Serum DHEA-S Level Is Associated with the Presence of Atherosclerosis in Postmenopausal Women with Type 2 Diabetes Mellitus

Kanazawa, Ippei; Yamaguchi, Toru; Yamamoto, Masahiro; Yamauchi, Mika; Kurioka, Soichi; Yano, Shozo; Sugimoto, Toshitsugu

doi:10.1507/endocrj.k07e-130

Cited by 30 publications

(23 citation statements)

References 49 publications

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“…On the other hand, AMPK phosphorylation occurred upon treatment with PDGF, a potent mitogen (Figs 2 and 3), which suggests that AMPK activation may not be strictly associated with growth inhibition. Although these data do not agree with the concept that AMPK has anti-proliferative activity (Motoshima et al 2006), two recent reports have shown that AMPK promotes the proliferation of osteoblastic cells and fibroblasts (Hattori et al 2006, Kanazawa et al 2008. In agreement with these findings, inhibition of AMPK blocked SMC proliferation in response to both PDGF and adiponectin, which thus implies that AMPK likely has a role in SMC proliferation.…”

Section: Discussioncontrasting

confidence: 53%

Inhibition of smooth muscle cell proliferation by adiponectin requires proteolytic conversion to its globular form

Fuerst¹,

Taylor²,

Wright³

et al. 2012

Journal of Endocrinology

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Accelerated atherosclerosis is the primary cardiovascular manifestation of diabetes and correlates inversely with levels of circulating adiponectin, an anti-atherosclerotic adipokine that declines in diabetes. We therefore initiated a study to examine the mechanisms by which adiponectin, a hormone released from adipose tissue, influences the proliferation of vascular smooth muscle cells (SMCs). Addition of adiponectin to quiescent porcine coronary artery SMCs increased both protein and DNA synthesis and concurrently activated ERK1/2 and Akt. By contrast, globular adiponectin, a truncated form of this protein, exhibited anti-mitogenic properties as indicated by the inhibition of protein and DNA synthesis in SMCs stimulated with platelet-derived growth factor (PDGF). Whereas globular adiponectin did not stimulate growth-related signal transduction pathways, it was able to block the PDGF-dependent phosphorylation of eukaryotic elongation factor 2 kinase, a regulator of protein synthesis. Proteolysis of adiponectin with trypsin, which produces globular adiponectin, reversed the growth-stimulating actions of the undigested protein. As the existence of globular adiponectin remains controversial, western blotting was used to establish its presence in rat serum. We found that globular adiponectin was detectable in rat serum, but this result was not obtained with all antibodies. The contrasting properties of adiponectin and its globular form with respect to SMC proliferation suggest that protection against atherosclerosis may therefore be mediated, in part, by the level of globular adiponectin.

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Section: Discussioncontrasting

confidence: 53%

Inhibition of smooth muscle cell proliferation by adiponectin requires proteolytic conversion to its globular form

Fuerst¹,

Taylor²,

Wright³

et al. 2012

Journal of Endocrinology

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“…Osteocalcin was found to be inversely associated with fasting plasma glucose (FPG) [7,9,10] , HbA1c [7,12] , body mass index (BMI) [10,13] , fat mass [10] , measures of insulin resistance [8,14] , and measures of lipid metabolism [12,15] . In these same studies, osteocalcin was positively associated with adiponectin [11] and measures of insulin sensitivity [7,15] . Among these studies, the positive relationship between osteocalcin and markers of metabolic phenotype were revealed mostly in the elderly population or subjects with diabetes mellitus.…”

Section: Introductionmentioning

confidence: 78%

“…A number of studies have evaluated the complex interactions between the skeleton and glucose and energy homeostasis in humans [7][8][9][10][11][12][13][14][15] . Osteocalcin was found to be inversely associated with fasting plasma glucose (FPG) [7,9,10] , HbA1c [7,12] , body mass index (BMI) [10,13] , fat mass [10] , measures of insulin resistance [8,14] , and measures of lipid metabolism [12,15] .…”

Section: Introductionmentioning

confidence: 99%

Serum osteocalcin levels are inversely associated with plasma glucose and body mass index in healthy Chinese women

et al. 2014

Acta Pharmacol Sin

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Aim: Osteocalcin, a biochemical marker of bone formation, has been suggested to be involved in the regulation of energy metabolism. The aim of this study was to investigate the possible association between serum osteocalcin and markers of glucose and lipid metabolism in a large sample of healthy Chinese women. Methods: A total of 2032 healthy Chinese women in Shanghai, aged 20-94 (including 1396 discovery-study subjects and 636 postmenopausal women for a reduplication analysis) were recruited. Their serum osteocalcin, calcium and the relevant measurements were analyzed. A Spearman correlation analysis was performed between osteocalcin and the other markers of energy metabolism including triglyceride, total cholesterol, fasting plasma glucose (FPG), serum insulin, body mass index and homeostasis model assessment-insulin resistance. Separate multiple regression analyses were performed with data from the discovery and reduplication subjects to determine whether serum osteocalcin concentration was an independent predictor of the glucose or lipid metabolism markers. Results: For the discovery-study subjects, serum osteocalcin was found to be negatively associated with weight (r=-0.08, P=0.002), BMI (r=-0.13, P<0.001) and FPG (r=-0.13, P=0.001). Similar results were also found in the reduplication subjects P=0.016; P=0.003; P<0.001). In the multiple regression analysis, serum osteocalcin was revealed as a potential independent predictor for FPG (β=-0.07 and -0.210 for discovery and reduplication, respectively, P<0.01) and BMI (β=-0.127 and -0.299 for discovery and reduplication, respectively, P<0.01). Conclusion: Serum osteocalcin is negatively associated with weight BMI and FPG in healthy Chinese women. Therefore, osteocalcin might contribute to obesity and diabetes.

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“…AMPK is well known as a key sensor of changes in cellular energy homeostasis such as lipid synthesis (Rutter & Leclerc 2009). With regard to bone metabolism, it has been shown that AMPK stimulates bone formation and mineralization (Kanazawa et al 2008, Shah et al 2010. It has recently been shown that AMPK stimulates osteoblast differentiation via induction of RUNX2 expression (Jang et al 2011).…”

Section: Discussionmentioning

confidence: 99%

Involvement of AMP-activated protein kinase in thrombin-stimulated interleukin 6 synthesis in osteoblasts

Tokuda¹,

Kato²,

Natsume³

et al. 2012

Journal of Molecular Endocrinology

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We previously demonstrated that thrombin stimulates synthesis of interleukin 6 (IL6), a potent bone resorptive agent, in part via p44/p42 MAP kinase and p38 MAP kinase but not through stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) among the MAP kinase superfamily in osteoblast-like MC3T3-E1 cells. In this study, we investigated the involvement of AMP-activated protein kinase (AMPK), a regulator of energy metabolism, in thrombin-stimulated IL6 synthesis in MC3T3-E1 cells. The phosphorylation of p44/p42 MAP kinase, p38 MAP kinase, SAPK/JNK, or AMPK was determined by western blot analysis. The release of IL6 was determined by the measurement of IL6 concentration in the conditioned medium using an ELISA kit. The expression of IL6 mRNA was determined by RT-PCR. Thrombin time dependently induced the phosphorylation of AMPK a-subunit (Thr-172). Compound C, an inhibitor of AMPK, dosedependently suppressed the thrombin-stimulated IL6 release in the range between 0 . 3 and 10 mM. Compound C reduced thrombin-induced acetyl-CoA carboxylase phosphorylation. The IL6 mRNA expression induced by thrombin was markedly reduced by compound C. Downregulation of AMPK by siRNA suppressed the thrombin-stimulated IL6 release. The thrombin-induced phosphorylation of p44/p42 MAP kinase and p38 MAP kinase was inhibited by compound C, which failed to affect SAPK/JNK phosphorylation. These results strongly suggest that AMPK regulates thrombin-stimulated IL6 synthesis via p44/p42 MAP kinase and p38 MAP kinase in osteoblasts.

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Serum DHEA-S Level Is Associated with the Presence of Atherosclerosis in Postmenopausal Women with Type 2 Diabetes Mellitus

Cited by 30 publications

References 49 publications

Inhibition of smooth muscle cell proliferation by adiponectin requires proteolytic conversion to its globular form

Inhibition of smooth muscle cell proliferation by adiponectin requires proteolytic conversion to its globular form

Serum osteocalcin levels are inversely associated with plasma glucose and body mass index in healthy Chinese women

Involvement of AMP-activated protein kinase in thrombin-stimulated interleukin 6 synthesis in osteoblasts

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