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Current Opinion in Endocrinology, Diabetes and Obesity - Current Table Of Contents

Editorial introductions.
Page: viiDOI: 10.1097/MED.0b013e328321b372
Endocrinology of female puberty.
Page: 1DOI: 10.1097/MED.0b013e3283207937Authors: DiVall, Sara A; Radovick, Sally
Endocrinology of male puberty.
Page: 5DOI: 10.1097/MED.0b013e32832029beAuthors: Lewis, Katherine; Lee, Peter A

PubMed: 0013-7227

Role of type I{alpha} phosphatidylinositol-4-phosphate 5-kinase in insulin secretion, glucose metabolism, and membrane potential in INS-1 {beta}-cells.
Zhang J, Luo R, Wu H, Wei S, Han W, Li G Related Articles Role of type I{alpha} phosphatidylinositol-4-phosphate 5-kinase in insulin secretion, glucose metabolism, and membrane potential in INS-1 {beta}-cells. Endocrinology. 2008 Dec 30; Authors: Zhang J, Luo R, Wu H, Wei S, Han W, Li G Insulin secretion from beta-cells is regulated by a complex signaling network. Our earlier study has reported that Rac1 participates in glucose- and cAMP-induced insulin secretion probably via maintaining a functional actin structure for recruitment of insulin granules. Type Ialpha phosphatidylinositol-4-phosphate 5-kinase (PIP5K-Ialpha) is a downstream effector of Rac1 and a critical enzyme for synthesis of phosphatidylinositol-4,5-bisphosphate (PIP2). By using RNA interference technique, PIP5K-Ialpha in INS-1 beta-cells could be specifically knocked down by 70-75%. PIP5K-Ialpha knockdown disrupted F-actin structure and caused changes in cell morphology. In addition, PIP2 content in the plasma membrane was reduced and glucose effect on PIP2 was abolished but without affecting glucose-induced formation of inositol 1,4,5-trisphosphate. At basal conditions (2.8 mM glucose), PIP5K-Ialpha knockdown doubled insulin secretion, elevated glucose metabolic rate, depolarized resting membrane potential and raised cytoplasmic free Ca(2+) levels ([Ca(2+)]i). The total insulin release at high glucose was increased upon PIP5K-Ialpha knockdown. However, the percentage increment of insulin secretion by high glucose and forskolin over the basal release was significantly reduced, an effect more apparent on the late phase of insulin secretion. Metabolism and [Ca(2+)]i rises at high glucose was also attenuated in cells after PIP5K-Ialpha knockdown. In contrast, PIP5K-Ialpha knockdown had no effect on cell growth and viability. Taken together, our data suggest that PIP5K-Ialpha may play an important role in both the proximal and distal steps of signaling cascade for insulin secretion in beta-cells. PMID: 19116346 [PubMed - as supplied by publisher]
Sphingosine kinase as an oncogene: autocrine sphingosine 1-phoshate modulates ML-1 thyroid carcinoma cell migration by a mechanism dependent on PKC-{alpha} and ERK1/2.
Bergelin N, Blom T, Heikkilä J, Löf C, Alam C, Balthasar S, Slotte JP, Hinkkanen A, Törnquist K Related Articles Sphingosine kinase as an oncogene: autocrine sphingosine 1-phoshate modulates ML-1 thyroid carcinoma cell migration by a mechanism dependent on PKC-{alpha} and ERK1/2. Endocrinology. 2008 Dec 30; Authors: Bergelin N, Blom T, Heikkilä J, Löf C, Alam C, Balthasar S, Slotte JP, Hinkkanen A, Törnquist K Sphingosine 1-phosphate (S1P) induces migration of the human thyroid follicular carcinoma cell line ML-1 by activation of S1P1- and S1P3-receptors, Gi-proteins and the PI-3K-Akt pathway. Since sphingosine kinase isoform 1 (SK) recently has been implicated as an oncogene in various cancer cell systems, we investigated the functions of SK1 in the migration, proliferation and adhesion of the ML-1 cell line. SK1 over-expressing ML-1 cells show an enhanced secretion of S1P, which can be attenuated, by inhibiting SK activity, and by inhibiting a multidrug resistant transport protein (ABCC1). Furthermore, over-expression of SK enhances serum-induced migration of ML-1 cells, which can be attenuated by blocking ABCC1 and SK1, suggesting that the migration is mediated by autocrine signalling through secretion of S1P. Inhibition of PKC-alpha, both with siRNA and small molecular inhibitors, attenuates migration in SK over-expressing cells. In addition, SK over-expressing cells show an impaired adhesion, slower cell growth, and an up-regulation of ERK1/2 phosphorylation, as compared to cells expressing a dominant negative SK. Taken together, we present evidence suggesting that SK enhances migration of ML-1 cells by an autocrine mechanism, and that the S1P-evoked migration is dependent on PKC-alpha, ERK1/2, and SK. PMID: 19116345 [PubMed - as supplied by publisher]
Akt2 regulation of Cdc2-like kinases (Clk/Sty), serine/arginine-rich (SR) protein phosphorylation, and insulin-induced alternative splicing of PKCssII mRNA.
Jiang K, Patel NA, Watson JE, Apostolatos H, Kleiman E, Hanson O, Hagiwara M, Cooper DR Related Articles Akt2 regulation of Cdc2-like kinases (Clk/Sty), serine/arginine-rich (SR) protein phosphorylation, and insulin-induced alternative splicing of PKCssII mRNA. Endocrinology. 2008 Dec 30; Authors: Jiang K, Patel NA, Watson JE, Apostolatos H, Kleiman E, Hanson O, Hagiwara M, Cooper DR Serine/arginine-rich (SR) proteins play essential roles in the constitutive and regulated splicing of precursor mRNAs. Phosphorylation of the arginine/serine dipeptide-rich (RS) domain by SR protein kinases such as Cdc2-like kinases (Clk/Sty) modulates their subcellular localization and activation. However, it remains unclear how these kinases and their target SR proteins are regulated by extracellular signals. Regulation of protein kinase C betaII (PKCbetaII) pre-mRNA alternative splicing via exon inclusion by Akt2, a central kinase in insulin action, involves phosphorylation of SR proteins. Here we showed that Akt2, in response to insulin, resulted in phosphorylation of Clk/Sty, which then altered SR protein phosphorylation in concert with Akt2. Insulin-stimulated PKCbetaII pre-mRNA splicing was blocked by Clk/Sty and phosphatidylinositol-3-kinase (PI3K) inhibitors, and diabetic Akt2-null mouse tissues had impaired phospho-Clk/Sty, SR protein phosphorylation and PKCbetaII expression. Furthermore, we observed that Akt2 phosphorylated several SR proteins distinct from Clk/Sty in response to insulin. Akt2-catalyzed phosphorylation of Clk/Sty and SR proteins revealed a role for both kinases in splicing regulation indicating dual functions for Akt2 in response to insulin in this pathway. PMID: 19116344 [PubMed - as supplied by publisher]
Pax6 haploinsufficiency causes abnormal metabolic homeostasis by down-regulating GLP-1 in mice.
Ding J, Gao Y, Zhao J, Yan H, Guo SY, Zhang QX, Li LS, Gao X Related Articles Pax6 haploinsufficiency causes abnormal metabolic homeostasis by down-regulating GLP-1 in mice. Endocrinology. 2008 Dec 30; Authors: Ding J, Gao Y, Zhao J, Yan H, Guo SY, Zhang QX, Li LS, Gao X Heterozygosity for the Pax6 allele is associated with impaired glucose tolerance in humans. With a Pax6 mutant mice model, we found many of the metabolic abnormalities were consistent with the effects of down-regulating the expression of glucagon-like peptide 1 (GLP-1). In addition to impaired glucose tolerance, adult heterozygous mutant mice (Pax6(m/+)) secreted less insulin responding to glucose and arginine administration compared to control mice. Moreover, Pax6(m/+) mice showed increased food intake than control mice although they were resistant to diet-induced fat accumulation. Indeed levels of circulating GLP-1 and intestinal transcription of Gcg/Proglucagon were dramatically reduced in Pax6(m/+) mice. Mutated Pax6 also failed to activate the Gcg/Proglucagon promoter by in vitro transfection assay. Finally, administering the GLP-1 receptor agonist exendin-4 to Pax6(m/+) mice largely reversed their abnormal food intake, glycemic excursion, and insulin secretion. Our studies suggested that disruption of metabolic homeostasis mainly caused by Pax6 haploinsufficiency was mainly mediated by down-regulation of GLP-1. Administration of exendin-4 may be a useful therapy in humans with similar mutation. PMID: 19116343 [PubMed - as supplied by publisher]
Identification of the potent phytoestrogen glycinol in elicited soybean (Glycine Max) Abbreviated Title: Glycinol: A Novel Phytoestrogen.
Boué SM, Tilghman SL, Elliott S, Zimmerman MC, Williams KY, Payton-Stewart F, Miraflor AP, Howell MS, Shih BY, Carter-Wientjes CH, Segar C, Beckman BS, Wiese TE, Cleveland TE, McLachlan JA, Burow ME Related Articles Identification of the potent phytoestrogen glycinol in elicited soybean (Glycine Max) Abbreviated Title: Glycinol: A Novel Phytoestrogen. Endocrinology. 2008 Dec 30; Authors: Boué SM, Tilghman SL, Elliott S, Zimmerman MC, Williams KY, Payton-Stewart F, Miraflor AP, Howell MS, Shih BY, Carter-Wientjes CH, Segar C, Beckman BS, Wiese TE, Cleveland TE, McLachlan JA, Burow ME The primary induced isoflavones in soybean, the glyceollins, have been shown to be potent estrogen antagonists in vitro and in vivo. The discovery of the glyceollins' ability to inhibit cancer cell proliferation has led to the analysis of estrogenic activities of other induced isoflavones. In this study, we investigate a novel isoflavone, glycinol, a precursor to glyceollin that is produced in elicited soy. Sensitive and specific in vitro bioassays were used to determine that glycinol exhibits potent estrogenic activity. Estrogen-based reporter assays were performed and glycinol displayed a marked estrogenic effect on ER signaling between 1-10 microM, which correlated with comparable colony formation of MCF-7 cells at 10 microM. Glycinol also induced the expression of estrogen responsive genes (PgR and SDF-1). Competitive binding assays revealed a high affinity of glycinol for both ERalpha (IC50=13.8 nM) and ERbeta (IC50=9.1 nM). In addition, ligand receptor modeling (docking) studies were performed and glycinol was shown to bind similarly to both ERalpha and ERbeta. Taken together, these results suggest for the first time that glycinol is estrogenic and may represent an important component of the health effects of soy-based foods. PMID: 19116342 [PubMed - as supplied by publisher]
Dorsal hindbrain AMP-Kinase as an intracellular mediator of energy balance.
Hayes MR, Skibicka KP, Bence KK, Grill HJ Related Articles Dorsal hindbrain AMP-Kinase as an intracellular mediator of energy balance. Endocrinology. 2008 Dec 30; Authors: Hayes MR, Skibicka KP, Bence KK, Grill HJ The fuel-sensing enzyme AMP-activated protein kinase (AMPK) has been implicated in CNS control of energy balance. Hypothalamic AMPK activity is increased by food deprivation and this elevation is inhibited by refeeding or by leptin treatment. The contribution of extra-hypothalamic AMPK activity in energy balance control has not been addressed. Here, we investigate the effects of physiological state on the AMPK activity in hindbrain nucleus tractus solitarius (NTS) neurons as treatments that reduce energy availability in these neurons trigger behavioral, endocrine, and autonomic responses to restore energy balance. Food-deprived rats showed significantly increased AMPK activity in both NTS- and hypothalamus-enriched lysates compared to those that were ad libitum fed. Pharmacological inhibition of AMPK activity in medial NTS neurons, by intraparenchymal injection of compound C, suppressed food intake and body weight gain compared to vehicle. Fourth ventricle (4(th) icv) compound C delivery increased heart rate and spontaneous activity in free-moving rats. Suppression of AMPK activity has been implicated in leptin's anorectic action in the hypothalamus. Given the role of leptin signaling in food intake inhibition within the medial NTS, we also examined whether stimulation of hindbrain AMPK by 4(th) icv administration of AICAR, an AMP-mimicking promoter of AMPK activity, could attenuate the inhibition of food intake by 4(th)v leptin. The intake-suppressive effects of leptin (at 2h and 4h) were completely reversed by AICAR. We conclude that: 1) hindbrain AMPK activity contributes to energy balance control through regulation of food intake and energy expenditure; 2) leptin's intake-reducing effects in the NTS are meditated by AMPK; 3) CNS AMPK controls whole-body homeostasis at anatomically distributed sites across the neuraxis. PMID: 19116341 [PubMed - as supplied by publisher]
Characterization of relaxin receptor (RXFP1) desensitization and internalization in primary human decidual cells and RXFP1 transfected HEK293 cells.
Kern A, Bryant-Greenwood GD Related Articles Characterization of relaxin receptor (RXFP1) desensitization and internalization in primary human decidual cells and RXFP1 transfected HEK293 cells. Endocrinology. 2008 Dec 30; Authors: Kern A, Bryant-Greenwood GD We report here the desensitization and internalization of the relaxin receptor (RXFP1) after agonist activation in both primary human decidual cells and HEK293 cells stably transfected with RXFP1. The importance of beta-arrestin 2 in these processes has also been demonstrated. Thus, in HEK-RXFP1 cells the desensitization of RXFP1 was significantly increased when beta-arrestin 2 was overexpressed. After relaxin activation, beta-arrestin 2 was translocated to the cell membrane and RXFP1 underwent rapid internalization. We have previously shown that RXFP1 forms dimers/oligomers during its biosynthesis and trafficking to the plasma membrane, we now show that internalization of RXFP1 occurs through this dimerization/oligomerization. In non-agonist stimulated cells, it is known that the majority of the RXFP1 is located intracellularly and was confirmed in the cells used here. Constitutive internalization of RXFP1 could account for this and indeed, slow but robust constitutive internalization, which was increased after agonist stimulation was demonstrated. A carboxyl-terminal deleted RXFP1 variant had a similar level of constitutive agonist-independent internalization as the wild-type RXFP1, but lost sensitivity to agonist stimulation. This demonstrated the importance of the carboxyl-terminus in agonist-stimulated receptor internalization. These data suggest that the autocrine/paracrine actions of relaxin in the decidua are under additional controls at the level of expression of its receptor on the surface of its target cells. PMID: 19116340 [PubMed - as supplied by publisher]
Nocturnal activation of Aurora C in rat pineal gland: its role in the norepinephrine-induced phosphorylation of histone H3 and gene expression.
Price DM, Kanyo R, Steinberg N, Chik CL, Ho AK Related Articles Nocturnal activation of Aurora C in rat pineal gland: its role in the norepinephrine-induced phosphorylation of histone H3 and gene expression. Endocrinology. 2008 Dec 30; Authors: Price DM, Kanyo R, Steinberg N, Chik CL, Ho AK We have shown previously that Ser10 phosphorylation of histone H3 occurs in rat pinealocytes following stimulation with norepinephrine (NE) and that histone modifications such as acetylation appear to play an important role in pineal gene transcription. Here we report the nocturnal phosphorylation of a Ser10 histone H3 kinase, Aurora C, in the rat pineal gland. The time profile of this phosphorylation parallels the increase in the level of phospho-Ser10 histone H3. Studies with cultured pinealocytes indicate that Aurora C phosphorylation is induced by NE and this induction can be blocked by co-treatment with propranolol or KT5720, a protein kinase A inhibitor. Moreover, only treatment with dibutyryl cAMP, but not other kinase activators, mimics the effect of NE on Aurora C phosphorylation. These results indicate that Aurora C is phosphorylated primarily by a beta-adrenergic/protein kinase A-mediated mechanism. Treatment with an Aurora C inhibitor reduces the NE-induced histone H3 phosphorylation, and suppresses the NE-stimulated induction of arylalkylamine N-acetyltransferase (AA-NAT), the rhythm-controlling enzyme of melatonin synthesis, and melatonin production. The effects of Aurora C inhibitors on adrenergic-induced genes in rat pinealocytes are gene-specific: inhibitory for Aa-nat and inducible cAMP repressor but stimulatory for c-fos. Together, our results support a role for the NE-stimulated phosphorylation of Aurora C and the subsequent remodelling of chromatin in NE-stimulated Aa-nat transcription. This phenomenon suggests that activation of this mitotic kinase can be induced by extracellular signals to participate in the transcriptional induction of a subset of genes in the rat pineal gland. PMID: 19116339 [PubMed - as supplied by publisher]
Epidermal Growth Factor Receptor Pathway Substrate 8 (Eps8) Is Overexpressed in Human Pituitary Tumors: Role in Proliferation and Survival.
Xu M, Shorts-Cary L, Knox AJ, Kleinsmidt-Demasters B, Lillehei K, Wierman ME Related Articles Epidermal Growth Factor Receptor Pathway Substrate 8 (Eps8) Is Overexpressed in Human Pituitary Tumors: Role in Proliferation and Survival. Endocrinology. 2008 Dec 30; Authors: Xu M, Shorts-Cary L, Knox AJ, Kleinsmidt-Demasters B, Lillehei K, Wierman ME Based on prior work showing that human pituitary tumors overexpress epidermal and fibroblast growth factor receptors, we hypothesized that downstream components of growth factor signaling pathways may also be dysregulated. Epidermal growth factor pathway substrate number 8 (Eps8) was identified as a transcript overexpressed (5.9 fold) in human pituitary tumors compared to normal pituitary by DNA microarrays. Eps8 mRNA upregulation was confirmed by semi-quantitative RT-PCR. Immunoblot analysis showed that Eps8 protein levels and its downstream target phosphorylated ERK were also upregulated in human pituitary tumors. Stable overexpression of Eps8 in LbetaT2 gonadotrope pituitary cells augmented colony formation in soft agar at day 21. Eps8 cells proliferated more robustly compared to controls in growth factor replete as well as growth restricted conditions. In addition, the Eps8 overexpressing cells were protected from serum withdrawal induced apoptosis compared to controls as assessed by caspase 3 cleavage. Epidermal growth factor (EGF) activated a robust amplification of ERK and modest upregulation of Akt in Eps8 overexpressing pituitary cells compared to vector controls. MEK inhibition or silencing of Eps8 blunted the proliferation of the cells in response to growth factor stimulation. Blockade of the PI3K pathway or silencing of Eps8 resulted in a loss of the Eps8 protection from growth factor withdrawal induced apoptosis. Together these data support a role of Eps8 in amplifying growth factor receptor signaling in human pituitary tumors to promote proliferation and cell survival. PMID: 19116338 [PubMed - as supplied by publisher]

PubMed: 0804-4643

Supplementation with cholecalciferol does not result in weight reduction in overweight and obese subjects.
Sneve M, Figenschau Y, Jorde R Related Articles Supplementation with cholecalciferol does not result in weight reduction in overweight and obese subjects. Eur J Endocrinol. 2008 Dec;159(6):675-84 Authors: Sneve M, Figenschau Y, Jorde R OBJECTIVE: Investigate whether cholecalciferol supplementation leads to weight loss in overweight and obese adults. DESIGN: Randomized double blind clinical trial with 20,000 IU cholecalciferol twice a week, or 20,000 IU once a week plus placebo, or placebo twice a week, for 12 months. All subjects were given 500 mg calcium supplementation. METHODS: Four hundred and forty five healthy, overweight, and obese men and women (age 21-70 years, body mass index (BMI) 28.0-47.0 kg/m(2)). Body weight, fatness, and fat distribution parameters were measured by dual-energy X-ray absorptiometry and anthropometry, blood samples and 24-h urinary samples were collected. RESULTS: At baseline, there were no significant differences between the groups, but there was a significant inverse relation between serum 25-hydroxyvitamin D (25(OH)D) levels and BMI, and a significant positive association between calorie intake and BMI. Three hundred and thirty four subjects completed the study. During the study, there was no significant change in weight, waist-to-hip ratio (WHR) or percentage body fat in any of the groups, nor between them. Parathyroid hormone decreased and 25(OH)D increased significantly in both groups receiving cholecalciferol, and serum levels of 25(OH)D stabilized after 3 months. Serum calcium was unchanged in all groups. Urinary calcium excretion increased in all groups, but there was no significant difference between the groups. Weekly dosage of 20,000-40,000 IU cholecalciferol for 12 months was associated with a low risk of adverse effects, at least in overweight and obese adults living at latitude 70 degrees N. CONCLUSION: Significant weight reduction in overweight and obese subjects is unlikely to occur with cholecalciferol supplementation. PMID: 19056900 [PubMed - indexed for MEDLINE]
Decreased lipin 1 beta expression in visceral adipose tissue is associated with insulin resistance in polycystic ovary syndrome.
Mlinar B, Pfeifer M, Vrtacnik-Bokal E, Jensterle M, Marc J Related Articles Decreased lipin 1 beta expression in visceral adipose tissue is associated with insulin resistance in polycystic ovary syndrome. Eur J Endocrinol. 2008 Dec;159(6):833-9 Authors: Mlinar B, Pfeifer M, Vrtacnik-Bokal E, Jensterle M, Marc J OBJECTIVE: In polycystic ovary syndrome (PCOS), insulin resistance (IR) appears with high prevalence and represents the major cause of cardiometabolic complications. Lipin 1beta regulates lipid metabolism and augments insulin sensitivity. The impact of lipin 1beta expression in visceral and subcutaneous adipose tissue of PCOS patients on IR was studied for the first time. METHODS: Eighty-five PCOS patients and 44 controls were enrolled for subcutaneous tissue biopsy, of whom 25 patients and 30 controls also underwent visceral adipose tissue biopsy. Gene expression of lipin 1beta was measured, together with that of peroxisome proliferator-activated receptor gamma, lipoprotein lipase, hormone-sensitive lipase, adiponectin and glucose transporter 4 in subcutaneous and visceral adipose tissue. Markers of obesity, IR and PCOS were also measured. RESULTS: In PCOS patients, lipin 1beta expression in both adipose depots was lower than in controls: 0.76 (0.67-0.84) vs 1.16 (0.90-1.43) for visceral and 0.91 (0.73-1.10) vs 1.30 (1.03-1.57) for s.c. depot (both P<10(-4)). The difference remained significant after adjustment for body mass index (BMI) and also when comparing only lean patients with lean controls. In PCOS patients, visceral adipose lipin 1beta expression correlated negatively with homeostasis model assessment-IR (r=-0.474, P=0.017), BMI (r=-0.511, P=0.009) and waist circumference (r=-0.473, P=0.017), waist circumference remaining significant (P=0.027) in multiple regression. Subcutaneous lipin 1beta expression in PCOS correlated negatively with BMI, waist circumference and plasma triglycerides, and positively with high density lipoprotein-cholesterol. Subcutaneous, but not visceral lipin 1beta expression, correlated positively with the studied genes. CONCLUSIONS: Lipin 1beta appears to be involved in the pathogenesis of IR in PCOS. PMID: 18829900 [PubMed - indexed for MEDLINE]
The appearance of the adrenal glands on computed tomography in multiple endocrine neoplasia type 1.
Whitley SA, Moyes VJ, Park KM, Brooke AM, Grossman AB, Chew SL, Rockall AG, Monson JP, Reznek RH Related Articles The appearance of the adrenal glands on computed tomography in multiple endocrine neoplasia type 1. Eur J Endocrinol. 2008 Dec;159(6):819-24 Authors: Whitley SA, Moyes VJ, Park KM, Brooke AM, Grossman AB, Chew SL, Rockall AG, Monson JP, Reznek RH AIMS: To review the morphology of the adrenal glands in multiple endocrine neoplasia type 1 (MEN1) on computed tomography (CT) to compare the results with established normal values for adrenal size and nodularity and to correlate adrenal size with serum cortisol secretory dynamics. MATERIALS AND METHODS: Two observers independently reviewed the adrenal CT in 28 patients with MEN1, measuring the maximum width of the body of the gland and the medial and lateral limbs. Incidence and location of nodules >5 mm within the gland were recorded. Following exclusion of known cases of Cushing's syndrome, adrenal gland size was compared with previously documented normative data. Adrenal gland size was compared between patients with normal and abnormal cortisol dynamics. RESULTS: Comparison of mean adrenal size in MEN1 patients with normative data showed that the adrenal limbs were significantly larger in MEN1 than normal (P<0.0001 in all four limbs). Adrenal body was also significantly larger (P<0.05). Nodules were demonstrated in 17 (60%) of patients (versus 0.4-2% in the normal population). No statistically significant correlation was demonstrated between adrenal limb hyperplasia and abnormal cortisol dynamics. CONCLUSIONS: In patients with MEN1, adrenal limb hyperplasia and adrenal nodules are significantly more common than in the normal population, a phenomenon not previously documented in a quantitative manner. There was no significant correlation between adrenal limb hyperplasia and abnormal cortisol dynamics. PMID: 18827064 [PubMed - indexed for MEDLINE]
Hyperleptinaemia rather than fasting hyperinsulinaemia is associated with obesity following hypothalamic damage in children.
Shaikh MG, Grundy RG, Kirk JM Related Articles Hyperleptinaemia rather than fasting hyperinsulinaemia is associated with obesity following hypothalamic damage in children. Eur J Endocrinol. 2008 Dec;159(6):791-7 Authors: Shaikh MG, Grundy RG, Kirk JM BACKGROUND: Obesity following hypothalamic damage is often severe and resistant to lifestyle changes. Disruption of hypothalamic feedback mechanisms that maintain energy homeostasis may be responsible for this intractable obesity. Adipocytokines including insulin and leptin are also known to be important regulators of appetite and weight. OBJECTIVE: To investigate the role of insulin, leptin, adiponectin and resistin in the aetiology of hypothalamic obesity (HO). DESIGN: This was a cross-sectional study of three groups of children, those with HO, congenital hypopituitarism (CH) and simple obesity (SO). RESULTS: A total of 69 children (HO=28, CH=18, SO=23) had leptin, resistin, adiponectin and insulin measured. Although fasting hyperinsulinaemia and insulin resistance were demonstrated, no differences in insulin or insulin resistance were seen between the groups. The HO group, however, had higher levels of leptin, adiponectin and resistin, which persisted even after adjusting for fat mass, compared with the other groups (P<0.05). CONCLUSION: No differences in fasting hyperinsulinaemia or insulin resistance were seen between the groups; however, leptin levels are elevated, even after adjusting for fat mass, suggesting that an element of leptin resistance is associated with HO. This is consistent with the inability of leptin to act on the hypothalamus, either due to transport across the blood-brain barrier or dysfunctional receptors. The lack of response to leptin may be more important in the development of obesity in these individuals, and the fasting hyperinsulinaemia is a result of the increased adipose tissue rather than the cause of the weight gain. PMID: 18819946 [PubMed - indexed for MEDLINE]
Mortality from thyroid cancer in patients with hyperthyroidism: the Theagenion Cancer Hospital experience.
Pazaitou-Panayiotou K, Perros P, Boudina M, Siardos G, Drimonitis A, Patakiouta F, Vainas I Related Articles Mortality from thyroid cancer in patients with hyperthyroidism: the Theagenion Cancer Hospital experience. Eur J Endocrinol. 2008 Dec;159(6):799-803 Authors: Pazaitou-Panayiotou K, Perros P, Boudina M, Siardos G, Drimonitis A, Patakiouta F, Vainas I BACKGROUND: Thyroid carcinoma has been reported in patients operated for different types of hyperthyroidism and the probability of a hot nodule being malignant seems to be low. The aim of the present study was to explore the relationship between thyroid cancer, hyperthyroidism and outcome in a large cohort of patients who presented to a tertiary cancer centre in Northern Greece. PATIENTS: Among 720 patients treated for thyroid cancer, 60 had a concomitant diagnosis of hyperthyroidism due to Graves' disease (n=14), solitary autonomous adenoma (n=17), or multinodular goiter (n=29). Adverse prognostic factors were common in patients with a previous history of hyperthyroidism at the time of diagnosis of thyroid cancer, including cases where the cancer was discovered coincidentally after thyroid surgery for hyperthyroidism and cases where tumor size was more than 10 mm. RESULTS: In 10 out of 17 patients with hyperthyroidism due to solitary autonomous adenomas, the tumor was located within the hot nodule and two of these patients developed local and distant metastases and died from the disease 4 and 15 years after thyroidectomy. CONCLUSION: Clinicians managing patients with hyperthyroidism need to be aware of the possible increased risk of thyroid cancer in this patient group. PMID: 18819945 [PubMed - indexed for MEDLINE]
Impaired subjective health status in chronic adrenal insufficiency: impact of different glucocorticoid replacement regimens.
Bleicken B, Hahner S, Loeffler M, Ventz M, Allolio B, Quinkler M Related Articles Impaired subjective health status in chronic adrenal insufficiency: impact of different glucocorticoid replacement regimens. Eur J Endocrinol. 2008 Dec;159(6):811-7 Authors: Bleicken B, Hahner S, Loeffler M, Ventz M, Allolio B, Quinkler M CONTEXT: Recent studies have suggested that current glucocorticoid replacement therapies fail to fully restore well-being in patients with adrenal insufficiency (AI). OBJECTIVE: To investigate the effect of different glucocorticoid preparations used for replacement therapy on subjective health status (SHS) in AI. DESIGN AND PATIENTS: In a cross-sectional study, primary and secondary AI patients were contacted by mail. Individual glucocorticoid replacement regimens, underlying diagnoses and comorbidities were verified by questionnaires and review of medical records. Patients were asked to complete three validated self-assessment questionnaires (Short Form 36 (SF-36), Giessen Complaint List (GBB-24), and Hospital Anxiety and Depression Scale). Results were compared with sex- and age-matched controls drawn from the questionnaire-specific reference cohort. RESULTS: Of the 883 patients identified, 526 agreed to participate in the study. Completed questionnaire sets were available from 427 patients (primary AI n=232; secondary AI n=195). AI patients showed significantly impaired SHS compared with controls irrespective of the glucocorticoid used for replacement. The only difference in SHS between patients on prednisolone (PR) and hydrocortisone (all patients and sub-analysis for primary AI) was significant higher bodily pain (lower Z-score in SF-36) in patients on PR (P<0.05, P<0.01 respectively). In patients with secondary AI, the PR group showed significantly (P<0.05) less heart complaints (lower Z-score) in the GBB questionnaire compared with the cortisone acetate group. CONCLUSIONS: Glucocorticoid replacement therapy with PR seems to be equivalent to hydrocortisone regarding SHS in patients with AI. However, SHS remains impaired in all patient groups suggesting a need for further improved glucocorticoid replacement strategies. PMID: 18819943 [PubMed - indexed for MEDLINE]

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