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This nation-wide study shows insufficiently reached treatment goals for haemoglobin A1c (HbA1c) in all treatment groups. Patients on insulin-based treatment regimens had the longest duration of diabetes, more cardiovascular risk factors and the highest proportions of patients not reaching HbA1c target.
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REMOVAL is the largest clinical trial of adjunct metformin therapy in T1D to date and will provide clinically meaningful information on its potential to impact CV disease and other complications.
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T24 and J82 cell lines were used as an in vitro model, and 24 female SD rats were used to build an N-methyl-N-nitrosourea (MNU)-induced orthotopic rat bladder cancer model. Transfection of lentivirus-based shRNA was used to construct the STAT3-KNOCKDOWN T24 cell line. After metformin treatment, the viability of bladde cancer cells was determined by CCK8. Cell cycle distribution and apoptosis were assessed by flow cytometry. The migration and invasion abilities of cells were evaluated by wound healing and transwell asssays. The inactivation of stat3 pahtway was examined by qRTPCR, western blot and Immunofluorescence.
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To investigate glucose and insulin metabolism in participants with ataxia telangiectasia in the absence of a diagnosis of diabetes.
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Within 7 months, 32 PCOS women were recruited in the study and equally allocated to the two groups. Baseline characteristics were similar in metformin group and placebo one. Ovulation was characterized by the presence of at least one mature follicle (> 16 mm), a circulating estradiol concentration in the edge of 150-250 pg and accessory an endometrial depth > 8 mm. The ovulation rate in the metformin group was 62.5% compared with 37.5% in the placebo group, a non-statistically significant (small study population) but important difference (1.66 times). Analyses show a higher mature follicle number and estradiol concentration in metformin group than in the placebo one. Metformin effect was, in our study, his only insulinosensitizer property consequence far away a 'making thinner' or Hyperandrogenism reducing ones.
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Insulin secretion is often diminished in hyperglycemic patients with type 2 diabetes. We examined whether chronic basal insulin treatment with insulin glargine improves glucose-induced insulin secretion.
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This is the first randomized trial utilizing multiple techniques to evaluate bone mass, structure, serum markers of bone remodeling, and potential reversibility of changes after discontinuation of rosiglitazone. This study will provide information about RSG bone effects in a population of postmenopausal women at risk for bone loss and subsequent fracture.
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In rats, metformin does not decrease neointimal growth after arterial injury, despite increasing whole body insulin sensitivity.
Albiglutide, as part of triple therapy, provided effective glucose-lowering and was generally well tolerated.
This was a prospective clinical study conducted at Kocaeli University Department of Obstetrics and Gynecology on 42 PCOS patients. Patients were randomly allocated into two groups [Group I (n = 22): drospirenone-ethinyl estradiol (DEE); Group II (n = 20): drospirenone-ethinyl estradiol + metformin (M)] according to Body Mass Index (BMI) findings. Patients were evaluated in terms of leptin-ghrelin, ultrasound, and body fat distribution before and 6 months after therapy. Main outcome measures were to investigate the effects of drospirenone-ethinyl estradiol and drospirenone-ethinyl estradiol + metformin on ovarian ultrasonographic markers, BFM index, leptin, and ghrelin.
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Six studies involving 2350 patients were included in the current meta-analysis. In all, the pooled HR of overall survival (OS) was 0.90 (95 % CI 0.84-0.96; P = 0.003). Sub-group analysis showed that when stratified by region the HR of OS was 0.52 (95 % CI 0.31-0.87; P = 0.012) and 0.86 (95 % CI 0.67-1.11, P = 0.361) for Asian and Western countries. When stratified by study design, the HR of OS was 0.78 (95 % CI 0.52-1.15, P = 0.206) and 0.82 (95 % CI 0.59-1.16, P = 0.264) for cohort and medical data-based studies. When stratified by lung cancer subtype, HR of OS was 0.52 (95 % CI 0.31-0.87; P = 0.012), 1.06 (95 % CI 0.51-2.19; P = 0.878) and 0.82 (95 % CI 0.59-1.16; P = 0.264) for SCLS, NSCLC and non-divided subtypes, respectively.
The near-normoglycemia rate at the third month in CSII alone and that in combination with rosiglitazone, metformin, or α-lipoic acid was 72.5%, 87.5%, 90%, and 75%, respectively (metformin group vs. CSII alone, P=0.045). The metformin group achieved euglycemia in a shorter time (2.6 ± 1.3 vs. 3.7 ± 1.8 days, P=0.020) with less daily insulin dosage and was more powerful in lowering total cholesterol, increasing AIR and HOMA β-cell function, whereas reduction of IMCL in the soleus was more obvious in the rosiglitazone group but not in the metformin group. The efficacy of combination with α-lipoic acid was similar to that of CSII alone.
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The aim of the study was to evaluate long-term effects of simvastatin and metformin on PCOS.
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A propensity score-matched cohort study was performed using Japanese pharmacy prescription receipt data for OHDs in order to confirm reported changes in OHD prescription behaviour for patients receiving sitagliptin before and after the safety alert.
To analyze the performance of the Programa Farmácia Popular do Brasil (FPB - Brazilian Popular Pharmacy Program) in the public and private sectors, in terms of availability and cost of medicines for hypertension and diabetes.
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LH levels increased in diabetic (p<0.001) and diabetic BA-treated mice (p=0.009). Plasma levels of testosterone (p< 0.001) and sperm count (p=0.04) decreased in these groups when compared to the control group. Furthermore, administration of 10 mg/kg (p=0.001), 20 mg/kg (p=0.004), or 40 mg/kg (p<0.001) of BA led to a greater reduction in plasma testosterone levels compared to the diabetes group. Seminiferous tubule vacuole numbers increased in diabetic and diabetic BA-treated mice, but testis morphology and FSH level assessment revealed no significant differences between the groups.
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Therapeutic options for the treatment of cardiometabolic risk include a multifactorial risk reduction for such individuals targeting each risk factor and emphasizing both lifestyle changes and pharmacologic therapy.
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Diabetes and tuberculosis coexist together, and influence each other's natural history and treatment outcomes significantly. This assumes clinical as well as public health significance. This article describes these associations, and discusses action that can be taken at the primary care level to tackle this challenge.
There is evidence that administration of sulfonylureas, such as glibenclamide and tolbutamide, blocks diclofenac-induced antinociception, suggesting that diclofenac activates ATP-sensitive K(+) channels. However, there is no evidence for the interaction between diclofenac and other hypoglycemic drugs, such as the biguanides metformin or phenformin. Therefore, this work was undertaken to determine whether two sulfonylureas, glibenclamide and glipizide, as well as two biguanides, metformin and phenformin, have any effect on the systemic antinociception that is induced by diclofenac and indomethacin using the rat formalin test as an animal model. Systemic injections of diclofenac (10 to 30mg/kg) and indomethacin (10 to 30mg/kg) produced dose-dependent antinociception during the second phase of the test. Systemic pretreatment with glibenclamide (3 and 10mg/kg), glipizide (3 and 10mg/kg), metformin (100 and 180mg/kg) or phenformin (100 and 180mg/kg) blocked diclofenac-induced systemic antinociception in the second phase of the test (P<0.05). In contrast, pretreatment with glibenclamide, glipizide, metformin or phenformin did not block indomethacin-induced systemic antinociception (P>0.05). These data suggest that diclofenac, but not indomethacin, activated K(+) channels and metformin and phenformin-dependent mechanisms, which resulted in systemic antinociceptive effects in the rat formalin test.
In this study we aimed to replicate the previously reported association between the glycaemic response to metformin and the SNP rs11212617 at a locus that includes the ataxia telangiectasia mutated (ATM) gene in multiple additional populations.
To observe the effect of Zhenqing Recipe (ZQR) on non-alcoholic fatty liver (NAFL), and the expression of hepatic salt-inducible kinase 1 (SIK1) and sterol-regulatory element binding protein-ic (SREBP-lc) in type 2 diabetes rats.
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Lectin-like oxidized LDL receptor-1 (LOX-1) is a class E oxidized LDL specific scavenger receptor that recognizes multiple ligands. Advanced glycation end products (AGEs) have been recently identified as other ligands to LOX-1 and shown to increase LOX-1 expressions in diabetes; therefore, we investigated the underlying mechanism involved.
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comorbidity, metabolic control, compliance and complications. Patients were followed for 2 years. The cost model differed direct health costs (primary care / specialist) and indirect (labor productivity).
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Metformin, generally considered nontoxic and remarkably inexpensive, might be used in combination with TKIs in patients with non-small cell lung cancer, harboring EGFR mutations to overcome TKI resistance and prolong survival.
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Diabesity is a new term for obesity-dependent diabetes, which is also associated with cardiovascular and other comorbidities with rising epidemic. Traditional treatments (sulfonylureas and thiazolidinediones) of diabetes are associated with weight gain, except metformin. Newer agents such as glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and Sodium glucose co-transporter 2 inhibitors (SGLT2i) are causing a modest weight reduction, whereas dipeptidyl peptidase-4 inhibitors (DPP-4i) are weight neutral. Oxyntomodulin, a native GLP-1/glucagon receptor agonist produced a superior weight loss and antihyperglycemic effects in obese mice and humans. Recent findings with synthetic dual GLP-1/glucagon receptor agonists have shown a good weight loss and antihyperglycemic profile in diet-induced obese (DIO) mice. Targeting combinations of GLP-1 receptor and glucagon receptor simultaneously with a single peptide may be the better strategy to achieve marked weight loss and considerable glycemic control in diabesity. Cardiovascular safety is very important with new antidiabetic agents due to rosiglitazone controversy. Current on-going clinical trials will clarify the cardiovascular effects of incretin-based therapies in near future. Based on current knowledge and rapid progress in the field, there is a strong possibility that the GLP-1/glucagon receptor co-agonists will likely be the new therapeutic treatment for diabesity for decades to come.
Ninety-eight patients with uncontrolled type 2 diabetes, who were previously prescribed metformin, acarbose, or both, were randomly assigned to a DP group (add-on pioglitazone; n = 49) or a DS group (add-on sulfonylurea; n = 49).
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Current processes of care for diabetes mellitus (DM) were shaped during the era when insulin therapy was considered inexorable to the management of advanced stage type 2 (T2DM), though this no longer appears to be categorically true. There are also dashed hopes that insulin therapy can prevent or stall diabetes. While exogenous insulin remains a life-sparing tool for fully insulin-dependent DM, insulin therapy-induced hyperinsulinemia now appears to contribute to serious safety issues beyond hypoglycemia and weight gain. Iatrogenic and compensatory hyperinsulinemia are metabolic disruptors of β-cells, liver, muscle, kidney, brain, heart and vasculature, inflammation, and lipid homeostasis, among other systems. This may compromise β-cells, exacerbate insulin resistance (IR), and increase risk of cardiovascular (CV) disease. Striking associations between exogenous insulin and risks of CV events, cancer, and all-cause mortality in clinical trial and real-world cohorts caution that insulin may pose more harm than previously evidenced. At our disposal are numerous alternate tools that, alone or in combination, efficaciously manage hyperglycemia and glucolipotoxicity, and do so without inducing hypoglycemia, weight gain, or hyperinsulinemia. Moreover, these new tools support true precision therapy, as modern day drug classes can be aligned with the various mediating pathways of hyperglycemia at work in any given patient. Some also appear to promote β-cell survival, with intriguing data being presented for newer agents, such as incretins. As such, we encourage preferential use of non-insulin antidiabetic agents to injected insulin for the management of non-insulin-dependent patients with T2DM, including in advanced stage T2DM. The goal of this article is to augment existing literature to 1) correct misconceptions on the rationale and necessity for insulin therapy in T2DM, 2) discuss emerging negative safety data with insulin therapy, and, 3) offer a practical means to reduce reliance on insulin through delayed initiation, minimized dose, and, drug switching to safer agents, and, potentially, reframes processes of care.
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In patients with type 2 diabetes, empagliflozin-induced glycosuria improved β cell function and insulin sensitivity, despite the fall in insulin secretion and tissue glucose disposal and the rise in EGP after one dose, thereby lowering fasting and postprandial glycemia. Chronic dosing shifted substrate utilization from carbohydrate to lipid. Trial registration. ClinicalTrials.Gov NCT01248364 (EudraCT no. 2010-018708-99). Funding. This study was funded by Boehringer Ingelheim.