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"insulin resistance", "islet cell function", "T2DM"

S-D Qi, Z-L He, Y Chen, J Ma, W-H Yu, Y-Y Li, F-M Yang, J-B Wang, L-X Chen, Y Zhao, S-Y Lu
Resistin is a type of hormone-like adipocytokines, which is secreted specifically by adipocytes. It may be a key factor in the development of type 2 diabetes mellitus (T2DM) from obesity- associated insulin resistance due to results that show that it has a close relationship with insulin resistance in rodents. We utilized the rhesus monkeys as study objects to preliminarily test the association with glucose metabolism and to conduct a correlation analysis for clinical parameters and serum resistin levels in obese rhesus monkey models of T2DM...
September 2015: Experimental and Clinical Endocrinology & Diabetes
Hongyun Lu, Fang Hu, Yingjuan Zeng, Lingling Zou, Shunkui Luo, Ying Sun, Hong Liu, Liao Sun
Diabetic ketosis had been identified as a characteristic of type 1 diabetes mellitus (T1DM), but now emerging evidence has identified that they were diagnosed as T2DM after long time follow up. This case control study was aimed at comparing the clinical characteristic, β-cell function, and insulin resistance of ketosis and nonketotic onset T2DM and providing evidence for treatment selection. 140 cases of newly diagnosed T2DM patients were divided into ketosis (62 cases) and nonketotic onset group (78 cases)...
2014: Journal of Diabetes Research
Shuangli Guo, Chunhua Dai, Min Guo, Brandon Taylor, Jamie S Harmon, Maike Sander, R Paul Robertson, Alvin C Powers, Roland Stein
Type 2 diabetes (T2DM) commonly arises from islet β cell failure and insulin resistance. Here, we examined the sensitivity of key islet-enriched transcription factors to oxidative stress, a condition associated with β cell dysfunction in both type 1 diabetes (T1DM) and T2DM. Hydrogen peroxide treatment of β cell lines induced cytoplasmic translocation of MAFA and NKX6.1. In parallel, the ability of nuclear PDX1 to bind endogenous target gene promoters was also dramatically reduced, whereas the activity of other key β cell transcriptional regulators was unaffected...
August 2013: Journal of Clinical Investigation
C A Carrera Boada, J M Martínez-Moreno
T2DM involves at least two primary pathogenic mechanisms: (a) a progressive decline in pancreatic islet cell function resulting in reduced insulin secretion and (b) peripheral insulin resistance resulting in a decrease in the metabolic responses to insulin. This dynamic interaction between insulin secretion and insulin resistance is essential to the maintenance of normal glucose tolerance (NGT). The transition from the normal control of glucose metabolism to type 2 diabetes mellitus occurs through the intermediate states of altered metabolism that worsen over time...
March 2013: Nutrición Hospitalaria: Organo Oficial de la Sociedad Española de Nutrición Parenteral y Enteral
R E van Genugten, D H van Raalte, M Diamant
Type 2 diabetes mellitus (T2DM) develops as a consequence of progressive β-cell dysfunction in the presence of insulin resistance. None of the currently-available T2DM therapies is able to change the course of the disease by halting the relentless decline in pancreatic islet cell function. Recently, dipeptidyl peptidase (DPP)-4 inhibitors, or incretin enhancers, have been introduced in the treatment of T2DM. This class of glucose-lowering agents enhances endogenous glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) levels by blocking the incretin-degrading enzyme DPP-4...
February 2012: Diabetes, Obesity & Metabolism
Qinghua Wang, Tianru Jin
The peptide hormone insulin not only regulates metabolic pathways, but also proliferative signaling pathways. Insulin regulates cell proliferation, protein synthesis and gene expression in most, if not all, mammalian tissues. Extensive recent studies have shown that insulin also plays an important role in the regulation of pancreatic islet β-cell function. In the development of peripheral insulin resistance leading to an increased demand for insulin production, increase in β-cell mass by compensatory hyperplasia and hypertrophy of β-cells and insulin output is a crucial mechanism to maintain euglycemia...
September 2009: Islets
Burkhard Göke
No abstract text is available yet for this article.
March 2008: International Journal of Clinical Practice. Supplement
P S Leung
Large clinical trials have shown that inhibition of the renin-angiotensin system (RAS) can delay and/or prevent the onset of Type 2 diabetes mellitus (T2DM) in high-risk individuals, such as those with hypertension or chronic heart failure. Moreover, a meta-analysis of these randomized clinical studies concluded that the mean weighted relative risk of development of T2DM was reduced by 25% in those patients treated with angiotensin II receptor blockers or angiotensin-converting enzyme inhibitors. In spite of these firm clinical data, the mechanistic pathways mediating the protective activity of RAS blockade have yet to be resolved...
February 2007: Diabetic Medicine: a Journal of the British Diabetic Association
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