PhysEmp :: Medicine :: Medical Specialties :: Endocrinology (4)

All Endocrinology Jobs

University City :: Kentucky :: Medical Search Consultants
Join Group of 3 This is an excellent opportunity for a BE/BC Endocrinologist to join 3 others as an expansion to this very practice. This expansion is needed due to increasing referral volume from
Great Location :: Massachusetts :: Intelligent Placement Solutions, Inc
We are developing an endocrinology center of excellence. Have one full time and one part time endo and need two more. Starting salary $185K + with sign on bonus of $25K+. NO CALL. Competitive salary
Not Disclosed :: Texas :: Locum Medical Group
A facility north of Dallas, Texas seeks to hire an Endocrinologist. Candidates must be either Board Certified or Board Eligible with an active Texas Medical license, DEA and DPS. Work Monday through Friday

pubmed: 0013-7227

Effects of TWEAK (TNF Superfamily Member 12) on Differentiation, Metabolism, and Secretory Function of Human Primary Preadipocytes and Adipocytes.
Tiller G, Fischer-Posovszky P, Laumen H, Finck A, Skurk T, Keuper M, Brinkmann U, Wabitsch M, Link D, Hauner H Related Articles Effects of TWEAK (TNF Superfamily Member 12) on Differentiation, Metabolism, and Secretory Function of Human Primary Preadipocytes and Adipocytes. Endocrinology. 2009 Nov 3; Authors: Tiller G, Fischer-Posovszky P, Laumen H, Finck A, Skurk T, Keuper M, Brinkmann U, Wabitsch M, Link D, Hauner H Expansion of adipose tissue mass by hypertrophy and hyperplasia is the hallmark of obesity. An automated cDNA screen was established to identify secreted human proteins with an inhibitory effect on adipocyte differentiation and, thereby, a potential inhibitory effect on adipose tissue growth. A member of the TNF superfamily, TNF-like weak inducer of apoptosis (TWEAK; TNF superfamily 12) was identified by means of high-throughput screening with the lipophilic dye Nile Red as an inhibitor of murine adipocyte differentiation and, subsequently, also of human adipocyte differentiation. TWEAK inhibited lipid deposition in a dose-dependent manner without causing cytotoxic effects. This inhibitory action was mimicked by an agonistic antibody of the TWEAK receptor. The TWEAK receptor (fibroblast growth factor inducible 14; CD266) was expressed on human primary preadipocytes and mature adipocytes. Knockdown of TWEAK receptor by short-hairpin RNA abolished the inhibitory effect of TWEAK on cell differentiation, demonstrating that the effects of TWEAK are mediated by its specific receptor. Inhibition of differentiation was the result of interference at an early step of transcriptional activation as assessed by decreased peroxisome proliferator-activated receptor-gamma, CCAAT enhancer-binding protein alpha (C/EBPalpha), and CCAAT enhancer-binding protein beta (C/EBPbeta) mRNA expression. In contrast to TNFalpha, basal and insulin-stimulated glucose uptake and lipolysis of terminally differentiated mature adipocytes and secretion of proinflammatory cytokines were not altered in the presence of TWEAK, and nuclear factor kappa B activity was only weakly induced. We conclude from our findings that TWEAK and the corresponding agonistic antibody have the potential to prevent adipose tissue growth without adversely influencing central metabolic pathways or proinflammatory cytokine secretion in adipose tissue. PMID: 19887572 [PubMed - as supplied by publisher]
Different Degrees of Somatotroph Ablation Compromise Pituitary Growth Hormone Cell Network Structure and Other Pituitary Endocrine Cell Types.
Waite E, Lafont C, Carmignac D, Chauvet N, Coutry N, Christian H, Robinson I, Mollard P, Le Tissier P Related Articles Different Degrees of Somatotroph Ablation Compromise Pituitary Growth Hormone Cell Network Structure and Other Pituitary Endocrine Cell Types. Endocrinology. 2009 Nov 3; Authors: Waite E, Lafont C, Carmignac D, Chauvet N, Coutry N, Christian H, Robinson I, Mollard P, Le Tissier P We have generated transgenic mice with somatotroph-specific expression of a modified influenza virus ion channel, (H37A)M2, leading to ablation of GH cells with three levels of severity, dependent on transgene copy number. GH-M2(low) mice grow normally and have normal-size pituitaries but 40-50% reduction in pituitary GH content in adult animals. GH-M2(med) mice have male-specific transient growth retardation and a reduction in pituitary GH content by 75% at 42 d and 97% by 100 d. GH-M2(high) mice are severely dwarfed with undetectable pituitary GH. The GH secretory response of GH-M2(low) and GH-M2(med) mice to GH-releasing peptide-6 and GHRH was markedly attenuated. The content of other pituitary hormones was affected depending on transgene copy number: no effect in GH-M2(low) mice, prolactin and TSH reduced in GH-M2(med) mice, and all hormones reduced in GH-M2(high) mice. The effect on non-GH hormone content was associated with increased macrophage invasion of the pituitary. Somatotroph ablation affected GH cell network organization with limited disruption in GH-M2(low) mice but more severe disruption in GH-M2(med) mice. The remaining somatotrophs formed tight clusters after puberty, which contrasts with GHRH-M2 mice with a secondary reduction in somatotrophs that do not form clusters. A reduction in pituitary beta-catenin staining was correlated with GH-M2 transgene copy number, suggesting M2 expression has an effect on cell-cell communication in somatotrophs and other pituitary cell types. GH-M2 transgenic mice demonstrate that differing degrees of somatotroph ablation lead to correlated secondary effects on cell populations and cellular network organization. PMID: 19887571 [PubMed - as supplied by publisher]
Wingless (Wnt)-3A Induces Trophoblast Migration and Matrix Metalloproteinase-2 Secretion through Canonical Wnt Signaling and Protein Kinase B/AKT Activation.
Sonderegger S, Haslinger P, Sabri A, Leisser C, Otten JV, Fiala C, Knöfler M Related Articles Wingless (Wnt)-3A Induces Trophoblast Migration and Matrix Metalloproteinase-2 Secretion through Canonical Wnt Signaling and Protein Kinase B/AKT Activation. Endocrinology. 2009 Nov 3; Authors: Sonderegger S, Haslinger P, Sabri A, Leisser C, Otten JV, Fiala C, Knöfler M Invasion of human trophoblasts is promoted through activation of wingless (Wnt) signaling, suggesting a role of the pathway in placental development and morphogenesis. However, details on the process such as involvement of canonical and/or noncanonical Wnt signaling cascades as well as their target genes are largely unknown. Hence, signal transduction via canonical Wnt signaling or phosphatidylinositide 3-kinase (PI3K)/AKT and their cross talk as well as trophoblast-specific protease expression were investigated in trophoblastic SGHPL-5 cells and primary extravillous trophoblasts purified from first-trimester placentas. Western blot analyses revealed that the recombinant Wnt ligand Wnt-3A increased phosphorylation of AKT and the downstream kinase glycogen synthase kinase (GSK)-3beta as well as accumulation of activated, nuclear beta-catenin. In accordance, luciferase expression of a canonical Wnt/TCF reporter and cell migration in first-trimester villous explant cultures and of SGHPL-5 cells were stimulated. Chemical inhibition of PI3K abolished Wnt-dependent phosphorylation of AKT and GSK-3beta and trophoblast motility but did not affect appearance of activated beta-catenin or Wnt/TCF reporter activity. In contrast, inhibition of the canonical pathway through soluble Dickkopf-1 did not influence AKT and GSK-3beta phosphorylation but reduced Wnt reporter activity, accumulation of active beta-catenin, and cell migration. Both inhibitors decreased Wnt-3A-induced secretion of pro- and active matrix metalloproteinase-2 from SGHPL-5 cells and pure EVT. The data suggest that Wnt-3A may activate canonical Wnt signaling and PI3K/AKT through distinct receptors. The two signaling cascades act independently in trophoblasts; however, both pathways promote Wnt-dependent migration and the release of matrix metalloproteinase-2, which has been identified as novel Wnt target in invasive trophoblasts. PMID: 19887570 [PubMed - as supplied by publisher]
Circadian Expression of Adiponectin and Its Receptors in Human Adipose Tissue.
GĂłmez-Abellán P, GĂłmez-Santos C, Madrid JA, Milagro FI, Campion J, MartĂ­nez JA, Ordovás JM, Garaulet M Related Articles Circadian Expression of Adiponectin and Its Receptors in Human Adipose Tissue. Endocrinology. 2009 Nov 3; Authors: Gómez-Abellán P, Gómez-Santos C, Madrid JA, Milagro FI, Campion J, Martínez JA, Ordovás JM, Garaulet M Adiponectin is one of the most clinically relevant cytokines associated with obesity. However, circadian rhythmicity of adiponectin in human adipose tissue (AT) has not been analyzed. To assess whether the mRNA levels of adiponectin and its receptors (ADIPOR1 and ADIPOR2) might show daily circadian rhythms in visceral and sc fat explants obtained from morbid obese women, visceral and sc abdominal AT biopsies (n = 6) were obtained from morbidly obese women (body mass index >/=40 kg/m(2)). Anthropometric variables were measured and fasting plasma glucose, lipid, and lipoprotein concentrations were analyzed. To investigate rhythmic expression pattern, AT explants were cultured during 24 h, and gene expression was analyzed at the following times: 0800, 1400, 2000, and 0200 h, using quantitative real-time PCR. All genes investigated showed a circadian rhythmicity and oscillated accurately and independently of the suprachiasmatic nucleus in both AT explants (P < 0.05). Adiponectin gene expression fluctuated in the same phase as its receptors. Correlation analyses between the genetic circadian oscillation and components of the metabolic syndrome revealed that adiposity and abdominal obesity correlated with a decrease in adiponectin and adiponectin receptors ADIPOR1 and ADIPOR2 amplitude (P < 0.05). Visceral fat showed a trend toward a phase delay and dampening of the mRNA amplitude of adiponectin as compared with sc fat. The mRNA expression of adiponectin and its receptors showed 24-h rhythmicity in human AT from morbidly obese patients. PMID: 19887569 [PubMed - as supplied by publisher]
Peroxisome Proliferator-Activated Receptor-{alpha} Control of Lipid and Glucose Metabolism in Human White Adipocytes.
Ribet C, Montastier E, Valle C, Bezaire V, Mazzucotelli A, Mairal A, Viguerie N, Langin D Related Articles Peroxisome Proliferator-Activated Receptor-{alpha} Control of Lipid and Glucose Metabolism in Human White Adipocytes. Endocrinology. 2009 Nov 3; Authors: Ribet C, Montastier E, Valle C, Bezaire V, Mazzucotelli A, Mairal A, Viguerie N, Langin D This work aimed at characterizing the role of peroxisome proliferator-activated receptors (PPAR)alpha in human white adipocyte metabolism and at comparing PPARalpha and PPARgamma actions in these cells. Primary cultures of human fat cells were treated with the PPARalpha agonist GW7647 or the PPARgamma agonist rosiglitazone. Changes in gene expression were determined using DNA microrrays and quantitative RT-PCR. Western blot and metabolic studies were performed to identify the biological effects elicited by PPAR agonist treatments. GW7647 induced an up-regulation of beta-oxidation gene expression and increased palmitate oxidation. Unexpectedly, glycolysis was strongly reduced at transcriptional and functional levels by GW7647 leading to a decrease in pyruvate and lactate production. Glucose oxidation was decreased. Triglyceride esterification and de novo lipogenesis were inhibited by the PPARalpha agonist. GW7647-induced alterations were abolished by a treatment with a PPARalpha antagonist. Small interfering RNA-mediated extinction of PPARalpha gene expression in hMADS adipocytes attenuated GW7647 induction of palmitate oxidation. Rosiglitazone had no major impact on glycolysis and beta-oxidation. Altogether these results show that PPARalpha can selectively up-regulate beta-oxidation and decrease glucose utilization in human white adipocytes. PMID: 19887568 [PubMed - as supplied by publisher]
Deletion of the Novel Oocyte-Enriched Gene, Gpr149, Leads to Increased Fertility in Mice.
Edson MA, Lin YN, Matzuk MM Related Articles Deletion of the Novel Oocyte-Enriched Gene, Gpr149, Leads to Increased Fertility in Mice. Endocrinology. 2009 Nov 3; Authors: Edson MA, Lin YN, Matzuk MM Through in silico subtraction and microarray analysis, we identified mouse Gpr149, a novel, oocyte-enriched transcript that encodes a predicted orphan G-protein-coupled receptor (GPR). Phylogenetic analysis of GPR149 from fish to mammals suggests that it is widely conserved in vertebrates. By multitissue RT-PCR analysis, we found that Gpr149 is highly expressed in the ovary and also in the brain and the digestive tract at low levels. Gpr149 levels are low in newborn ovaries but increase throughout folliculogenesis. In the ovary, we found that granulosa cells did not express Gpr149, whereas germinal vesicle and meiosis II stage oocytes showed high levels of Gpr149 expression. After fertilization, Gpr149 expression declined, becoming undetectable by the two-cell stage. To study the function of GPR149 in oocyte growth and maturation, we generated Gpr149 null mice. Surprisingly, Gpr149 null mice are viable and have normal folliculogenesis, but demonstrate increased fertility, enhanced ovulation, increased oocyte Gdf9 mRNA levels, and increased levels of FSH receptor and cyclin D2 mRNA levels in granulosa cells. Thus, Gpr149 null mice are one of the few models with enhanced fertility, and GPR149 could be a target for small molecules to enhance fertility in the assisted reproductive technology clinic. PMID: 19887567 [PubMed - as supplied by publisher]
Central Insulin Signaling Is Attenuated by Long-Term Insulin Exposure via Insulin Receptor Substrate-1 Serine Phosphorylation, Proteasomal Degradation, and Lysosomal Insulin Receptor Degradation.
Mayer CM, Belsham DD Related Articles Central Insulin Signaling Is Attenuated by Long-Term Insulin Exposure via Insulin Receptor Substrate-1 Serine Phosphorylation, Proteasomal Degradation, and Lysosomal Insulin Receptor Degradation. Endocrinology. 2009 Nov 3; Authors: Mayer CM, Belsham DD Central insulin signaling is critical for the prevention of insulin resistance. Hyperinsulinemia contributes to insulin resistance, but it is not yet clear whether neurons are subject to cellular insulin resistance. We used an immortalized, hypothalamic, clonal cell line, mHypoE-46, which exemplifies neuronal function and expresses the components of the insulin signaling pathway, to determine how hyperinsulinemia modifies neuronal function. Western blot analysis indicated that prolonged insulin treatment of mHypoE-46 cells attenuated insulin signaling through phospho-Akt. To understand the mechanisms involved, time-course analysis was performed. Insulin exposure for 4 and 8 h phosphorylated Akt and p70-S6 kinase (S6K1), whereas 8 and 24 h treatment decreased insulin receptor (IR) and IR substrate 1 (IRS-1) protein levels. Insulin phosphorylation of S6K1 correlated with IRS-1 ser1101 phosphorylation and the mTOR-S6K1 pathway inhibitor rapamycin prevented IRS-1 serine phosphorylation. The proteasomal inhibitor epoxomicin and the lysosomal pathway inhibitor 3-methyladenine prevented the degradation of IRS-1 and IR by insulin, respectively, and pretreatment with rapamycin, epoxomicin, or 3-methyladenine prevented attenuation of insulin signaling by long-term insulin exposure. Thus, a sustained elevation of insulin levels diminishes neuronal insulin signaling through mTOR-S6K1-mediated IRS-1 serine phosphorylation, proteasomal degradation of IRS-1 and lysosomal degradation of the IR. PMID: 19887566 [PubMed - as supplied by publisher]
Up-Regulation of Toll-Like Receptor 4/Nuclear Factor-{kappa}B Signaling Is Associated with Enhanced Adipogenesis and Insulin Resistance in Fetal Skeletal Muscle of Obese Sheep at Late Gestation.
Yan X, Zhu MJ, Xu W, Tong JF, Ford SP, Nathanielsz PW, Du M Related Articles Up-Regulation of Toll-Like Receptor 4/Nuclear Factor-{kappa}B Signaling Is Associated with Enhanced Adipogenesis and Insulin Resistance in Fetal Skeletal Muscle of Obese Sheep at Late Gestation. Endocrinology. 2009 Nov 3; Authors: Yan X, Zhu MJ, Xu W, Tong JF, Ford SP, Nathanielsz PW, Du M Maternal obesity is increasing at an alarming rate. We previously showed that maternal obesity induces an inflammatory response and enhances adipogenesis in fetal skeletal muscle at midgestation. The objective of this study was to evaluate effects of maternal obesity on adipogenesis, inflammatory signaling, and insulin pathways at late gestation when ovine fetal skeletal muscle matures. Nonpregnant ewes were assigned to a control diet (Con, fed 100% of National Research Council nutrient recommendations, n = 6) or obesogenic diet (OB, fed 150% of National Research Council recommendations, n = 6) from 60 d before to 135 d after conception (term 148 d) when the fetal semitendenosus skeletal muscle was sampled. Expression of the adipogenic marker, peroxisome proliferator-activated receptor-gamma, was increased in OB compared with Con fetal semitendenosus muscle, indicating up-regulation of adipogenesis. More intramuscular adipocytes were observed in OB muscle. Phosphorylation of inhibitor-kappaB kinase-alpha/beta and nuclear factor-kappaB RelA/p65 were both increased in OB fetal muscle, indicating activation of nuclear factor-kappaB pathway. Phosphorylation of c-Jun N-terminal kinase and c-Jun (at Ser 63 and Ser 73) was also elevated. Toll-like receptor 4 expression was higher in OB than Con fetal muscle. Moreover, despite higher insulin concentrations in OB vs. Con fetal plasma (2.89 +/- 0.53 vs. 1.06 +/- 0.52 ng/ml; P < 0.05), phosphorylation of protein kinase B at Ser 473 was reduced, indicating insulin resistance. In conclusion, our data show maternal obesity-induced inflammatory signaling in late gestation fetal muscle, which correlates with increased im adipogenesis and insulin resistance, which may predispose offspring to later-life obesity and diabetes. PMID: 19887565 [PubMed - as supplied by publisher]
Decreased Expression of A-Kinase Anchoring Protein 150 in GT1 Neurons Decreases Neuron Excitability and Frequency of Intrinsic Gonadotropin-Releasing Hormone Pulses.
Chen Q, Weiner RI, Blackman BE Related Articles Decreased Expression of A-Kinase Anchoring Protein 150 in GT1 Neurons Decreases Neuron Excitability and Frequency of Intrinsic Gonadotropin-Releasing Hormone Pulses. Endocrinology. 2009 Nov 3; Authors: Chen Q, Weiner RI, Blackman BE The frequency of intrinsic pulsatile GnRH secretion from endogenous GnRH neurons and GT1 GnRH cell lines is stimulated by increased intracellular cAMP levels. The downstream molecules comprising the cAMP signaling pathway are organized in microdomains by a family of scaffolding proteins, A-kinase anchoring proteins (AKAPs). These molecules tether protein kinase A, cAMP-specific phosphodiesterases, phosphatases to known substrates. In neurons AKAP150 organizes many of the signaling molecules known to regulate the excitability and intrinsic pulsatile activity of GnRH neurons. AKAP150 was expressed in both the GT1-1 and GT1-7 cells. We determined the role of AKAP150 in coordinating GT1-1 cell excitability and intrinsic GnRH pulsatile secretion by lowering AKAP150 levels with a small interfering RNA (siRNA) adenovirus construct to AKAP150 (Ad-AKAP150-siRNA). Infection with Ad-AKAP150-siRNA specifically decreased AKAP150 mRNA levels by 74% and protein levels by 53% relative to uninfected cells or cells infected with a luciferase control adenovirus siRNA vector. In GT1 cells, spontaneous Ca(2+) oscillations, an index of neuron excitability, are stimulated by increased levels of intracellular cAMP and lowered by decreased levels. The frequency of spontaneous Ca(2+) oscillations in Ad-AKAP150-siRNA-treated GT1-1 cells decreased by 47.2% relative to controls. A dramatic decrease in the number of spontaneous GnRH pulses was also observed after infection with Ad-AKAP150-siRNA. The interpulse interval increased to 143 +/- 20.25 min in Ad-AKAP150-siRNA infected cells from 32.2 +/- 7.3 min in luciferase control adenovirus siRNA vector-infected cells. These data demonstrate an important role of AKAP150 in coordinating signaling events regulating the frequency of intrinsic pulsatile GnRH secretion. PMID: 19887564 [PubMed - as supplied by publisher]

pubmed: 0804-4643

Cytotoxic T lymphocyte antigen-4 Ala17 polymorphism is a genetic marker of autoimmune adrenal insufficiency: Italian association study and meta-analysis of European studies.
Brozzetti A, Marzotti S, Tortoioli C, Bini V, Giordano R, Dotta F, Betterle C, De Bellis A, Arnaldi G, Toscano V, Arvat E, Bellastella A, Mantero F, Falorni A Related Articles Cytotoxic T lymphocyte antigen-4 Ala17 polymorphism is a genetic marker of autoimmune adrenal insufficiency: Italian association study and meta-analysis of European studies. Eur J Endocrinol. 2009 Nov 2; Authors: Brozzetti A, Marzotti S, Tortoioli C, Bini V, Giordano R, Dotta F, Betterle C, De Bellis A, Arnaldi G, Toscano V, Arvat E, Bellastella A, Mantero F, Falorni A Objective: CTLA4 gene polymorphism has been associated with human autoimmune diseases, but discordant data are available on its association with autoimmune Addison's disease (AAD). We tested the HLA-independent association of CTLA4 +49 (A/G) (Ala 17) and/or CTLA4 CT60 (A/G) polymorphism with AAD. Design: DNA samples from 180 AAD patients and 394 healthy control subjects, from continental Italy were analyzed and association statistical analyses and meta-analysis of published studies performed. Methods: TaqMan Minor Groove Binder chemistry assays and PCR fragment length polymorphysm assays were used. Results: Frequency of allele G of CTLA4 +49 was significantly increased among AAD patients (40% alleles) than among healthy controls (27% alleles) (p<0.0001). CTLA4 CT60 polymorphism was associated with AAD only in the heterozygous A/G individuals. The frequency of +49 AG+GG genotypes was significantly higher among AAD patients than among healthy control subjects, in both a co-dominant (p<0.0001) and a G dominant model (p<0.0001). CTLA4 +49 allele G was significantly associated with disease risk in both patients with isolated AAD and in patients with autoimmune polyendocrine syndrome. Multivariate logistic regression analysis showed that CTLA4 +49 allele G was positively associated with AAD (p<0.0001, OR=2.43, 95%CI=1.54-3.86) also after correction for DRB1*03-DQA1*0501-DQB1*0201, DRB1*04-DQA1*0301-DQB1*0302 and sex. Meta-analysis of five studies revealed a significant association of CTLA4 +49 allele G with AAD (p<0.0001) with an overall OR of 1.48 (1.28-1.71). Conclusions: The CTLA4 +49 polymorphism is strongly associated with genetic risk for AAD, independentenly from the well known association with HLA class II genes. PMID: 19884265 [PubMed - as supplied by publisher]
Raloxifene and body composition and muscle strength in postmenopausal women: A randomized, double-blind, placebo-controlled trial.
Jacobsen D, Samson M, Emmelot M, Verhaar H Related Articles Raloxifene and body composition and muscle strength in postmenopausal women: A randomized, double-blind, placebo-controlled trial. Eur J Endocrinol. 2009 Nov 2; Authors: Jacobsen D, Samson M, Emmelot M, Verhaar H Objective To compare the effects of raloxifene and placebo on body composition and muscle strength. Design Randomized, double-blind, placebo-controlled trial involving 198 healthy women aged 70 years or older conducted between July 2003 and January 2008 at the University Medical Centre, Utrecht, the Netherlands. Methods Participants were randomly assigned to receive raloxifene 60 mg or placebo daily for 12 months. Measurements were taken at baseline, 3, 6, and 12 months, and change from baseline was calculated. Main outcome measures are body composition (bioelectrical impedance analysis), muscle strength, and muscle power (maximum voluntary isometric knee extension strength, explosive leg extensor power, and handgrip strength). Results At 12 months, the body composition of women taking raloxifene was significantly different from that of women taking placebo: fat-free mass had increased by a mean of 0.83 (2.4) kg in the raloxifene group versus 0.03 (1.5) kg in the placebo group (p=0.05), and total body water had increased by a mean of 0.6 (1.8) L in the raloxifene group versus a decrease of 0.06 (1.1) L in the placebo group (p=0.02). Muscle strength and power were not significantly different. Conclusion Raloxifene significantly changed (increased fat-free mass; increased water content) body composition compared with placebo in postmenopausal women. Keywords: Raloxifene; body composition, postmenopausal Trial registration number: NTR: 1232. PMID: 19884264 [PubMed - as supplied by publisher]
Increased suppression of serum ghrelin concentration by hyperinsulinemia in women with anorexia nervosa.
Karczewska-Kupczewska M, Straczkowski M, Adamska A, Nikolajuk A, Otziomek E, Gorska M, Kowalska I Related Articles Increased suppression of serum ghrelin concentration by hyperinsulinemia in women with anorexia nervosa. Eur J Endocrinol. 2009 Nov 2; Authors: Karczewska-Kupczewska M, Straczkowski M, Adamska A, Nikolajuk A, Otziomek E, Gorska M, Kowalska I Context: Ghrelin is a peptide secreted mainly by stomach, which has the ability to stimulate appetite and food intake. Serum ghrelin concentration decreases rapidly after the meal, probably because of the concurrent increase in serum insulin. Anorexia nervosa (AN) is an eating disorder, which is characterized by high serum ghrelin concentration, however, regulation of circulating ghrelin by insulin in this disorder remains unclear. Objective: To estimate serum ghrelin concentration in the fasting state and after hyperinsulinemia in women with AN. Design and participants: We examined 19 women with AN, 26 lean healthy women and 25 women with overweight or obesity. Serum ghrelin concentration was measured in the fasting state and after euglycemic hyperinsulinemic clamp. Results: Insulin sensitivity was similar in AN and normal-weight women and was markedly decreased in the obese subjects. In fasting state, serum ghrelin was higher in AN in comparison with other groups (normal-weight, p=0.017; obese, p=0.0001) and in normal-weight in comparison with the obese (p=0.044). Hyperinsulinemia resulted in a marked decrease in serum ghrelin in AN (p<0.0001) and normal-weight women (p=0.002). The fall in serum ghrelin was higher in AN in comparison with other groups (normal-weight, p=0.0008; obese, p=0.0001) and was related to insulin sensitivity (r=0.24, p<0.05). In multiple regression analysis, only fasting serum ghrelin and the presence of AN were independent predictors of this fall. Conclusions: Women with AN have an increased suppression of serum ghrelin by hyperinsulinemia. This phenomenon might lead to an increased and more rapid feeling of satiety in AN. PMID: 19884263 [PubMed - as supplied by publisher]
No recurrence of sporadic primary hyperparathyroidism when cure is established 6 months after parathyroidectomy.
Witteveen J, Kievit J, Morreau H, Romijn J, Hamdy N Related Articles No recurrence of sporadic primary hyperparathyroidism when cure is established 6 months after parathyroidectomy. Eur J Endocrinol. 2009 Nov 2; Authors: Witteveen J, Kievit J, Morreau H, Romijn J, Hamdy N Objective: Cure rate for primary hyperparathyroidism is reported to be 94-100% one year after surgery, but recent data suggest recurrence in 4% of patients 1-5 years postoperatively. The aim of our study was to establish the cure rate and its maintenance in the long-term after parathyroidectomy in patients with sporadic primary hyperparathyroidism. Design: Evaluation of recurrence in patients with sporadic hyperparathyroidism who underwent parathyroidectomy 1-24 years prior to the study. Patients &amp; Methods: We identified 111 patients who underwent initial PTx between 1984 and 2008 and had no MEN-1, MEN-2 or CaR mutation, parathyroid carcinoma, history of lithium use or renal failure. Thirty-eight patients were lost to follow-up or were unwilling or unable to participate in the study. Cure was defined as maintenance of normal serum calcium and PTH concentrations 6 months after PTx. Results: Cure was achieved in 68 of 73 patients studied (93%) and was sustained in all for 6+/-5 years. Conclusion: The cure rate of sporadic primary hyperparathyroidism after initial surgery is 93%. When cure is achieved, this is sustained in 100% of patients for up to 24 years post-operatively. Our data suggest that closer early follow-up is advocated in all patients undergoing PTx to definitively establish cure and to provide a safety net for those with residual gland pathology. The data do not support the need for long term follow-up when cure is established 6 months after PTx. PMID: 19884262 [PubMed - as supplied by publisher]

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