Background: Mean platelet volume (MPV) is associated with cardiovascular morbidity and mortality in type 2 diabetic patients. However, the effects of blood glucose regulation and treatment regime on MPV has not been adequately studied in type 2 diabetic patients. Aims: We studied the effects of blood glucose regulation and treatment regimen on mean platelet volume in Type 2 diabetic patients.
Subjects And Methods: A total of 232 diabetic patients who were admitted to the hospital in short intervals of 3 months in the last 2 years were included in the study. When the second admission HbA was greater than the first admission HbA, they were classified as being in the deteriorated blood glucose regulation group, otherwise they were classified in the improved blood glucose regulation group. Also, the deteriorated and improved blood glucose regulation groups were classified based on therapy modalities as the sulfonylurea + metformin group and the insulin + metformin group. Paired t-test was used for comparison of the groups.
Results: Of the 232 patients, 98 (42.2%) were male and 134 (57.8%) were female. There were 126 (55.2%) patients using sulfonylurea + metformin, while 106 (44.8%) patients were using insulin + metformin. MPV levels were significantly increased in patients with deteriorating glucose regulation (p = 0.003). This increase in MPV was only seen in the oral hypoglycemic treatment group (p = 0.003).
Conclusions: Our results suggested a close relationship between poor glycemic control and increased platelet activity in type 2 diabetic patients with oral antidiabetic therapy when compared to the insulin and metformin therapy modality.
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http://dx.doi.org/10.4103/njcp.njcp_477_19 | DOI Listing |
Open Med (Wars)
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Department of Obstetrical, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang Street, Ouhai District, Wenzhou, Zhejiang, 325000, China.
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Research Center, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, China.
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View Article and Find Full Text PDFJ Exp Zool B Mol Dev Evol
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Department for Integrative Evolutionary Biology, Max-Planck Institute for Biology Tübingen, Tübingen, Germany.
Developmental plasticity, the ability of a genotype to produce different phenotypes in response to environmental conditions, has been subject to intense studies in the last four decades. The self-fertilising nematode Pristionchus pacificus has been developed as a genetic model system for studying developmental plasticity due to its mouth-form polyphenism that results in alternative feeding strategies with a facultative predatory and non-predatory mouth form. Many studies linked molecular aspects of the regulation of mouth-form polyphenism with investigations of its evolutionary and ecological significance.
View Article and Find Full Text PDFSci China Life Sci
January 2025
CAS Engineering Laboratory for Nanozyme, Key Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.
Alternative treatment for the highly prevalent Helicobacter pylori infection is imperative due to rising antibiotic resistance. We unexpectedly discovered that the anti-H. pylori component in garlic is hydrogen polysulfide (HS, n⩾2), not organic polysulfides.
View Article and Find Full Text PDFJ Pharmacokinet Pharmacodyn
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Department of Clinical Pharmacy and Pharmacy Administration, West China school of Pharmacy, Sichuan University, Chengdu, 610064, China.
Alogliptin is a highly selective inhibitor of dipeptidyl peptidase-4 and primarily excreted as unchanged drug in the urine, and differences in clinical outcomes in renal impairment patients increase the risk of serious adverse reactions. In this study, we developed a comprehensive physiologically-based quantitative systematic pharmacology model of the alogliptin-glucose control system to predict plasma exposure and use glucose as a clinical endpoint to prospectively understand its therapeutic outcomes with varying renal function. Our model incorporates a PBPK model for alogliptin, DPP-4 activity described by receptor occupancy theory, and the crosstalk and feedback loops for GLP-1-GIP-glucagon, insulin, and glucose.
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