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      Influence of Apelin-13 on osteoporosis in Type-2 diabetes mellitus: A clinical study

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          Abstract

          Objective:

          To investigate the relationship between serum level of Apelin-13 and bone mineral density (BMD) as well as other parameters, and determine the influence of Apelin-13 on osteoporosis in patients with Type-2 diabetes mellitus.

          Methods:

          Seventy-six patients with Type-2 diabetes mellitus were recruited from Department of Endocrinology of our hospital between January 2013 and July2017. The clinical data, including age, gender, height, weight, body mass index (BMI) and disease duration were recorded for all patients. Blood sample was collected for measurement of Apelin-13, Procollagen type-I N propeptide (PINP) and Cross-linked carboxy terminal telopeptide of type-I collagen (ICTP), and BMD was tested with a dual-energy X-ray absorptiometry scanner.

          Results:

          The patients were divided into three groups, in which 19 patients were assigned in osteoporosis group, 25 in osteopenia group and 32 in normal group. The level of Apelin-13 in osteoporosis group was significantly lower than that in osteopenia and normal groups (p<0.05), and the value in osteopenia group was significant lower than that in normal group (p<0.05). Correlation analysis showed in the included patients the level of Apelin-13 was positively correlated to the value of BMD and PINP (p<0.05), but negatively correlated to age and ICTP (p<0.05).

          Conclusion:

          In conclusion, this study demonstrated that there was a close relationship among Apelin-13, BMD, ICTP and PINP, and Apelin-13 plays an important role in the occurrence of osteoporosis in patients with Type-2 diabetes mellitus.

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          Most cited references16

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          Mechanisms of diabetes mellitus-induced bone fragility

          Diabetes mellitus is associated with an increased risk of fragility fractures. Here, Napoli and colleagues discuss the complex interactions between glucose homeostasis and bone fragility, the epidemiology of fractures in patients with diabetes mellitus and the effects of antidiabetic drugs on bone health.
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            PINP as a biological response marker during teriparatide treatment for osteoporosis

            Postmenopausal women with severe osteoporosis may require treatment with the bone anabolic drug teriparatide. While changes in bone mineral density (BMD) are one measure of response, BMD changes often require a minimum of one year to observe measureable changes. Biochemical markers of bone turnover change within 1 to 3 months of initiating osteoporosis therapy. Monitoring with a marker such as procollagen type I N propeptide (PINP), an osteoblast-derived protein, during teriparatide treatment may provide clinically useful information for managing patients with osteoporosis. Clinical trials have shown consistent increases in PINP within 3 months of initiating teriparatide, increases that are significantly greater than placebo and significantly different from baseline. Increases in PINP concentrations during teriparatide treatment correlate well with increases in skeletal activity assessed by radioisotope bone scans and quantitative bone histomorphometry parameters. Individuals treated with teriparatide in clinical trials usually experienced an increase in PINP > 10 mcg/L from baseline, while those given placebo usually did not. In the clinical setting, patients experiencing a significant increase in PINP > 10 mcg/L after initiating teriparatide therapy may receive an earlier confirmation of anabolic effect, while those who do not may be assessed for adherence, proper injection technique, or undetected secondary conditions that might mitigate an anabolic response. PINP monitoring may provide information supplemental to BMD monitoring and be a useful aid in managing patients receiving anabolic osteoporosis treatment in the same way that biochemical markers of bone resorption are useful in monitoring antiresorptive therapy. This review examines PINP as a biological response marker during teriparatide treatment for osteoporosis.
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              Apelin inhibits the development of diabetic nephropathy by regulating histone acetylation in Akita mouse.

              Diabetic nephropathy is the primary cause of end-stage renal disease. Increasing numbers of patients are suffering from this disease and therefore novel medications and therapeutic approaches are urgently needed. Here, we investigated whether apelin-13, the most active member of the adipokine apelin group, could effectively suppress the development of nephropathy in Akita mouse, a spontaneous type 1 diabetic model. Apelin-13 treatment decreased diabetes-induced glomerular filtration rate, proteinuria, glomerular hypertrophy, mesangial expansion and renal inflammation. The inflammatory factors, activation of NF-κB, histone acetylation and the enzymes involved in histone acetylation were further examined in diabetic kidneys and high glucose- or sodium butyrate-treated mesangial cells in the presence or absence of apelin-13. Apelin-13 treatment inhibited diabetes-, high glucose- and NaB-induced elevation of inflammatory factors, and histone hyperacetylation by upregulation of histone deacetylase 1. Furthermore, overexpression of apelin in mesangial cells induced histone deacetylation under high glucose condition. Thus, apelin-13 may be a novel therapeutic candidate for treatment of diabetic nephropathy via regulation of histone acetylation.
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                Author and article information

                Journal
                Pak J Med Sci
                Pak J Med Sci
                Pakistan Journal of Medical Sciences
                Professional Medical Publications (Pakistan )
                1682-024X
                1681-715X
                Jan-Feb 2018
                : 34
                : 1
                : 159-163
                Affiliations
                [1 ]Supin Liu, Blood Collection Centre, The Centre Hospital of Cangzhou, Cangzhou City, Hebei Province, China
                [2 ]Wenlong Wang, Department of Clinical Laboratory, The Centre Hospital of Cangzhou, Cangzhou City, Hebei Province, China
                [3 ]Linlin Yin, Department of Clinical Laboratory, The Centre Hospital of Cangzhou, Cangzhou City, Hebei Province, China
                [4 ]Yitang Zhu, Department of Clinical Laboratory, The Centre Hospital of Cangzhou, Cangzhou City, Hebei Province, China
                Author notes
                Correspondence: Supin Liu, Blood Collection Centre, The centre hospital of Cangzhou, 16 Xinhuaxiroad, Cangzhou City, Hebei Province, 061001, China. Email: cl2778@ 123456126.com
                Article
                PJMS-34-159
                10.12669/pjms.341.14135
                5857004
                4fcd36de-4bb7-4e07-ab43-669f646bdb05
                Copyright: © Pakistan Journal of Medical Sciences

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 31 October 2017
                : 10 January 2018
                : 14 January 2018
                Categories
                Original Article

                apelin-13,bone mineral density (bmd),osteoporosis,type-2 diabetes mellitus

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