4 research outputs found

    The polymorphism in insulin receptor substrate-1 gene and birth weight in neonates at term

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    Wstęp: Mutacja genu substratu 1 receptora insuliny (IRS-1, insulin receptor substrate-1) jest jednym z genetycznych czynników ryzyka, przypuszczalnie związanych z występowaniem zjawiska oporności na insulinę lub predyspozycją do wystąpienia cukrzycy typu 2. Celem niniejszego badania była ocena potencjalnych zależności między polimorfizmem Gly972Arg w genie IRS-1 a masą ciała u noworodków urodzonych o czasie. Materiał i metody: W badaniu wzięło udział 100 noworodków urodzonych o czasie (38-42 tydzień ciąży), których matki nie chorowały podczas ciąży. Po wyekstrahowaniu genomowego DNA z leukocytów krwi pępowinowej przeprowadzono z użyciem metody PCR ocenę polimorfizmu Gly972Arg genu IR-1. Wyniki: Urodzeniowa masa ciała była istotnie niższa u noworodków z polimorfizmem Gly972Arg genu IRS-1 w porównaniu z grupą kontrolną (3161,75 ± 380,86 g vs. 3427,92 ± 468,86 g). U noworodków z tym polimorfizmem zaobserwowano również mniejszą długość ciała oraz mniejszy obwód głowy (odpowiednio: 54,38 ± 3,13 cm vs. 52,69 ± 2,91 cm oraz 34,08 ± 1,47 cm vs. 33,63 ± 0,81 cm). Wnioski: Wyniki sugerują, że genotyp Gly972Arg u noworodków urodzonych o czasie wiąże się z niższą urodzeniową masą ciała, mniejszą długością ciała oraz mniejszym obwodem głowy.Background: The mutation of the IRS-1 gene is one of the genetic risk factors which, it is speculated, is associated with insulin resistance or predisposition to type 2 diabetes. The aim of our study was to evaluate the association between the Gly972Arg polymorphism in the IRS-1 gene and birth weight in newborn children with adequate gestational age. Material and methods: 100 newborn children with adequate gestational age (38–42 weeks), whose mother had no disorders during pregnancy, were studied. Genomic DNA was extracted from umbilical cord blood leukocytes, and Gly972Arg polymorphism in the IRS-1 gene was genotyped using the PCR-based method. Results: Birth weight was significantly lower in the newborn with the IRS-1 Gly972Arg polymorphism compared with a control group (3161.75 ± 380.86 g vs. 3427.92 ± 468.86 g). Body length and head circumference at birth were also lower in the neonates with that polymorphism (54.38 ± 3.13 cm vs. 52.69 ± 2.91 cm, and 34.08 ± 1.47 vs. 33.63 ± 0.81, respectively). Conclusions: The results suggest that the Gly972Arg genotype is associated with lower birth weight, body length and head circumference in neonates with adequate gestational age

    Perspectives of Patients with Insulin-treated Type 1 and Type 2 Diabetes on Hypoglycemia: Results of the HAT Observational Study in Central and Eastern European Countries

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    <p></p><p><b>Article full text</b></p> <p><br></p> <p>The full text of this article can be found here<b>.</b> <a href="https://link.springer.com/article/10.1007/s13300-018-0388-2">https://link.springer.com/article/10.1007/s13300-018-0388-2</a></p><p></p><p></p><p> </p><p><br></p> <p><b>Provide enhanced content for this article</b></p> <p><br></p> <p>If you are an author of this publication and would like to provide additional enhanced content for your article then please contact <a href="http://www.medengine.com/Redeem/”mailto:[email protected]”"><b>[email protected]</b></a>.</p> <p><br></p> <p>The journal offers a range of additional features designed to increase visibility and readership. All features will be thoroughly peer reviewed to ensure the content is of the highest scientific standard and all features are marked as ‘peer reviewed’ to ensure readers are aware that the content has been reviewed to the same level as the articles they are being presented alongside. Moreover, all sponsorship and disclosure information is included to provide complete transparency and adherence to good publication practices. This ensures that however the content is reached the reader has a full understanding of its origin. No fees are charged for hosting additional open access content.</p> <p><br></p> <p>Other enhanced features include, but are not limited to:</p> <p><br></p> <p>• Slide decks</p> <p>• Videos and animations</p> <p>• Audio abstracts</p> <p>• Audio slides</p><br><p></p

    Sequential Intensification of Metformin Treatment in Type 2 Diabetes With Liraglutide Followed by Randomized Addition of Basal Insulin Prompted by A1C Targets

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    OBJECTIVE-We evaluated the addition of liraglutide to metformin in type 2 diabetes followed by intensification with basal insulin (detemir) if glycated hemoglobin (A1C) >= 7%. RESEARCH DESIGN AND METHODS-In 988 participants from North America and Europe uncontrolled on metformin +/- sulfonylurea, sulfonylurea was discontinued and liraglutide 1.8 mg/day added for 12 weeks (run-in). Subsequently, those with A1C >= 7% were randomized 1:1 to 26 weeks' open-label addition of insulin detemir to metformin + liraglunde (n = 162) or continuation without insulin detemir (n = 161). Patients achieving A1C <7% continued unchanged treatment (observational arm). The primary end point was A1C change between randomized groups. RESULTS-Of 821 participants completing the run-in, 61% (n = 498) achieved A1C <7% (mean change -1.3% from 7.7% at start), whereas 39% (n = 323) did not (-0.6% from 8.3% at start). During run-in, 167 of 988 (17%) withdrew; 46% of these due to gastrointestinal adverse events. At week 26, A1C decreased further, by 0.5% (from 7.6% at randomization) with insulin detemir (n = 162) versus 0.02% increase without insulin detemir (n = 157) to 7.1 and 7.5%, respectively (estimated treatment difference -0.52 [95% CI -0.68 to -0.36]; P <0.0001). Forty-three percent of participants with insulin detemir versus 17% without reached A1C <7%. Mean weight decreased by 3.5 kg during run-in, then by 0.16 kg with insulin detemir or 0.95 kg without insulin detemir. In the randomized phase, no major hypoglycemia occurred and minor hypoglycemia rates were 0.286 and 0.029 events per participant-year with and without insulin detemir (9.2 vs. 1.3%). CONCLUSIONS-Supplementation of metformin with liraglutide and then insulin detemir was well tolerated in the majority of patients, with good glycemic control, sustained weight loss, and very low hypoglycemia rate

    Liraglutide and renal outcomes in type 2 diabetes

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    BACKGROUND In a randomized, controlled trial that compared liraglutide, a glucagon-like peptide 1 analogue, with placebo in patients with type 2 diabetes and high cardiovascular risk who were receiving usual care, we found that liraglutide resulted in lower risks of the primary end point (nonfatal myocardial infarction, nonfatal stroke, or death from cardiovascular causes) and death. However, the long-term effects of liraglutide on renal outcomes in patients with type 2 diabetes are unknown. METHODS We report the prespecified secondary renal outcomes of that randomized, controlled trial in which patients were assigned to receive liraglutide or placebo. The secondary renal outcome was a composite of new-onset persistent macroalbuminuria, persistent doubling of the serum creatinine level, end-stage renal disease, or death due to renal disease. The risk of renal outcomes was determined with the use of time-to-event analyses with an intention-to-treat approach. Changes in the estimated glomerular filtration rate and albuminuria were also analyzed. RESULTS A total of 9340 patients underwent randomization, and the median follow-up of the patients was 3.84 years. The renal outcome occurred in fewer participants in the liraglutide group than in the placebo group (268 of 4668 patients vs. 337 of 4672; hazard ratio, 0.78; 95% confidence interval [CI], 0.67 to 0.92; P=0.003). This result was driven primarily by the new onset of persistent macroalbuminuria, which occurred in fewer participants in the liraglutide group than in the placebo group (161 vs. 215 patients; hazard ratio, 0.74; 95% CI, 0.60 to 0.91; P=0.004). The rates of renal adverse events were similar in the liraglutide group and the placebo group (15.1 events and 16.5 events per 1000 patient-years), including the rate of acute kidney injury (7.1 and 6.2 events per 1000 patient-years, respectively). CONCLUSIONS This prespecified secondary analysis shows that, when added to usual care, liraglutide resulted in lower rates of the development and progression of diabetic kidney disease than placebo. (Funded by Novo Nordisk and the National Institutes of Health; LEADER ClinicalTrials.gov number, NCT01179048.
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