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fasting plasma glucose (FPG), glycated hemoglobin (HbA1c) and insulin resistance (IR) ( 9 , 10 , 11 ). A large number of studies have shown that adenosine can play a role in cardiac protection by dilating the coronary artery, scavenging oxygen free
Guangdong Provincial Key Laboratory of Diabetology, Guangzhou, China
Department of Ultrasound, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China
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Guangdong Provincial Key Laboratory of Diabetology, Guangzhou, China
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Guangdong Provincial Key Laboratory of Diabetology, Guangzhou, China
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Guangdong Provincial Key Laboratory of Diabetology, Guangzhou, China
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Guangdong Provincial Key Laboratory of Diabetology, Guangzhou, China
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Guangdong Provincial Key Laboratory of Diabetology, Guangzhou, China
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Guangdong Provincial Key Laboratory of Diabetology, Guangzhou, China
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compared to the HFD mice ( Fig. 1F ). Taken together, these data showed that liraglutide improves body weight, glucose tolerance, and insulin resistance in HFD-challenged mice. Figure 1 Liraglutide decreased body weight and improved glucose
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soluble leptin receptor levels and free leptin index in women with polycystic ovary syndrome: relationship to insulin resistance and androgens . Fertility and Sterility 2006 85 1441 – 1447 . ( https://doi.org/10.1016/j.fertnstert.2005.10.038 ) 24
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Type 1 diabetes mellitus (T1DM) results from the autoimmune destruction of β cells of the endocrine pancreas. Pathogenesis of T1DM is different from that of type 2 diabetes mellitus, where both insulin resistance and reduced secretion of insulin by the β cells play a synergistic role. We will present genetic, environmental and immunologic factors that destroy β cells of the endocrine pancreas and lead to insulin deficiency. The process of autoimmune destruction takes place in genetically susceptible individuals under the triggering effect of one or more environmental factors and usually progresses over a period of many months to years, during which period patients are asymptomatic and euglycemic, but positive for relevant autoantibodies. Symptomatic hyperglycemia and frank diabetes occur after a long latency period, which reflects the large percentage of β cells that need to be destroyed before overt diabetes become evident.
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Hyperinsulinemia is a major complication associated with the development of insulin resistance. In addition to its normal spectrum of metabolic effects, insulin can act as a growth factor and has the ability to promote mitogenic activity. Thus, hyperinsulinemia is regarded as a potentially important cancer risk factor among diabetic patients. However, the mechanisms of action of insulin in the specific context of prostate cancer (PCa) and, in particular, the specific receptor that mediates its actions have not been elucidated yet. The aims of this study were to investigate whether insulin can directly induce mitogenic activities in PCa-derived cell lines and to examine the mechanisms responsible for these actions. To this end, we used several PCa-derived cell lines, representing early and advanced stages of the disease. Our results indicated that insulin induces cell proliferation in a dose-dependent fashion in the LNCaP, C4-2, and P69 cell lines. We also demonstrated that insulin enabled LNCaP and C4-2 cells to progress through the cell cycle. Immunoprecipitation assays revealed that insulin activated the insulin receptor (INSR), but not the IGF1 receptor (IGF1R). In addition, INSR was able to compensate for and mediate IGF1 mitogenic signals following IGF1R inhibition. In conclusion, insulin exhibits direct mitogenic activities in PCa cells, which are mediated exclusively through the INSR. Further research is needed to fully dissect the molecular mechanisms underlying the biological actions of insulin in PCa.
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Background: Fatty acid-binding protein 4 (FABP4) is an adipokine that plays significant roles in the development of insulin resistance and atherosclerosis. High levels of soluble tumor necrosis factor receptors (TNFRs) including TNFR1 and TNFR2 are associated with renal dysfunction and increased mortality in patients with diabetes mellitus (DM). However, the association between circulating levels of FABP4 and TNFRs remains unclear.
Methods: We investigated the associations of FABP4 with TNFRs and metabolic markers in Japanese patients with type 1 DM (T1DM, n=76, men/women: 31/45) and type 2 DM (T2DM, n=575, men/women: 312/263).
Results: FABP4 concentration was positively correlated with levels of TNFR1 and TNFR2 in both patients with T1DM and those with T2DM. Multivariable regression analyses showed that there were independent associations of FABP4 concentration with body mass index (BMI) and estimated glomerular filtration rate (eGFR) after adjustment of age and sex in both patients with T1DM and those with T2DM. FABP4 concentration was independently associated with circulating levels of TNFR1 and TNFR2 after adjustment of the confounders in patients with T2DM but not in those with T1DM. Similarly, levels of TNFR1 and TNFR2 were independently associated with FABP4 concentration after adjustment of age, sex, systolic blood pressure, duration of DM and levels of eGFR, high-density lipoprotein cholesterol and C-reactive protein in patients with T2DM but not in those with T1DM.
Conclusion: FABP4 concentration is independently associated with levels of TNFRs in patients with DM, but the association is more evident in patients with T2DM than in those with T1DM.
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Background: Bariatric surgery induces significant weight loss, increases insulin sensitivity and improves dyslipidemia. As one of the most widely performed bariatric surgeries, laparoscopic sleeve gastrectomy (LSG) is thought to improve metabolic profile along with weight loss. The objective of this study was to evaluate longitudinal changes in serum metabolite levels after LSG and elucidate the underlying mechanisms of metabolic improvement.
Methods: Clinical metabolic parameters and serum samples were collected preoperatively and at 1, 3, and 6 months postoperatively from nine patients with obesity undergoing LSG. Serum metabolites were measured using non-targeted metabolic liquid chromatography-mass spectrometry (LC-MS) method.
Results: During the 1, 3, and 6 months postoperative follow-up, the BMI, HOMA-IR, liver fat content showed a gradual descending trend. A total of 328 serum metabolites were detected and 38 were differentially expressed. The up-regulated metabolites were mainly enriched in ketone body metabolism, alpha linolenic acid and linoleic acid metabolism, pantothenate and CoA biosynthesis, glycerolipid metabolism, fructose and mannose degradation, while the down-regulated metabolites were closely related to caffeine metabolism, oxidation of branched chain fatty acids, glutamate metabolism, and homocysteine degradation. Notably, nine metabolites (oxoglutarate, 2-ketobutyric acid, succinic acid semialdehyde, phthalic acid, pantetheine, eicosapentaenoate, 3-hydroxybutanoate, oxamic acid, and dihydroxyfumarate) showed persistent differential expression at 1, 3, and 6 months follow-up. Some were found to be significantly associated with weight loss, insulin resistance improvement and liver fat content reduction.
Conclusions: This finding may provide a new perspective for revealing novel biomarkers and mechanisms of metabolic improvement in obesity and related comorbidities.
Department of Endocrinology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
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). It was first reported by Berson and coworkers ( 2 ) that clinical hypersensitivity and insulin resistance were associated with circulating insulin antibodies (IAs) in patients receiving exogenous animal insulin therapy. Over the past few decades, with
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Federation (IDF), the waist circumference has to be measured at ≥80 cm in women and ≥94 cm in men ( http://www.idf.org , 09/08/2011). Mesenteric and omental fat is of greater importance in the development of insulin resistance, because their fatty acids and
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aim of this article is to explore and review current evidence that associates PCOS with cardiometabolic abnormalities and possibly an increased risk of cardiovascular disease. Insulin resistance, metabolic syndrome, obesity and sleep disturbances
