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4,359 results for “Insulin”
Effect of acupuncture and metformin on insulin sensitivity in women with polycystic ovary syndrome and insulin resistance: a three-armed randomized controlled trial
<p>STUDY QUESTION</p> <p>Does acupuncture improve insulin sensitivity more effectively than metformin or sham acupuncture in women with polycystic ovary syndrome (PCOS) and insulin resistance (IR)?</p> <p>SUMMARY ANSWER</p> <p>Among women with PCOS and IR, acupuncture was not more effective than metformin or sham acupuncture in improving insulin sensitivity.</p> <p>WHAT IS KNOWN ALREADY</p> <p>Uncontrolled trials have shown that acupuncture improved insulin sensitivity with fewer side effects compared with metformin in women with PCOS and IR. However, data from randomized trials between acupuncture and metformin or sham acupuncture are lacking.</p> <p>STUDY DESIGN, SIZE, DURATION</p> <p>This was a three-armed randomized controlled trial enrolling a total of 342 women with PCOS and IR from three hospitals between November 2015 and February 2018, with a 3-month follow-up until October 2018.</p> <p>PARTICIPANTS/MATERIALS, SETTING, METHODS</p> <p>Women aged from 18 to 40 years with PCOS and homeostasis model assessment of insulin resistance (HOMA-IR) ≥2.14 were randomly assigned (n = 114 per group) to receive true acupuncture plus placebo (true acupuncture), metformin plus sham acupuncture (metformin, 0.5 g three times daily) or sham acupuncture plus placebo (sham acupuncture) for 4 months, with an additional 3-month follow-up. True or sham acupuncture was given three times per week, and 0.5 g metformin or placebo was given three times daily. The primary outcome was change in HOMA-IR from baseline to 4 months after baseline visit. Secondary outcomes included changes in the glucose AUC during an oral glucose tolerance test, BMI and side effects at 4 months after baseline visit.</p> <p>MAIN RESULTS AND THE ROLE OF CHANCE</p> <p>After 4 months of treatment, the changes of HOMA-IR were –0.5 (decreased 14.7%) in the true acupuncture group, –1.0 (decreased 25.0%) in the metformin group and –0.3 (decreased 8.6%) in the sham acupuncture group, when compared with baseline. True acupuncture is not as effective as metformin in improving HOMA-IR at 4 months after baseline visit (difference, 0.6; 95% CI, 0.1–1.1). No significant difference was found in change in HOMA-IR between true and sham acupuncture groups at 4 months after baseline visit (difference, –0.2; 95% CI, –0.7 to 0.3). During the 4 months of treatment, gastrointestinal side effects were more frequent in the metformin group, including diarrhea, nausea, loss of appetite, fatigue, vomiting and stomach discomfort (31.6%, 13.2%, 11.4%, 8.8%, 14.0% and 8.8%, respectively). Bruising was more common in the true acupuncture group (14.9%).</p> <p>LIMITATIONS, REASONS FOR CAUTION</p> <p>This study might have underestimated the sample size in the true acupuncture group with 4 months of treatment to enable detection of statistically significant changes in HOMA-IR with fixed acupuncture (i.e. a non-personalized protocol). Participants who withdrew because of pregnancy did not have further blood tests and this can introduce bias.</p> <p>WIDER IMPLICATIONS OF THE FINDINGS</p> <p>True acupuncture did not improve insulin sensitivity as effectively as metformin in women with PCOS and IR, but it is better than metformin in improving glucose metabolism (which might reduce the risk of type 2 diabetes) and has less side effects. Metformin had a higher incidence of gastrointestinal adverse effects than acupuncture groups, and thus acupuncture might be a non-pharmacological treatment with low risk for women with PCOS. Further studies are needed to evaluate the effect of acupuncture combined with metformin on insulin sensitivity in these women.</p> <p>STUDY FUNDING/COMPETING INTEREST(S)</p> <p>This work was supported by grants 2017A020213004 and 2014A020221060 from the Science and Technology Planning Project of Guangdong Province. The authors have no conflicts of interest.</p> <p>TRIAL REGISTRATION NUMBER</p> <p>Clinicaltrials.gov number: NCT02491333.</p> <p>TRIAL REGISTRATION DATE</p> <p>8 July 2015.</p> <p>DATE OF FIRST PATIENT'S ENROLLMENT</p> <p>11 November 2015.</p>
Supplementary Information - Circulating insulin-like growth factor system adaptations in hibernating brown bears indicate increased tissue IGF availability
<p>Supplementary figures and tables for the manuscript entitled “Circulating insulin-like growth factor system adaptations in hibernating brown bears indicate increased tissue IGF availability”.</p>
Conformational changes in insulin receptor illuminated by live-cell linear dichroism imaging and a FLIP biosensor
<p>Response of GP2(1)-eGFP-CD59, a FLIP biosensor co transfected with insulin receptor against anatgonists and agonists of IR was measured and qunatified using polarization-resolved fluorescence microscopy. Linear dichoirism values were measured by analyinzing cells using already published imageJ macros (Bondar, Rybakova et al. 2021). This data set contains both raw images obtained from polarization micrscopy and analyzed data.</p>
Data from: Low fasting serum insulin and dementia in nondiabetic women followed for 34 years
Objective: A previous study reported a U-shaped association between fasting insulin and dementia in a 5-year follow-up of a male cohort, which was now re-investigated in a representative population of women followed over 34 years, and taking into account the incidence of diabetes. Methods: Fasting values for insulin and glucose were obtained from serum samples in 1212 non-diabetic women aged 38-60 at the 1968 baseline. Risk of dementia was assessed by Cox proportional hazard regression adjusting for insulin, glucose, and other covariates, and, in a second model, after censoring for incident cases of diabetes. Incident diabetes was considered as a third endpoint, for comparison with dementia. Results: Over 34 years, we observed 142 incident cases of dementia. The low tertile of insulin displayed excess risk for dementia, hazard ratio (HR) = 2.34, 95% confidence interval = (1.52, 3.58), compared to the medium tertile, but the high tertile of insulin did not, HR = 1.28 (0.81, 2.03). These associations were also seen for dementia without diabetes comorbidity. In contrast, high but not low insulin predicted incident diabetes (115 cases), HR = 1.70 (1.08, 2.68) and HR = 0.76 (0.43, 1.37), respectively. Conclusions: Our results revealed a non-linear association between fasting serum insulin and dementia in a female population, with high risk at low insulin values that was not attributable to preclinical dementia or impaired insulin secretion. This condition suggests a new pathway to dementia, which differs from the metabolic pathway involving diabetes.
Supplementary data for article: Central insulin modulates dopamine signaling in the human striatum
<p><b>Objective:</b> Activity in the dopaminergic pathways of the brain is highly sensitive to body weight and metabolic states. Animal studies show that dopamine neurons are important targets for the metabolic hormone insulin with abolished effects in the insulin resistant state, leading to increases in body weight and food intake. In humans, the influence of central acting insulin on dopamine and effects of their interplay are still elusive.</p> <p><b>Research Design and Methods:</b> We investigated whether central administered insulin influences dopaminergic activity in striatal regions and whole-brain neural activity. Using a PET/MRI hybrid scanner, we simultaneously performed [<sup>11</sup>C]-raclopride-PET and resting state fMRI in 10 healthy normal weight men after application of intranasal insulin or placebo on two separate days in a randomized, placebo-controlled, blinded, crossover trial.</p> <p><b>Results:</b> In response to central insulin compared to placebo administration, we observed greater [<sup>11</sup>C]-raclopride binding potential (BP<sub>nd</sub>) in the bilateral ventral and dorsal striatum. This suggests an insulin-induced reduction in synaptic dopamine levels. Resting-state striatal activity was lower 15 and 30 min after nasal insulin compared to placebo. Functional connectivity of the mesocorticolimbic circuitry associated with differences in dopamine levels: individuals with a stronger insulin-induced effect on dopamine levels showed a stronger increase in functional connectivity 45 min after intranasal insulin.</p> <p><b>Conclusions</b>: This study indicates that central insulin modulates dopaminergic tone in the striatum, which may affect regional brain activity and connectivity. Our results deepen the understanding of the insulin-dopamine interaction and the complex network that underlies the regulation of whole-body metabolism.</p>
Electrogenetic cellular insulin release for real-time glycemic control in type 1 diabetic mice
<p>Data underlying the figures in the publication “Electrogenetic cellular insulin release for real-time glycemic control in type 1 diabetic mice”, published in <em>Science</em>, <strong>2020</strong>, 368, 993-1001. <a href="https://science.sciencemag.org/content/368/6494/993">https://science.sciencemag.org/content/368/6494/993</a></p> <p>Table of contents:</p> <p><strong>1. Electrogenetics source data file</strong>; File openable with Graphpad Prism containing the source data for the main <em>Figures: 1-4 </em>(Transgene expression by SEAP measurement), <em>5b, 6a, 6f</em> (Insulin by ELISA), <em>5c, 6b, 6e </em>(NanoLuc luciferase), 7c (NanoLuc luciferase in vivo) and <em>7a, 7d</em> (Glycemia).</p> <p><strong>Transgene expression by SEAP measurement</strong></p> <p>Data for main <em>Figures 1, 2, 3, 4</em>.</p> <p>SEAP (human placental secreted alkaline phosphatase) levels were profiled in cell culture supernatants using a colorimetric assay. 100 µL 2x SEAP assay buffer (20 mM homoarginine, 1 mM MgCl2, 21% diethanolamine, pH 9.8) was mixed with 80 µL heat-inactivated (30 min at 65°C) cell culture supernatant. After the addition of 20 µL substrate solution (120 mM p-nitrophenyl phosphate; cat. no. AC128860100, Thermo Fisher Scientific), the absorbance time course was recorded for 45 min at 405 nm and 37°C using a Tecan Genios PRO plate reader (cat. no. P97084; Tecan Group AG, Maennedorf, Switzerland) and the SEAP levels were determined as follows: first, absorbance change over time (slope) was calculated. According to the Beer–Lambert’s law, absorbance is proportional to the concentration of a colored compound and depends on the light path length (d) and extinction coefficient (ε) (ε for p-nitrophenyl (εpNP) = 18.600 M−1 cm−1). Enzymatic activity EA [U/L] was calculated from the equation: EA = slope × dilution factor × εpNP−1 × d−1 </p> <p>Values in the file present determined SEAP levels.</p> <p><strong>Insulin by ELISA</strong></p> <p>Data for <em>Figures 5b, 6a, 6f</em>.</p> <p>Values in the file present Insulin level as determined by ELISA kit. The assay was performed according to manufacturer’s instructions.</p> <p><strong>NanoLuc luciferase </strong></p> <p>Data for <em>Figures 5c, 6b, 6e</em>.</p> <p>NanoLuc® luciferase was quantified in cell culture supernatants using the Nano-Glo® Luciferase Assay System (cat. no. N1110; Promega, Duebendorf, Switzerland). In brief, 7.5 µL of cell culture supernatant was added per well of a black 384-well plate and mixed with 7.5 µL substrate-containing assay buffer. Total luminescence was quantified using a Tecan Genios PRO plate reader (Tecan Group AG).</p> <p>Values in the file present measured luminescence levels.</p> <p><strong>NanoLuc luciferase in vivo </strong></p> <p>Data for <em>Figure 7c.</em></p> <p>Aliquots of 15 µL of whole-blood samples were diluted in 5 μL of 50 mM EDTA and frozen at -20 °C until NanoLuc® quantification as described above.</p> <p>Values in the file present measured luminescence levels normalized to time point 0 (Normalization individually for each mouse).</p> <p><strong>Glycemia </strong></p> <p>Data for <em>Figures 7a, 7d</em>.</p> <p>Blood glucose level was determined using a glucometer (Contour®Next, Bayer Healthcare, Leverkusen, Germany).</p> <p>Values in the file present measured glucose levels.</p> <p><strong>2. Figure 7b</strong>; Data for <em>Figure 7b</em>. File openable with Graphpad Prism.</p> <p>Blood glucose level was determined using a glucometer (Contour®Next, Bayer Healthcare, Leverkusen, Germany).</p> <p>Values in the file present measured glucose levels.</p> <p><strong>3. Figure 6c and 6d</strong>; Excel file with the data for <em>Figures 6c, 6d</em>.</p> <p>NanoLuc® luciferase was quantified in cell culture supernatants using the Nano-Glo® Luciferase Assay System (cat. no. N1110; Promega, Duebendorf, Switzerland). In brief, 7.5 µL of cell culture supernatant was added per well of a black 384-well plate and mixed with 7.5 µL substrate-containing assay buffer. Total luminescence was quantified using a Tecan Genios PRO plate reader (Tecan Group AG).</p> <p>Values in the file present measured luminescence levels.</p>
Intranasal Insulin Treatment Alters Gene Expression Profile in the Hippocampus of Rats with Perinatal Iron Deficiency
<p>Datasets for rat hippocampal RNAseq experiment. </p>
Underlying data for Association between Serum Insulin and Interleukin-6 levels with Breast Cancer in Post-Menopausal Iraqi Women
<p>Underlying data for Association between Serum Insulin and Interleukin-6 levels with Breast Cancer in Post-Menopausal Iraqi Women</p>
Thiazides attenuate insulin secretion through inhibition of mitochondrial carbonic anhydrase 5b in β-islet cells in mice
<p><span><em><strong>Background</strong></em>:</span><span> Thiazides </span><span>are associated with glucose intolerance and new onset diabetes mellitus. Previous studies demonstrated that thiazides attenuate insulin secretion, but the molecular mechanisms remain elusive. We hypothesized that thiazides attenuate insulin secretion via one of the known molecular thiazide targets</span> <span>in β-cells.</span></p> <p><span><em><strong>Methods</strong></em>:</span><span> We performed static insulin secretion experiments with islets of wild-type, NCC (SLC12A3) and NDCBE (SLC4A8) knock-out (KO) mice and with murine Min6 cells with individual knock-down of carbonic anhydrase (CA) isoforms to identify the molecular target of thiazides in </span><span>β-cells</span><span>. CA5b KO mice were then used to assess the role of the putative thiazide target CA5b in </span><span>β-cell </span><span>function and in mediating thiazide sensitivity<em> in vitro</em> and<em> in vivo</em>.</span></p> <p><span><em><strong>Results</strong></em>:</span><span> Thiazides inhibited glucose- and sulfonylurea-stimulated insulin secretion in islets and Min6 cells at pharmacologically relevant concentrations.</span> <span>Inhibition of insulin secretion by thiazides was CO2/HCO3--dependent, not additive to unselective CA inhibition with acetazolamide and independent of extracellular potassium. In contrast, insulin secretion was unaltered in islets of mice lacking the known molecular thiazide targets NCC or NDCBE. CA expression profiling with subsequent knock-down of individual CA isoforms suggested mitochondrial CA5b as molecular target.</span><span> In support of these findings, thiazides significantly attenuated Krebs cycle anaplerosis through reduction of mitochondrial oxaloacetate synthesis</span><span>. </span><span>CA5b KO mice were resistant to thiazide-induced glucose intolerance, and thiazides did not alter insulin secretion in CA5b KO islets. </span></p> <p><span><em><strong>Conclusions</strong></em>:</span><span> In summary, our study reveals that thiazides attenuate insulin secretion via inhibition of the mitochondrial CA5b isoform in </span><span>β</span><span>-cells.</span></p>
Improvement of Insulin self-injection accuracy in patients with diabetes mellitus by a nursing project
<p>Supplementary material of manuscript <strong>Improvement of Insulin self-injection accuracy in patients with diabetes mellitus by a nursing project</strong></p>
Evaluation of Chitosan based orally delivered insulin nanoparticle
<p>Data sets</p> <p>Ethical approval</p> <p>Figures</p> <p> </p>
Fig. 6 in Germacranolide- and guaianolide-type sesquiterpenoids from Achillea alpina L. reduce insulin resistance in palmitic acid-treated HepG2 cells via inhibition of the NLRP3 inflammasome pathway
Fig. 6. The inhibitory effects of 4 on the production of IL-1β and ROS in HepG2-IR cells. The expression levels of IL-1β were measured by ELISA analysis (A), Fluorescence intensity of ROS was recorded by a multimode microplate reader (B). ##P <0.01 vs CON group, *P <0.05, **P <0.01 vs PA treatment group.
Fig. 5 in Germacranolide- and guaianolide-type sesquiterpenoids from Achillea alpina L. reduce insulin resistance in palmitic acid-treated HepG2 cells via inhibition of the NLRP3 inflammasome pathway
Fig. 5. The glucose consumption assay of compounds 4–6, 10 and 11 in different concentrations. The concentrations of these compounds were from 1.56 to 50 μM, ROSI was the positive control. *p <0.05, **p <0.01, compared to the PA treatment group. ##p <0.01, compared to the control (CON) group.
Fig. 7 in Germacranolide- and guaianolide-type sesquiterpenoids from Achillea alpina L. reduce insulin resistance in palmitic acid-treated HepG2 cells via inhibition of the NLRP3 inflammasome pathway
Fig. 7. Inhibitory effects of 4 on the expression of proteins related to NLRP3 inflammasome in PA-induced HepG2-IR cells. Representative protein bands of Western blot (A and B). Densitometric analysis of the Western blot analysis results (C). Glibenclamide (1 μM, Gliben) was a positive control. ##P <0.01 vs CON group, *P <0.05, **P <0.01 vs PA treatment group.
Fig. 6 in Spiroganodermaines A G from Ganoderma species and their activities against insulin resistance and renal fibrosis
Fig. 6. Compounds inhibit renal fibrosis in vitro. (A) NRK-52E cells were treated with 20 μM for 48 h, and cell viability was determined by using the CCK-8 assay. (B, E and F) Compounds at 20 μM affect renal fibrosis-related protein expression. GW788388 was used as a positive control. (C) NRK-52E cells were treated with 5, 10 and 20 μM of ()-7 for 48 h, and cell viability was determined by using the CCK-8 assay. (D, G and H) Compound ()-7 dose-dependently inhibits fibronectin and α-SMA expression. GW788388 was used as a positive control. The results were represented Mean ± SEM. *P <0.05, **P <0.01, ***P <0.001, ****P <0.0001 compared with TGF-β1 alone. #P <0.05 ##P <0.01, ###P <0.001, and ####P <0.0001 compared with DMSO alone.
Fig. 5 in Spiroganodermaines A G from Ganoderma species and their activities against insulin resistance and renal fibrosis
Fig. 5. Attenuation of insulin-induced IR in myotubes. (A) C2C12 cell proliferation in response to compounds at 40 μM by CCK-8 assay. (B) C2C12 were treated with 40 μM for 24 h, and glucose uptake was determined. Metformin (Met) was used as a positive control. (C) Compound (+)-7 improves insulin-stimulated glucose uptake in IR model. (D–F) Expression of p-AKT and p-IRS1 were determined by Western blot. Compound (+)-7 improves attenuated insulin signal pathway disruption in dose-dependent manner. #P <0.05 and ###P <0.001 compared with no-insulin treatment control; *P <0.05 and **P <0.01 compared with insulin treatment alone; $$$P <0.001 and $$$$P <0.0001 compared with insulin treatment control.
Fig. 3 in Stimulation of insulin secretion by 5-methylcoumarins and its sulfur analogues isolated from Clutia lanceolata Forssk
Fig. 3. Effects of test compounds (from Clutia lanceoleta) on the glucose-triggered secretion of insulin from murine islets. Islets were incubated for 1 h at 37 °C in KRB buffer containing glucose (16.7 mM) in the absence (Control) or presence of test compounds and the secreted insulin was measured. Values are mean ± SD from three independent experiments. *P <0.05, **P <0.01, ***P <0.001 compared with the control value.
Fig. 2. X-Ray crystal structures determined for 1,8,9,11,12,14–17,19,20 in Stimulation of insulin secretion by 5-methylcoumarins and its sulfur analogues isolated from Clutia lanceolata Forssk
Fig. 2. X-Ray crystal structures determined for 1,8,9,11,12,14–17,19,20. Atoms are shown as thermal ellipsoids drawn at the 50% probability level.
Fig. 1 in Stimulation of insulin secretion by 5-methylcoumarins and its sulfur analogues isolated from Clutia lanceolata Forssk
Fig. 1. Structures of 5-methylcoumarins isolated from Clutia lanceolata. Compounds 1–13 are undescribed, whereas 14–21 are known but are isolated from this plant for the first time. Also shown is the chemical numbering scheme for the ring and its substituents.
Effect of COX-2 Selective Inhibitors on Postoperative Insulin Resistance After Gastrointestinal Laparoscopic Surgery
ClinicalTrials.gov study NCT01930318. IPD Sharing: Not stated. Countries: 1. Publications: 1.
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