GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Serum Osteocalcin Level Is Associated with Glucose Metabolism and Atherosclerosis Parameters in Type 2 Diabetes Mellitus
    The Endocrine Society ; 2009
    In:  The Journal of Clinical Endocrinology & Metabolism Vol. 94, No. 1 ( 2009-01-01), p. 45-49
    Details
    In: The Journal of Clinical Endocrinology & Metabolism, The Endocrine Society, Vol. 94, No. 1 ( 2009-01-01), p. 45-49
    Type of Medium: Online Resource
    ISSN: 0021-972X , 1945-7197
    URL: Article
    DOI: 10.1210/jc.2008-1455
    RVK:
    XA 10000
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2009
    detail.hit.zdb_id: 2026217-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Adiponectin Is Associated with Changes in Bone Markers during Glycemic Control in Type 2 Diabetes Mellitus
    The Endocrine Society ; 2009
    In:  The Journal of Clinical Endocrinology & Metabolism Vol. 94, No. 8 ( 2009-08-01), p. 3031-3037
    Details
    In: The Journal of Clinical Endocrinology & Metabolism, The Endocrine Society, Vol. 94, No. 8 ( 2009-08-01), p. 3031-3037
    Abstract: Objective: Although several experiments show that adiponectin is associated with bone metabolism, a relationship between adiponectin and bone markers is still unclear. We monitored chronological changes in hyperglycemia, serum adiponectin, and bone markers during glycemic control in type 2 diabetes and analyzed relationships among these parameters. Subjects and Results: A total of 50 Japanese patients with poorly controlled type 2 diabetes [initial hemoglobin A1c (HbA1c) = 10.0 ± 2.5%] were recruited, and biochemical data were collected before and after glycemic control for a month. Of b one formation markers, bone-specific alkaline phosphatase was decreased with a mean change of −3.11 [95% confidence interval (CI), −5.03 to −1.20; P & lt; 0.01], whereas osteocalcin (OC) was increased with a mean change of 1.94 (95% CI, 1.45–2.42; P & lt; 0.001) and undercarboxylated OC (ucOC)/OC ratio was decreased with a mean change of −0.15 (95% CI, −0.27 to −0.03; P & lt; 0.01). Although adiponectin level was not significantly different before and after glycemic control, baseline adiponectin level, but not HbA1c, was positively correlated with changes in OC, ucOC, and urinary N-terminal cross-linked telopeptide of type I collagen (uNTX) (r = 0.30, P =0.04; r = 0.32, P = 0.03; and r = 0.36, P = 0.01, respectively). Changes in adiponectin were also negatively correlated with changes in OC and uNTX (r = −0.42, P & lt; 0.01; and r = −0.38, P & lt; 0.01, respectively). Changes in HbA1c were negatively correlated with changes in OC (r = −0.30, P = 0.03). Conclusion: These findings show that treatments for hyperglycemia enhance OC level and suggest that serum adiponectin level before starting to compensate poorly controlled diabetics could predict the subsequent improvement of bone remodeling markers during glycemic control.
    Type of Medium: Online Resource
    ISSN: 0021-972X , 1945-7197
    URL: Article
    DOI: 10.1210/jc.2008-2187
    RVK:
    XA 10000
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2009
    detail.hit.zdb_id: 2026217-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Menin Missense Mutants Encoded by the MEN1 Gene that Are Targeted to the Proteasome: Restoration of Expression and Activity by CHIP siRNA
    The Endocrine Society ; 2012
    In:  The Journal of Clinical Endocrinology & Metabolism Vol. 97, No. 2 ( 2012-02-01), p. E282-E291
    Details
    In: The Journal of Clinical Endocrinology & Metabolism, The Endocrine Society, Vol. 97, No. 2 ( 2012-02-01), p. E282-E291
    Abstract: In multiple endocrine neoplasia type 1 (MEN1) characterized by tumors of parathyroid, enteropancreas, and anterior pituitary, missense mutations in the MEN1 gene product, menin, occur in a subset of cases. The mutant proteins are degraded by the proteasome. However, whether their expression and activity can be restored is not known. Objective: Our objective was to functionally characterize a panel of 16 menin missense mutants, including W423R and S443Y identified in new MEN1 families, with respect to protein stability, targeting to the proteasome and restoration of expression by proteasome inhibitors and expression and function by small interfering RNA technology. Methods: Flag-tagged wild-type (WT) and missense menin mutant expression vectors were transiently transfected in human embryonic kidney (HEK293) and/or rat insulinoma (Rin-5F) cells. Results: The majority of mutants were short-lived, whereas WT menin was stable. Proteasome inhibitors MG132 and PS-341 and inhibition of the chaperone, heat-shock protein 70 (Hsp70), or the ubiquitin ligase, COOH terminus of Hsp70-interacting protein (CHIP), by specific small interfering RNA, restored the levels of the mutants, whereas that of WT menin was largely unaffected. Inhibition of CHIP restored the ability of mutants to mediate normal functions of menin: TGF-β up-regulation of the promoters of its target genes, the cyclin-dependent kinase inhibitors p15 and p21 as well as TGF-β inhibition of cell numbers. Conclusion: When the levels of missense menin mutants that are targeted to the proteasome are normalized they may function similarly to WT menin. Potentially, targeting specific components of the proteasome chaperone pathway could be beneficial in treating a subset of MEN1 cases.
    Type of Medium: Online Resource
    ISSN: 0021-972X , 1945-7197
    URL: Article
    DOI: 10.1210/jc.2011-0241
    RVK:
    XA 10000
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2012
    detail.hit.zdb_id: 2026217-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Advanced Glycation End Product 3 (AGE3) Suppresses the Mineralization of Mouse Stromal ST2 Cells and Human Mesenchymal Stem Cells by Increasing TGF-β Expression and Secretion
    The Endocrine Society ; 2014
    In:  Endocrinology Vol. 155, No. 7 ( 2014-07-01), p. 2402-2410
    Details
    In: Endocrinology, The Endocrine Society, Vol. 155, No. 7 ( 2014-07-01), p. 2402-2410
    Abstract: In diabetic patients, advanced glycation end products (AGEs) cause bone fragility because of deterioration of bone quality. We previously showed that AGEs suppressed the mineralization of mouse stromal ST2 cells. TGF-β is abundant in bone, and enhancement of its signal causes bone quality deterioration. However, whether TGF-β signaling is involved in the AGE-induced suppression of mineralization during the osteoblast lineage remains unknown. We therefore examined the roles of TGF-β in the AGE-induced suppression of mineralization of ST2 cells and human mesenchymal stem cells. AGE3 significantly (P & lt; .001) inhibited mineralization in both cell types, whereas transfection with small interfering RNA for the receptor for AGEs (RAGEs) significantly (P & lt; .05) recovered this process in ST2 cells. AGE3 increased (P & lt; .001) the expression of TGF-β mRNA and protein, which was partially antagonized by transfection with RAGE small interfering RNA. Treatment with a TGF-β type I receptor kinase inhibitor, SD208, recovered AGE3-induced decreases in osterix (P & lt; .001) and osteocalcin (P & lt; .05) and antagonized the AGE3-induced increase in Runx2 mRNA expression in ST2 cells (P & lt; .001). Moreover, SD208 completely and dose dependently rescued AGE3-induced suppression of mineralization in both cell types. In contrast, SD208 intensified AGE3-induced suppression of cell proliferation as well as AGE3-induced apoptosis in proliferating ST2 cells. These findings indicate that, after cells become confluent, AGE3 partially inhibits the differentiation and mineralization of osteoblastic cells by binding to RAGE and increasing TGF-β expression and secretion. They also suggest that TGF-β adversely affects bone quality not only in primary osteoporosis but also in diabetes-related bone disorder.
    Type of Medium: Online Resource
    ISSN: 0013-7227 , 1945-7170
    URL: Article
    DOI: 10.1210/en.2013-1818
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2014
    detail.hit.zdb_id: 2011695-0
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Osteoblast AMP-Activated Protein Kinase Regulates Postnatal Skeletal Development in Male Mice
    The Endocrine Society ; 2018
    In:  Endocrinology Vol. 159, No. 2 ( 2018-02-01), p. 597-608
    Details
    In: Endocrinology, The Endocrine Society, Vol. 159, No. 2 ( 2018-02-01), p. 597-608
    Abstract: Studies have shown that AMP-activated protein kinase (AMPK), a crucial regulator of energy homeostasis, plays important roles in osteoblast differentiation and mineralization. However, little is known about in vivo roles of osteoblastic AMPK in bone development. Thus, to investigate in vivo roles of osteoblast AMPK, we conditionally inactivated Ampk in osterix (Osx)–expressing cells by crossing Osx-Cre mice with floxed AMPKα1 to generate mice lacking AMPKα1 in osteoblasts (Ampk−/− mice). Compared with wild-type and Ampk+/− mice, Ampk−/− mice displayed retardation of postnatal bone development, although bone deformity was not observed at birth. Microcomputed tomography showed significant reductions in trabecular bone volume, cortical bone length, and density, as well as increased cortical porosity in femur as well as development defects of skull in 8-week-old Ampk−/− mice. Surprisingly, histomorphometric analysis demonstrated that the number of osteoclasts was significantly increased, although bone formation rate was not altered. Loss of trabecular network connections and mass, as well as shortened growth plates and reduced thickness of cartilage adjacent to the growth plate, was observed in Ampk−/− mice. In primary cultured osteoblasts from calvaria, the expressions of alkaline phosphatase, type 1 collagen, osteocalcin, bone morphogenetic protein 2, Runx2, and osterix were significantly inhibited in Ampk−/− osteoblasts, whereas the expression of receptor activator of nuclear κB ligand (RANKL) and the RANKL/osteoprotegerin ratio were significantly increased. These findings indicate that osteoblastic AMPK plays important roles in bone development in vivo and that deletion of AMPK in osteoblasts decreases osteoblastic differentiation and enhances bone turnover by increasing RANKL expression.
    Type of Medium: Online Resource
    ISSN: 1945-7170
    URL: Article
    DOI: 10.1210/en.2017-00357
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2018
    detail.hit.zdb_id: 2011695-0
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...