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4,359 results for “Insulin”
Reduced gray matter volume in the default-mode network associated with insulin resistance
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Data from: Complex evolution of insect insulin receptors and homologous decoy receptors, and functional significance of their multiplicity
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Data from: ApoA-I protects pancreatic β-cells from cholesterol-induced mitochondrial damage and restores their ability to secrete insulin
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Insulin sensitivity in mesolimbic pathways predicts and improves with weight loss in older dieters
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Data from: A clinal polymorphism in the insulin signaling transcription factor foxo contributes to life-history adaptation in Drosophila
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Data from: Compensatory growth is accompanied by changes in insulin-like growth factor-1 but not markers of cellular aging in a long-lived seabird
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Yogurt supplementation attenuates insulin resistance in obese mice by reducing metabolic endotoxemia and inflammation
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Weight loss, insulin resistance, and study design confound results in a meta-analysis of animal models of fatty liver
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Supplemental data for: Daily rhythms of glucose, insulin and nonesterified fatty acid responses to an intravenous glucose tolerance test in dairy cows
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Assessing the evolutionary lability of insulin signaling in the regulation of nutritional plasticity across traits and species of horned dung beetles
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Numeric data from: Non-autonomous insulin signaling delays mitotic progression in C. elegans germline stem and progenitor cells
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Insulin infusion is linked to increased NPPC expression in muscle and plasma C-type natriuretic peptide levels in dogs
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Interleukin-6 response to insulin-induced hypoglycemia is associated with hypothalamic-pituitary-adrenal axis activation
<p>Raw data (excel table) concerning 23 patients who underwnt ITT for evaluation of IL-6 and counter-regulatory responses </p>
Supplemental Materials: Identification of proteins associated with the early restoration of insulin sensitivity after biliopancreatic diversion
<p><b>ABSTRACT</b></p> <p><b>CONTEXT:</b> Insulin resistance (IR) is a risk factor for type 2 diabetes, diabetic kidney disease, cardiovascular disease and non-alcoholic steatohepatitis. Biliopancreatic diversion (BPD) is the most effective form of bariatric surgery for improving insulin sensitivity.</p> <p><b>OBJECTIVE:</b> To identify plasma proteins correlating with the early restoration of insulin sensitivity after BPD.</p> <p><b>DESIGN: </b>Prospective single centre study including twenty insulin resistant men with morbid obesity scheduled for BPD. Patient characteristics and blood samples were repeatedly collected from baseline up to four weeks post-surgery. IR was assessed by HOMA-IR, Matsuda Index and by studying metabolic profiles during meal tolerance tests. Unbiased proteomic analysis was performed to identify plasma proteins altered by BPD. Detailed plasma profiles were made on a selected set of proteins by targeted multiple reaction monitoring mass spectrometry (MRM/MS). Changes in plasma proteome were evaluated in relation to metabolic and inflammatory changes.</p> <p><b>RESULTS</b>: BPD resulted in improved insulin sensitivity and reduced body weight. Proteomic analysis identified 29 proteins changed following BPD. Changes in plasma levels of afamin, apolipoprotein A-IV (ApoA4) and apolipoprotein A-II (ApoA2) correlated significantly with changes in IR.</p> <p><b>CONCLUSION:</b> Circulating levels of afamin, ApoA4 and ApoA2 were associated with and may contribute to the rapid improvement in insulin sensitivity after BPD.</p>
Dual GIP and GLP-1 receptor agonist tirzepatide improves beta-cell function and insulin sensitivity in type 2 diabetes
<p><span><b>Context:</b> Novel dual GIP and GLP-1 receptor agonist (RA) tirzepatide demonstrated substantially greater glucose control and weight loss (WL) compared with selective GLP-1RA dulaglutide.</span></p> <p><span><b>Objective:</b> Explore mechanisms of glucose control by tirzepatide. </span></p> <p><span><b>Design:</b> <i>Post-hoc</i> analyses of fasting biomarkers and multiple linear regression analysis.</span></p> <p><span><b>Setting:</b> 47 sites in 4 countries.</span></p> <p><span><b>Patients or Other Participants:</b> 316 subjects with Type 2 diabetes.</span></p> <p><span><b>Interventions:</b> Tirzepatide (1, 5, 10, 15 mg), dulaglutide (1.5 mg), placebo. </span></p> <p><span><b>Main Outcome Measures:</b> Analyze biomarkers of beta-cell function and insulin resistance (IR) and evaluate WL contributions to IR improvements at 26 weeks. </span></p> <p><span><b>Results:</b> HOMA2-B significantly increased with dulaglutide and tirzepatide 5, 10, and 15 mg compared with placebo (p<u><</u>0.02). Proinsulin/insulin and proinsulin/C-peptide ratios significantly decreased with tirzepatide 10 and 15 mg compared with placebo and dulaglutide (p<u><</u>0.007). Tirzepatide 10 and 15 mg significantly decreased fasting insulin (p<u><</u>0.033) and tirzepatide 10 mg significantly decreased HOMA2-IR (p=0.004) compared with placebo and dulaglutide. Markers of improved insulin sensitivity (IS) adiponectin, IGFBP-1, and IGFBP-2 significantly increased by one or more doses of tirzepatide (p<0.05). To determine whether improvements in IR were directly attributable to WL, multiple linear regression analysis with potential confounding variables age, sex, metformin, triglycerides, and HbA1c was conducted. WL significantly (p<u><</u>0.028) explained only 13% and 21% of improvement in HOMA2-IR with tirzepatide 10 and 15 mg, respectively. </span></p> <p><span><b>Conclusions:</b> Tirzepatide improved markers of IS and beta-cell function to a greater extent than dulaglutide. IS effects of tirzepatide were only partly attributable to WL, suggesting dual receptor agonism confers distinct mechanisms of glycemic control.</span></p>
Differential Proteomic Expression of Equine Cardiac and Lamellar Tissue During Insulin-Induced Laminitis
<p><span><span>Endocrinopathic laminitis is pathologically similar to the multi-organ dysfunction and peripheral neuropathy found in human patients with metabolic syndrome. Similarly, endocrinopathic laminitis has been shown to partially result from vascular dysfunction. However, despite extensive research, the pathogenesis of this disease is not well elucidated and laminitis remains without an effective treatment. Here, we sought to identify novel proteins and pathways underlying the development of equine endocrinopathic laminitis. Healthy Standardbred horses (n=4/group) were either given an electrolyte infusion, or a 48-hour euglycemic-hyperinsulinemic clamp. Cardiac and lamellar tissues were analyzed by mass spectrometry (FDR=0.05). All hyperinsulinemic horses developed laminitis despite being previously healthy. We identified 538 and 737 unique proteins in the cardiac and lamellar proteomes, respectively. In the lamellar tissue, we identified 14 proteins which were significantly upregulated and 13 proteins which were significantly downregulated in the hyperinsulinemic group as compared to controls. These results were confirmed via real-time reverse-transcriptase PCR. A STRING analysis of protein-protein interactions revealed that these upregulated proteins were primarily involved in coagulation and complement cascades, platelet activity, and ribosomal function, while downregulated proteins were involved in focal adhesions, spliceosomes, and cell-cell matrices. Novel significant differentially expressed proteins associated with hyperinsulinemia-induced laminitis include talin -1, vinculin, cadherin-13, fibrinogen, alpha-2-macroglobulin, and heat shock protein 90. In contrast, no proteins were found to be significantly differentially expressed in the heart of hyperinsulinemic horses compared to controls. Together,</span> <span>these data indicate that while hyperinsulinemia induced, in part, microvascular damage, complement activation, and ribosomal dysfunction in the lamellae, but a similar effect was not seen in the heart. In brief, this proteomic investigation of a unique equine model of hyperinsulinemia identified novel proteins and signaling pathways, which may lead to the discovery of molecular biomarkers and/or therapeutic targets for endocrinopathic laminitis.</span></span></p>
Data from: Insulin-like growth factor 1 and life-history evolution of passerine birds
1. Natural selection has generated a diversity of ways in which vertebrates allocate their resources between fundamental life-history traits. The availability of possible evolutionary trajectories of these traits is limited by various genetic, physiological, and phylogenetic constraints. This causes trade-offs due to shared resource pools for, or genetic linkage of, competing traits. The majority of these trade-offs are mediated by hormones and create the variability of phenotypes that can be observed in nature. 2. Insulin-like growth factor 1 (IGF-1) is an evolutionarily conserved peptide, which has been shown to be essential in the regulation of body size, the pattern of reproductive investment and lifespan across a broad taxonomic range of model species in laboratory and domesticated conditions. However, studies addressing corresponding evolutionary hypotheses on a broader scale and in free-living vertebrates are very rare. 3. In this phylogenetic comparative study on free-living passerines (Passeriformes), we explore the way in which plasma IGF-1 levels underlie the evolution of body size and demographic fitness correlates (clutch size, egg weight, lifespan). 4. We showed firstly that IGF-1 levels were positively associated with the body size of passerines, although smaller birds had larger IGF-1-mediated investment into building up their body faster. IGF-1 levels were negatively associated with lifespan of passerines, and more so in birds with smaller body weight. Finally, IGF-1 levels were negatively associated with clutch size in heavier species, and positively associated with egg weight in species with higher body weight and longer duration of parental care. The pattern was opposite in species with smaller body weight and shorter duration of parental care. 5. The described evolutionary framework indicates that variation in IGF-1 levels can be regarded as an important mechanism that may underlie life-history evolution in passerines. IGF-1 could act as a physiological link mediating the inter-regulatory growth–reproduction–lifespan "life-history triangle" on the pace-of-life continuum. Interestingly, body weight and investment into parental care have likely imposed a constraining effect on the IGF-1-mediated co-evolution of demographic fitness traits, such as lifespan or reproductive investment. This has limited the availability of adaptive pathways via which those traits could evolve as passerines diversified.
Fig. 5. C2C12 in Insulin-mimetic activity of 23-glycosyl oleanane triterpenoids isolated from Gymnema latifolium
Fig. 5. C2C12 myotube cells were exposed to compounds 2 and 4 (5 μM and 20 μM, respectively) and incubated for 1 h. The phosphorylation of the protein AMPK in the cells was assessed by Western blot analysis. Fold expression was calculated as p-AMPK/AMPK and normalized to the protein level of β-actin. Values are expressed as the mean ± SD (n = 3).
Fig. 2. Key 1H–1H in Insulin-mimetic activity of 23-glycosyl oleanane triterpenoids isolated from Gymnema latifolium
Fig. 2. Key 1H–1H COSY (bold) and HMBC (1H → 13C, green arrows) correlations for compounds 1, 2, 5, and 7. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 4 in Insulin-mimetic activity of 23-glycosyl oleanane triterpenoids isolated from Gymnema latifolium
Fig. 4. Stimulatory effects of compounds 1⎯9 on glucose uptake in 3T3-L1 adipocytes using the fluorescent glucose derivative 2-NBDG. (A) Differentiated adipocytes were treated with isolated compounds (1–9) at a concentration of 20 μM and insulin (100 nM) as a positive control. After 1 h of incubation with or without 2-NBDG, images were captured by fluorescence microscopy. (B) The fluorescence signal in the adipocytes was measured and analyzed. After the cells were incubated for 1 h with or without 2-NBDG, the fluorescence signals were measured at Ex/Em = 450/535 nm. The results are presented as the mean ± SD (n = 3) of experiments performed in triplicate; *p <0.05, **p <0.01, and ***p <0.001, compared to the vehicle group. (C) Differentiated 3T3-L1 adipocytes were treated with compounds 2 and 4 at concentrations of 1, 5, and 20 μM or insulin at 100 nM. After 1 h of incubation, the fluorescence intensities were measured using a fluorescence microscope. (D) The concentration–response effects on glucose uptake in 3T3-L1 adipocytes. Cells were exposed to compounds at various concentrations (5, 10, and 20 μM) and incubated for 1 h. The cells were lysed, and the fluorescence signals were measured at Ex/Em =450/535 nm. Data are expressed as the mean ±SD (n =3) of experiments performed in triplicate; *p <0.05, **p <0.01, and ***p <0.001, compared to the negative control.
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
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