Complete data were obtained for 35 of the 61 patients enrolled to the study. At three and six months no changes were reported for any of the cardiovascular risk factors except for lipids where there was a modest rise in plasma triglycerides. These effects were achieved with a reduced dose of metformin XR compared to pre-study dosing with standard metformin (1500 mg +/- 402 vs 1861 +/- 711 p = 0.004). A total of 77% of patients were free of gastrointestinal side effects and 83% of patients stated a preference for metformin XR at the end of the study. Ghost tablets were reported in the faeces by the majority of the patients (54.1%).
After 36 weeks of insulin therapy, insulin doses were comparable between the G+MET (68 ± 5.7 U/day) and NPH+MET (71 ± 6.2 U/day) groups (p = 0.68). Before insulin therapy, circulating IGF-I bioactivity was similar between the G+MET (134 ± 9 pmol/l) and NPH+MET (135 ± 10 pmol/l) groups (p = 0.83). After 36 weeks, IGF-I bioactivity had decreased significantly (p = 0.001) and did not differ between the G+MET (116 ± 9 pmol/l) and NPH+MET (117 ± 10 pmol/l) groups (p = 0.91). At baseline and after insulin therapy, total IGF-I concentrations were comparable in both groups (baseline: G+MET 13.3 ± 1.0 vs NPH+MET 13.3 ± 1.0 nmol/l, p = 0.97; and 36 weeks: 13.4 ± 1.0 vs 13.1 ± 0.9 nmol/l, p = 0.71). Total IGF-I concentration did not change during insulin therapy (13.3 ± 0.7 vs 13.3 ± 0.7 nmol/l, baseline vs 36 weeks, p = 0.86).
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Our study showed that NAFLD is a common disease in women with polycystic ovaries, especially with high BMI, but an incidence rate of 40% in lean women too was found. Because steatohepatitis is a risk factor for the developmente of cirrhosis and hepatocellular carcinoma, it is therefore prudent to carry out an ultrasound evaluation of liver in all young patients suffering from polycystic ovary syndrome, regardless of their BMI and the results of serological evaluation of liver.
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We tested genetic associations with weight loss and weight regain in the Diabetes Prevention Program, a randomized controlled trial of weight loss-inducing interventions (lifestyle and metformin) versus placebo.
As part of study, among 500 patients evaluated, three most common diagnosis were upper respiratory infections (URIs; 18%), acute gastroenteritis including water-borne diseases (15.8%), and anemia (10.4%). Treatment given to these patients comprised of mostly of antipyretic, analgesic, and antimicrobial agents. Most common drug prescribed was paracetamol for fever. Other common drugs prescribed were amoxicillin/clavulanic acid, chloroquine, artemisin derivative, doxycycline, co-trimoxazole, miltefosine, cephalexin, ceftriaxone sodium, cefixime, oral rehydration salts, ranitidine, omeprazole, pantoprazole, metronidazole, albendazole, ondansetron, diclofenac sodium, piroxicam, ibuprofen, diphenhydramine, codeine-sulfate, amlodipine, ramipril, hydrochlorothiazide, atenolol, salbutamol, etophyline, metformin, glimepiride, fluoxetine, flavoxate, tamsulosin, iron-folic acid, etc. The fact that three or more drugs are given in most of the prescriptions, can be justified due to multiple morbidity and the severity of disease than to irresponsible prescribing.
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Prospective observational study.
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Streptozotocin- and methylglyoxal-induced pain models were established in rats, and the anti-nociceptive effects of the methylglyoxal scavenging agents, selective transient receptor potential channel ankyrin 1 (TRPA1) antagonist, and Nav1.8 antagonist were tested.
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To explain the subadditive efficacy typically observed with initial combination treatments for type 2 diabetes.
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To determine incidence of dementia in type 2 diabetic (T2DM) patients, and whether there are adverse or favorable effects of oral agents (OA) in DM, we obtained a representative cohort of 800,000 from Taiwan’s National Health Insurance database. Those who, as of on January 1, 2000, were 50 years or older and dementia free (n = 127,209) were followed until December 31, 2007, in relation to absence (n = 101,816) or presence (n = 25,393) of T2DM, and whether any OA was used. Dementia was ascertained by ICD9-CM or A-code. Dementia incidence densities (DID) and fully adjusted Cox proportional hazard models were used to estimate association between dementia, DM, and OA. Notably, DID (per 10,000 person-years)was markedly increased with DM (without medication), compared to DM free subjects (119 versus 46). Using non-DM as reference, the adjusted hazard ratios (HRs) (95% confidence interval) for DM without and with OA were 2.41 (2.17–2.66) and 1.62 (1.49–1.77), respectively. For T2DM, compared with no medication, sulfonylureas alone reduced the HR from 1 to 0.85 (0.71–1.01), metformin alone to 0.76 (0.58–0.98), while with combined oral therapy the HR was 0.65 (0.56–0.74). Adjustments included cerebrovascular diseases so that non-stroke related dementias were found to be decreased in DM with sulfonylurea and metformin therapy. T2DM increases the risk of dementia more than 2-fold. On the other hand, sulfonylureas may decrease the risk of dementia, as does metformin; together, these 2 OAs decrease the risk of dementia in T2DM patients by 35% over 8 years.
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Metformin is widely used in the treatment of Type 2 diabetes, however, mechanisms of its antihyperglycemic effect were not yet fully elucidated. Complex I of mitochondrial respiration chain is considered as one of the possible targets of metformin action. In this paper, we present data indicating that the inhibitory effect of metformin can be tested also in liver homogenate. Contrary to previous findings on hepatocytes or mitochondria under our experimental conditions, lower metformin concentrations and shorter time of preincubation give significant inhibitory effects. These conditions enable to study the mechanism of the inhibitory effect of metformin in small samples of biological material (50-100 mg wet weight) and compare more experimental groups of animals because isolation of mitochonria is unnecessary.
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To compare the efficacy and safety of liraglutide versus sitagliptin as add-on to metformin after 26 weeks of treatment in Chinese patients with type 2 diabetes mellitus (T2DM).
The mechanism for the association between diabetes mellitus and lung function impairment is unknown, as are any respiratory effects of antidiabetic agents. We aimed to assess whether treatment with metformin, an oral insulin-sensitising agent, improved lung function or symptoms in individuals with COPD and glucose intolerance. A prospective open-label observational study was conducted. Participants with moderate or severe COPD, BMI > 25 kg/m(2), and type 2 diabetes mellitus or impaired glucose tolerance took metformin twice daily for 6 months. Clinical outcomes included St George's Respiratory Questionnaire (SGRQ), transition dyspnoea index, and incremental shuttle walk test. Physiological outcomes including pulmonary function tests, exhaled nitric oxide, respiratory mouth pressures and handgrip strength. In total, 17 participants completed the study. SGRQ score improved by a median of 5 points, and TDI scores improved by 2 points. Inspiratory mouth pressures increased by 7.5 cmH2O. There were trends to improvements in hyperinflation, gas trapping and shuttle walk distance. Spirometry and exhaled nitric oxide were unchanged. In this proof-of-concept study, metformin was associated with improved dyspnoea and health status in COPD, possibly related to increased inspiratory muscle strength. These and other endpoints should be examined in a definitive study.
Adenosine monophosphate-activated protein kinase (AMPK) is a sensor for cellular energy status. When the cellular energy level is decreased, AMPK is activated and functions to suppress energy-consuming processes, including protein synthesis. Recently, AMPK has received attention as an attractive molecular target for cancer therapy. Several studies have revealed that the activation of AMPK by chemical stimulators, such as metformin, induces apoptosis in a variety of hematologic malignant cells. From another perspective, these results suggest that the function of AMPK is impaired in hematologic tumor cells. However, the precise mechanisms by which this impairment occurs are not well understood. In melanoma cells, oncogenic BRAF constitutively activates the extracellular signal-regulated kinase (ERK) pathway and phosphorylates liver kinase B1, an upstream activator of 5' adenosine monophosphate-activated protein kinase (AMPK), resulting in the inactivation of liver kinase B1 and AMPK. In this study, we analyzed whether ERK is involved in the suppression of AMPK activity using established and primary human leukemia cells. We found an inverse correlation between the intensity of ERK activity and the degree of AMPK activation after stimulation with either glucose deprivation or metformin. We also found that the inhibition of ERK activity by U0126 restored AMPK activation after metformin treatment. Furthermore, a combined treatment with metformin and U0126 enhanced the antileukemic activity of metformin. Importantly, metformin induced ERK activation by suppressing the protein levels of dual specificity phosphatase 6, a negative regulator of ERK. This crosstalk between AMPK and ERK could diminish the antileukemic activity of metformin. Taken together, our present observations suggest a novel therapeutic strategy for improving the efficacy of metformin in treating leukemia.
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To review current evidence of pharmacological options for managing pediatric obesity and provide potential areas for future research.
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Type 2 diabetes (T2D) in youth is recognized as a pediatric disease, but few reports describe the characteristics during diagnosis. We describe the clinical presentation of 503 youth with T2D.
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Transfer of bioactive organic compounds from soil to plants might represent animal and human health risks. Sewage sludge and manure are potential sources for bioactive compounds such as human- and veterinary drugs. In the present study, uptake of the anti-diabetic compound, metformin, the antibiotic agent ciprofloxacin and the anti-coccidial narasin in carrot (Daucuscarota ssp. sativus cvs. Napoli) and barley (Hordeumvulgare) were investigated. The pharmaceuticals were selected in order to cover various chemical properties, in addition to their presence in relevant environmental matrixes. The root concentration factors (RCF) found in the present study were higher than the corresponding leaf concentration factors (LCF) for the three test pharmaceuticals. The uptake of metformin was higher compared with ciprofloxacin and narasin for all plant compartments analyzed. Metformin was studied more explicitly with regard to uptake and translocation in meadow fescue (Festucapratense), three other carrot cultivars (D.carota ssp. sativus cvs. Amager, Rothild and Nutri Red), wheat cereal (Triticumaestivum) and turnip rape seed (Brassicacampestris). Uptake of metformin in meadow fescue was comparable with uptake in the four carrot cultivars (RCF 2-10, LCF approximately 1.5), uptake in wheat cereals were comparable with barley cereals (seed concentration factors, SCF, 0.02-0.04) while the accumulation in turnip rape seeds was as high as 1.5. All three pharmaceuticals produced negative effects on growth and development of carrots when grown in soil concentration of 6-10 mg kg(-1) dry weight.
The aim of the present study was to compare the effects of low glycemic index diet versus metformin on MetS components in adults with MetS.
TZD and berberine increased 2DG uptake by 3.3-fold (with respect to control) at 15 μM and 25 μM, respectively. The same concentrations of arecoline and vanillic acid increased 2DG uptake by 3.2-and 2.9-fold, respectively, when compared with the basal level. Berberine and arecoline acted synergistically with both the OHDs, whereas vanillic acid had an additive interaction with TZD and an antagonistic interaction with metformin. Arecoline significantly increased the translocation of GLUT4 via the PPAR(γ) pathway, whereas berberine and vanillic acid did this via the AMPK-dependent pathway.
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The pathways through which fatty acids induce insulin resistance have been the subject of much research. We hypothesise that by focussing on the reversal of insulin resistance, novel insights can be made regarding the mechanisms by which insulin resistance can be overcome. Using global gene and lipid expression profiling, we aimed to identify biological pathways altered during the prevention of palmitate-induced glucose production in hepatocytes using metformin and sodium salicylate. FAO hepatoma cells were treated with palmitate (0.075 mM, 48 h) with or without metformin (0.25 mM) and sodium salicylate (2 mM) in the final 24 h of palmitate treatment, and effects on glucose production were determined. RNA microarray measurements followed by gene set enrichment analysis were performed to investigate pathway regulation. Lipidomic analysis and measurement of secreted bile acids and cholesterol were also performed. Reversal of palmitate-induced glucose production by metformin and sodium salicylate was characterised by co-ordinated down-regulated expression of pathways regulating acetyl-CoA to cholesterol and bile acid biosynthesis. All 20 enzymes that regulate the conversion of acetyl-CoA to cholesterol were reduced following metformin and sodium salicylate. Selected findings were confirmed using primary mouse hepatocytes. Although total intracellular levels of diacylglycerol, triacylglycerol and cholesterol esters increased with palmitate, these were not, however, further altered by metformin and sodium salicylate. 6 individual diacylglycerol, triacylglycerol and cholesterol ester species containing 18:0 and 18:1 side-chains were reduced by metformin and sodium salicylate. These results implicate acetyl-CoA metabolism and C18 lipid species as modulators of hepatic glucose production that could be targeted to improve glucose homeostasis.
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DiaRegis is a multicentre registry including 3,810 patients with type-2 diabetes. For the present analysis we selected patients being treated with metformin monotherapy at baseline (n = 1,373), with the subsequent addition of incretin-based drugs (Met/Incr; n = 783), sulfonylureas (Met/SU; n = 255), or insulin (n = 220).
At baseline, compared with the TN group, the Met group had higher fasting glycaemia (9.1 ± 1.7 vs 8.2 ± 1.3 mmol/l), lower fasting and postmeal insulin secretion, lower beta cell glucose sensitivity (37  vs 58  pmol min(-1) m(-2) [mmol/l](-1), median [interquartile range]) and insulin:glucagon ratio, and higher fasting EGP (15.9 [4.3] vs 12.1 [2.7] μmol kgFFM (-1) min(-1)). Change from baseline in fasting EGP after single dose and 4 weeks of treatment with empagliflozin was similar in the Met and TN groups (19.6 [4.2] and 19.0 [2.3] in Met vs 16.2 [3.6] and 15.5 [3.2] μmol kgFFM (-1) min(-1) in TN for acute and chronic dosing, respectively). Beta cell glucose sensitivity increased less in Met than TN patients, whereas substrate utilisation shifted from carbohydrate to fat more in Met than TN patients.
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This case describes an unusual pattern of the disease, in which obstetric cholestasis occurred in five consecutive pregnancies with a different course of the disease in the fifth pregnancy.
Ovarian cancer is one of the most common lethal gynecological malignancies world-wide. Despite an initial 70-80% response rate, most patients relapse within 1-2 years and develop chemo-resistance. Hence, the identification of novel drugs or the repositioning of known drugs to re-sensitize ovarian cancer cells to existing chemotherapy regimens is needed. Here, we evaluated the effect of metformin (an anti-diabetic drug) on ovarian cancer cells, based on its putative effect on other solid tumors.
Over the last decade, guidelines for the treatment of type 2 diabetes have increasingly favored tighter glycemic control, necessitating the use of more aggressive pharmacological therapy. The objective of this study was to describe trends in the prescription of anti-diabetic medications among patients with type 2 diabetes in the United Kingdom (UK).
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In the NDTI database, the most common diagnoses associated with metformin use were diabetes (34·9%), followed by metabolic syndrome (20·9%), PCOS (17·2%) and obesity (6·5%). In the MarketScan(®) Commercial database, T2DM was the most common diagnosis among girls aged 10-14 years (22·8-23·6%), boys aged 10-14 years (20·5-24·5%) and boys aged 15-19 years (37·1-43·1%), whereas PCOS (24·1-28·3%) was the most common diagnosis among girls aged 15-19 years. In the Medicaid database, T2DM was the most common diagnosis among all four groups and the proportions were higher than their counterparts in the Commercial database.
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A total of 5689 patients with treated hypothyroidism and 59,937 euthyroid patients were included in the subcohorts. Among patients with treated hypothyroidism, 495 events of low TSH levels were observed during follow-up (incidence rate 119.7/1000 person-years). In the euthyroid group, 322 events of low TSH levels were observed (incidence rate 4.5/1000 person-years). Compared with sulfonylurea monotherapy, metformin monotherapy was associated with a 55% increased risk of low TSH levels in patients with treated hypothyroidism (incidence rate 79.5/1000 person-years v. 125.2/1000 person-years, adjusted hazard ratio [HR] 1.55, 95% confidence interval [CI] 1.09-2.20), with the highest risk in the 90-180 days after initiation (adjusted HR 2.30, 95% CI 1.00-5.29). No association was observed in euthyroid patients (adjusted HR 0.97, 95% CI 0.69-1.36).
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Comorbidity, young age, central obesity and poor baseline glycaemic control are important predictors of therapy one year after Type 2 diabetes mellitus debut.
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The global burden of diabetes mellitus (DM) is immense and predicted to reach 438 million by 2030, with 80% of the cases being in the developing world. The management of chronic non-communicable diseases like DM is poor in most resource-limited settings, and the 'directly observed therapy, short course' (DOTS) framework for tuberculosis control has been proposed as a feasible way to improve this situation. In late 2009, aspects of the DOTS model were applied to the management of persons with DM in the diabetes clinic in Queen Elizabeth Central Hospital, Blantyre, Malawi, and a point-of-care electronic medical record system was set up to support and monitor patients in care. This is the first quarterly and cumulative report of persons with DM registered for care stratified by treatment outcomes, complications and medication history up to 31 December 2010. There were 170 new patients registered between October and December 2010, with 1864 ever registered by 31 December 2010. Most patients were alive and in care; 3 died, 53 defaulted and 3 transferred out. Of those on oral hypoglycaemic agents, metformin was most commonly used. Complications were common. The monitoring and evaluation will be further refined, and at the same time, the systems developed in Blantyre will be expanded to other parts of the country.
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Further research, including larger randomized controlled trials and meta-analyses, is needed to clarify the role of metformin and thiazolidinediones in the treatment of clinical and biochemical PCOS characteristics.