-body insulin resistance with impaired beta-adrenergic response and reduced expression of genes that are critical regulators of glucose and lipid metabolism in skeletal muscle. We identify impaired beta-adrenergic signal transduction as a potential mechanism for impaired metabolic health after artificial selection for low intrinsic exercise capacity. PMID: 19819977 [PubMed - indexed for MEDLINE]
Colony-stimulating factor-1 (CSF-1) directly inhibits receptor activator of nuclear factor-{kappa}B ligand (RANKL) expression by osteoblasts.
Wittrant Y, Gorin Y, Mohan S, Wagner B, Abboud-Werner SL Related Articles Colony-stimulating factor-1 (CSF-1) directly inhibits receptor activator of nuclear factor-{kappa}B ligand (RANKL) expression by osteoblasts. Endocrinology. 2009 Nov;150(11):4977-88 Authors: Wittrant Y, Gorin Y, Mohan S, Wagner B, Abboud-Werner SL Colony-stimulating factor-1 (CSF-1), released by osteoblasts, stimulates the proliferation of osteoclast progenitors via the c-fms receptor (CSF-1R) and, in combination with receptor activator of nuclear factor-kappaB ligand (RANKL), leads to the formation of mature osteoclasts. Whether the CSF-1R is expressed by osteoblasts and mediates specific biological effects in osteoblasts has not been explored. Wild-type primary calvaria osteoblasts (OB) were analyzed for CSF-1R expression (RT-PCR and Western blot) and functionality (immunocomplex kinase assay). OB were serum starved for 24 h, and the effect of CSF-1 (0-100 ng/ml) on OB biological activities was determined at 48 h. In wild-type mouse bone marrow cultures, CSF-1 was tested for its effect on RANKL mRNA and osteoclast formation. Because ROS influence osteoblast RANKL expression, studies analyzed the effect of CSF-1 on reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and Nox1 and Nox4 proteins. Results indicate that OB express CSF-1R mRNA and protein and that CSF-1R could be phosphorylated in the presence of CSF-1. In osteoblasts, CSF-1 decreased RANKL mRNA in a dose- and time-dependent manner. Incubation of bone marrow cultures with CSF-1 resulted in a significant decline in tartrate-resistant acid phosphatase (TRACP) activity and CTR expression. RANKL-decreased expression by CSF-1 was correlated with a decrease of NADPH oxidase activity as well as Nox1 and Nox4 protein levels. These findings provide the first evidence that osteoblasts express CSF-1R and are a target for CSF-1 ligand. CSF-1-mediated inhibition of RANKL expression on osteoblasts may provide an important mechanism for coupling bone formation/resorption and preventing excessive osteoclastogenesis during normal skeletal growth. PMID: 19819976 [PubMed - indexed for MEDLINE]

pubmed: 0804-4643

HDL cholesterol response to growth hormone replacement is associated with common cholesteryl ester transfer protein gene variation (-629C>A) and modified by glucocorticoid treatment.
Dullaart R, van den Berg G, van der Knaap A, Dijck-Brouwer J, Dallinga-Thie G, Zelissen P, Sluiter W, van Beek A Related Articles HDL cholesterol response to growth hormone replacement is associated with common cholesteryl ester transfer protein gene variation (-629C>A) and modified by glucocorticoid treatment. Eur J Endocrinol. 2009 Nov 19; Authors: Dullaart R, van den Berg G, van der Knaap A, Dijck-Brouwer J, Dallinga-Thie G, Zelissen P, Sluiter W, van Beek A Objective: Growth hormone (GH) replacement lowers total cholesterol and low density lipoprotein cholesterol (LDL-C) in GH deficient adults, but effects on HDL cholesterol (HDL-C) are variable. GH and glucocorticoids both decrease cholesteryl ester transfer protein (CETP) activity, which is important in HDL metabolism. We determined the extent to which the changes in HDL-C in response to GH replacement are predicted by the -629C>A CETP promoter polymorphism, and questioned whether this association is modified by concomitant glucocorticoid treatment. Design and Methods: 91 GH deficient adults (63 receiving glucocorticoids) were genotyped for the -629 CETP C>A polymorphism. Fasting serum lipids were measured before and after 1.2 +/- 0.4 years of GH treatment (Genotropin, Pfizer Inc.). Results: In the whole group, total cholesterol and LDL-C decreased (P<0.05) after GH treatment, but the changes in HDL-C were not significant. In CC carriers receiving glucocorticoids (n=19), HDL-C rose by 0.15 +/- 0.25 mmol/l (P=0.02; P<0.03 from unchanged HDL-C in -629 AA+CA carriers on glucocorticoids and from CC homozygotes not receiving glucocorticoids). Multivariate regression analysis showed that individual changes in HDL-C were predicted by the CETP polymorphism (CC vs. AA+CC, P=0.006) in glucocorticoid users, independently of baseline HDL-C and other variables including ApolipoproteinE4 carrier status; an opposite association with the CETP polymorphism was found in patients not receiving glucocorticoids (P=0.053). Conclusions: We suggest a common CETP variant -glucocorticoid treatment interaction concerning the effect of GH replacement on HDL-C. This may explain some of the reported variation in the HDL-C response to GH. PMID: 19926784 [PubMed - as supplied by publisher]
Pilot study on the assessment of the setpoint of the hypothalamus-pituitary-thyroid axis in healthy volunteers.
Benhadi N, Fliers E, Visser T, Reitsma J, Wiersinga W Related Articles Pilot study on the assessment of the setpoint of the hypothalamus-pituitary-thyroid axis in healthy volunteers. Eur J Endocrinol. 2009 Nov 19; Authors: Benhadi N, Fliers E, Visser T, Reitsma J, Wiersinga W Objective.To determine the log-linear relationship between TSH and in healthy subjects, and the variation in baseline TSH/FT4 combination in each individual. Subjects and methods. Twenty-one healthy volunteers were randomized to receive at 23.00 h with 2-wks intervals a single dose of placebo, 125 mug T4 and 250 mug T4 (arm 1) or placebo, 25 mug T3 and 50 mug T3 (arm 2). Blood samples were taken in the morning (8-11 h) before and following administration of the drug for assessment of TSH, FT4 and T3. Results. Intra- and inter-individual variation, and the individuality index of four baseline serum samples were for TSH 21.6%, 41.9% and 0.52 respectively, for FT4 9.9%, 16.5% and 0.60, and for T3 9.3%, 16.0% and 0.58. Substantial differences existed in the location of individual working points within the reference range. T4 administration increased FT4 (but not T3) and decreased TSH, resulting in a log-linear relationship (log TSH = 1.50-0.059* FT4, p0.05) for the whole group. T3 administration increased T3 and decreased TSH (but not FT4), resulting in a log-linear relationship (log TSH = 0.790 -0.245* T3, p0.001) for the whole group. Log-linear relationships were not always significant when assessed for each subject separately. Conclusion. Individuality-indices of TSH, FT4 and T3 are all </= 0.6, thereby limiting the usefulness of population-based reference values. Accurate assessment of individual setpoints of the HPT-axis was not possible with the applied single doses of T4 or T3, and will require either prolonged administration or higher single doses of thyroid hormone. PMID: 19926783 [PubMed - as supplied by publisher]
Treatment with the PPAR-gamma agonist rosiglitazone down-regulates interleukin-1 receptor antagonist in individuals with metabolic syndrome.
Halvorsen B, Heggen E, Ueland T, Smith C, Sandberg W, DamÃ¥s J, Otterdal K, Tonstad S, Aukrust P Related Articles Treatment with the PPAR-gamma agonist rosiglitazone down-regulates interleukin-1 receptor antagonist in individuals with metabolic syndrome. Eur J Endocrinol. 2009 Nov 19; Authors: Halvorsen B, Heggen E, Ueland T, Smith C, Sandberg W, Damås J, Otterdal K, Tonstad S, Aukrust P Objectives: Thiazolidinediones reduce insulin resistance, but also have pleiotropic properties including effects on inflammation. The balance between protective and pro-atherogenic effects may differ in various patient populations. We studied the effect of rosiglitazone on inflammatory markers in patients with metabolic syndrome (MetSyn). Methods: In a cross-over randomized controlled trial 23 subjects with MetSyn were assigned to treatment with rosiglitazone that was up-titrated from 4 mg/day for 6 weeks followed by 8 mg/day for 6 weeks or matching placebo for 12 weeks, and then to the opposite treatment for 12 weeks. Plasma levels of inflammatory and metabolic markers were measured during follow-up. Results: Our main findings were: (i) Compared to placebo, rosiglitazone significantly decreased plasma levels of the naturally occurring IL-1 inhibitor, interleukin-1 receptor antagonist (IL-1Ra) (p=0.001), potentially reflecting inflammatory effects on the IL-1 system. (ii) Parallel to this, rosiglitazone decreased plasma levels of IL-10 (p=0.029) further suggesting inflammatory effects. (iii) Rosiglitazone decreased uric acid levels (p=0.001), and monocyte chemoattractant protein-1 (p=0.05) and C-reactive protein (p=0.06) tended to be lower after rosiglitazone than placebo, suggesting potential pro- and anti-inflammatory effects simultaneously. (iv) In vitro, rosiglitazone enhanced IL-1Ra and decreased IL-1beta in THP-1 monocytes, illustrating the complex effects of these medications, potentially exhibiting anti-inflammatory effects on the IL-1 system in certain tissues or cells at least at certain concentrations. Conclusion: Our findings suggest inflammatory effects on the IL-1 system during rosiglitazone therapy in MetSyn. However, anti-inflammatory effects were also observed, and the net effect of thiazolidinediones in MetSyn should be further investigated. PMID: 19926782 [PubMed - as supplied by publisher]

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