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Haijiang Wu, Xinna Deng, Yonghong Shi, Ye Su, Jinying Wei, and Huijun Duan

Hepatitis C virus infection and type 1 and type 2 diabetes mellitus . World Journal of Diabetes 5 586 – 600 . ( doi:10.4239/wjd.v5.i5.586 ) Aoi W Naito Y Yoshikawa T 2013 Role of oxidative stress in impaired insulin signaling associated

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PM Jehle, DR Jehle, S Mohan, and BO Bohm

Osteopenia has been ascribed to diabetics without residual insulin secretion and high insulin requirement. However, it is not known if this is partially due to disturbances in the IGF system, which is a key regulator of bone cell function. To address this question, we performed a cross-sectional study measuring serum levels of IGF-I, IGF-binding protein-1 (IGFBP-1), IGFBP-3, IGFBP-4 and IGFBP-5 by specific immunoassays in 52 adults with Type 1 (n=27) and Type 2 (n=25) diabetes mellitus and 100 age- and sex-matched healthy blood donors. In the diabetic patients, we further determined serum levels of proinsulin, intact parathyroid hormone (PTH), 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3 and several biochemical bone markers, including osteocalcin (OSC), bone alkaline phosphatase (B-ALP), carboxy-terminal propeptide of type I procollagen (PICP), and type I collagen cross-linked carboxy-terminal telopeptide (ICTP). Urinary albumin excretion was ascertained as a marker of diabetic nephropathy. Bone mineral density (BMD) of hip and lumbar spine was determined by dual-energy X-ray absorptiometry. Data are presented as means+/-s.e.m. Differences between the experimental groups were determined by performing a one-way analysis of variance (ANOVA), followed by Newman-Keuls test. Correlations between variables were assessed using univariate linear regression analysis and partial correlation analysis. Type 1 diabetics showed significantly lower IGF-I (119+/-8 ng/ml) and IGFBP-3 (2590+/-104 ng/ml) but higher IGFBP-1 levels (38+/-10 ng/ml) compared with Type 2 patients (170+/-13, 2910+/-118, 11+/-3 respectively; P<0.05) or healthy controls (169+/-5, 4620+/-192, 3.5+/-0.4 respectively; P<0.01). IGFBP-5 levels were markedly lower in both diabetic groups (Type 1, 228+/-9; Type 2, 242+/-11 ng/ml) than in controls (460+/-7 ng/ml,P<0. 01), whereas IGFBP-4 levels were similar in diabetics and controls. IGF-I correlated positively with IGFBP-3 and IGFBP-5 and negatively with IGFBP-1 and IGFBP-4 in all subjects. Type 1 patients showed a lower BMD of hip (83+/-2 %, Z-score) and lumbar spine (93+/-2 %) than Type 2 diabetics (93+/-5 %, 101+/-5 % respectively), reaching significance in the female subgroups (P<0.05). In Type 1 patients, BMD of hip correlated negatively with IGFBP-1 (r=-0.34, P<0.05) and IGFBP-4 (r=-0.3, P<0.05) but positively with IGFBP-5 (r=0.37, P<0. 05), which was independent of age, diabetes duration, height, weight and body mass index, as assessed by partial correlation analysis. Furthermore, biochemical markers indicating bone loss (ICTP) and increased bone turnover (PTH, OSC) correlated positively with IGFBP-1 and IGFBP-4 but negatively with IGF-I, IGFBP-3 and IGFBP-5, while the opposite was observed with bone formation markers (PICP, B-ALP) and vitamin D3 metabolites. In 20 Type 2 patients in whom immunoreactive proinsulin could be detected, significant positive correlations were found between proinsulin and BMD of hip (r=0.63, P<0.005), IGF-I (r=0.59, P<0.01) as well as IGFBP-3 (r=0.49, P<0.05). Type 1 and Type 2 patients with macroalbuminuria showed a lower BMD of hip, lower IGFBP-5 but higher IGFBP-4 levels, suggesting that diabetic nephropathy may contribute to bone loss by a disturbed IGF system. In conclusion, the findings of this study support the hypothesis that the imbalance between individual IGF system components and the lack of endogenous proinsulin may contribute to the lower BMD in Type 1 diabetics.

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Richard W Nelson and Claudia E Reusch

illustrates the similarities among dogs, cats, and humans. Type 1 diabetes mellitus: dogs The most common clinically recognized form of diabetes mellitus in the dog resembles type 1 diabetes mellitus in humans and is characterized by permanent hypoinsulinemia

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Yoko Yagishita, Akira Uruno, Dionysios V Chartoumpekis, Thomas W Kensler, and Masayuki Yamamoto

Introduction Type 1 diabetes is caused by destruction or dysfunction of insulin-producing pancreatic β-cells, and its incidence is increasing in the modern world ( Tuomilehto 2013 ). Protecting β-cells from inflammation and destruction is an

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Rosalia C M Simmen, Dustin M Brown, Charles M Quick, Iad Alhallak, Tyler Rose, Shi J Liu, and Angela S Kelley

Introduction Type 1 diabetes mellitus (T1DM) is an autoimmune disease, resulting from the destruction of insulin-producing β-cells of the pancreatic islets of Langerhans, which leads to a state of hypoinsulinemia and hyperglycemia. In 2015, 1

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Sachiko Kitanaka, Utako Sato, and Takashi Igarashi

. 2004 ). The molecular mechanism of diabetes mellitus by HNF-1α mutations in MODY3 has been attributed to the decreased transcription of genes including insulin, glucose transporter 2, and L-type pyruvate kinase ( Wang et al. 1998 , 2000 ). However

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Haiyong Chen, Hui-Yao Lan, Dimitrios H Roukos, and William C Cho

2013 ). DM is a complex disease characterized by high blood glucose levels. There are two major forms of diabetes. Type 1 diabetes (T1D) results from a lack of insulin production in pancreatic β-cells. T2D is due to resistance to insulin, resulting in

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L van Bloemendaal, J S ten Kulve, S E la Fleur, R G Ijzerman, and M Diamant

glargine, titrated QD +1.4 (0.2) –   Gallwitz et al . (2011) 363 26 T2DM Exenatide 10 μg BID −4.1 (0.2) <0.001 Insulin BIAsp 70/30, titrated +1.0 (0.2) – BIAsp, biphasic insulin aspart; BID, twice daily; NS, not significant; T2DM, type 2 diabetes mellitus

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Corinne A Schuyler, Nga N Ta, Yanchun Li, Maria F Lopes-Virella, and Yan Huang

of coronary atherosclerotic plaques . Lancet 2 941 – 944 doi:10.1016/S0140-6736(89)90953-7 . Soedamah-Muthu SS Stehouwer CD 2005 Cardiovascular disease morbidity and mortality in patients with type 1 diabetes mellitus: management

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Karen Oliva, Gillian Barker, Gregory E Rice, Mark J Bailey, and Martha Lappas

). Gestational diabetes mellitus (GDM), defined as any degree of glucose intolerance with onset or first recognition during pregnancy ( Kuhl 1998 ), affects up to 18% of all pregnancies ( Pregnancy 2010 ). Like type 2 diabetes, the prevalence rate of GDM has also