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31.
Nazarii Kobyliak Tetyana Falalyeyeva Galyna Mykhalchyshyn Dmytro Kyriienko Iuliia Komissarenko 《Diabetes & Metabolic Syndrome: Clinical Research & Reviews》2018,12(5):617-624
Background
Probiotics have beneficial effect on obesity related disorders in animal models. Despite a large number of animal data, randomized placebo-controlled trials (RCT) concluded that probiotics have a moderate effect on glycemic control-related parameters. However, effect of probiotics on insulin resistance are inconsistent.Aim
In a double-blind single center RCT, effect of alive multistrain probiotic vs. placebo on insulin resistance in type 2 diabetes patient were assessed.Methods
A total of 53 patients met the criteria for inclusion. They were randomly assigned to receive multiprobiotic “Symbiter” (concentrated biomass of 14 probiotic bacteria genera Bifidobacterium, Lactobacillus, Lactococcus, Propionibacterium) or placebo for 8-weeks administered as a sachet formulation. The primary main outcome was the change HOMA-IR (homeostasis model assessment-estimated insulin resistance) which calculated using Matthews et al.’s equation. Secondary outcomes were the changes in glycemic control-related parameters, anthropomorphic variables and cytokines.Results
Supplementation with alive multiprobiotic for 8 weeks was associated with significant reduction of HOMA-IR from 6.85?±?0.76 to 5.13?±?0.49 (p?=?0.047), but remained static in the placebo group. With respect to our secondary outcomes, HbA1c insignificant decreased by 0.09% (p?=?0.383) and 0.24% (p?=?0.068) respectively in placebo and probiotics groups. However, in probiotic responders (n?=?22, patient with decrease in HOMA-IR) after supplementation a significant reduction in HbA1c by 0.39% (p?=?0.022) as compared to non-responders was observed. In addition, from markers of chronic systemic inflammatory state only TNF-α and IL-1β changes significantly after treatment with probiotics.Conclusion
Probiotic therapies modestly improved insulin resistance in patients with type 2 diabetes. 相似文献32.
Xie X Van Deusen AL Vitko I Babu DA Davies LA Huynh N Cheng H Yang N Barrett PQ Perez-Reyes E 《Assay and drug development technologies》2007,5(2):191-203
T-type Ca(2+) channels encoded by voltage-gated Ca(2+) channel (Ca(v)) 3.1, 3.2, and 3.3 genes play important physiological roles and serve as therapeutic targets for neurological and cardiovascular disorders. Currently there is no selective T-channel blocker. To screen for such a blocker, we developed three stable cell lines expressing human recombinant Ca(v)3.1, 3.2, or 3.3 channels and then examined their usefulness in high throughput screens. All three cell lines displayed an increase in intracellular Ca(2+) in response to changes in extracellular Ca(2+) as detected with Ca(2+)-sensitive dyes using a fluorometric imaging plate reader (FLIPR [Molecular Devices, Sunnyvale, CA] or FlexStation [Molecular Devices]). The signal-to-noise ratio was 2-4. Co-expression of Ca(v)3.2 with a mouse leak K(+) channel, which by virtue of being open at rest hyperpolarizes the cell membrane, blocked the fluorescent signal. Co-addition of KCl to these cells induced a Ca(2+) signal that was similar to that observed in the cell line expressing Ca(v)3.2 alone. These results confirm that the detection of intracellular Ca(2+) increase in cells expressing Ca(v)3.2 alone results from Ca(2+) entry through channels that are open at the resting membrane potential of each cell line (i.e., window currents). Testing known drugs on Ca(v)3 channels showed that block could be reliably detected using the FlexStation assay, FLIPR assay, or voltage clamp recordings using the IonWorks HT system (Molecular Devices). These results support the use of the FLIPR window current assay for primary drug screening and high throughput patch recordings for secondary screening of novel T-channel blockers. 相似文献
33.
Kiselyov A Balakin KV Tkachenko SE Savchuk NP 《Mini reviews in medicinal chemistry》2006,6(6):711-717
The majority of marketed and late stage development kinase inhibitors are reported to be ATP-competitive. As a result, many promising drug candidates display non-specific activity that results in undesired physiological effects. There is growing interest towards non-ATP competitive kinase inhibitors, as they are expected to yield highly specific and efficacious molecules devoid of non-mechanistic toxicity. Recent developments in this area are summarized in our review. 相似文献
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Isabel Viola Wagner Iuliia Savchuk Lena Sahlin Alexandra Kulle Nora Klting Arne Dietrich Paul-Martin Holterhus Jrg Dtsch Matthias Blüher Olle Sder 《Obesity facts》2022,15(2):281
IntroductionObesity in women is often associated with hyperandrogenism, but the role of adipose tissue (AT) in androgen synthesis remains unclear. Therefore, we studied whether AT could be a source of androgens promoting hyperandrogenism.MethodsSubcutaneous and visceral (visc) AT was collected from lean and obese women. Androgen levels were evaluated in serum, AT, and cell-culture supernatant. Gene and protein expression of steroidogenic enzymes were determined.ResultsObese subjects had elevated serum androgen levels, which reduced after weight loss. Androgens were measurable in AT and in cell-culture supernatants of adipocytes. Steroids were higher in AT from obese women, with the highest difference for testosterone in visc AT (+7.9-fold, p = 0.032). Steroidogenic enzymes were expressed in human AT with depot-specific differences. Obese women showed a significantly higher expression of genes of the backdoor pathway and of CYP19 in visc AT.ConclusionThe whole steroidogenic machinery of the classical and backdoor pathways of steroidogenesis, and the capacity for androgen biosynthesis, were found in both AT depots and cultured adipocytes. Therefore, we hypothesize that AT is a de novo site of androgen production and the backdoor pathway of steroidogenesis might be a new pathomechanism for hyperandrogenism in women with obesity. 相似文献
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