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4,359 results for “Insulin”
Differential Proteomic Expression of Equine Cardiac and Lamellar Tissue During Insulin-Induced Laminitis
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Dual GIP and GLP-1 receptor agonist tirzepatide improves beta-cell function and insulin sensitivity in type 2 diabetes
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Data from: An exploratory association analysis of the insulin gene region with diabetes mellitus in two dog breeds
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Data from: Causal link between insulin-like growth factor 1 and growth in nestlings of a wild passerine bird
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Data from: Life in the fat lane: seasonal regulation of insulin sensitivity, food intake, and adipose biology in brown bears
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Supplementary data for article: Central insulin modulates dopamine signaling in the human striatum
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PDX1-/NKX6.1+ progenitors derived from human pluripotent stem cells as a novel source of insulin-secreting cells
<p>PDX1-/NKX6.1+ progenitors derived from hESCs were differentiated to pancreatic beta cell stage where they generated glucose-responsive, insulin-secreting cells. The transcriptome profile of hESC- derived PDX1-/NKX6.1+ progenitors were compared with hPSC-derived PDX1+/NKX6.1+ pancreatic progenitors as described in the article entitled "<strong>PDX1<sup>-</sup>/NKX6.1<sup>+</sup>progenitors derived from human pluripotent stem cells as a novel source of insulin-secreting cells</strong>" by Memon et al. 2020. Furthermore, beta cells derived from PDX1-/NKX6.1+ progenitors (3D-beta) were compared with their own endocrine progenitors at an earlier stage (stage 5, 3D-S5) to map their development. </p> <p>The file name is : Sample name_replicate_sample ID_read direction_001 where:</p> <p>-3D-beta: insulin-expressing cells derived from self-detached, 3D, PDX1-/NKX6.1+ progenitors</p> <p>-3D-S5: endocrine progenitors from stage 5, derived from self-detached, 3D, PDX1-/NKX6.1+ progenitors</p> <p>- RNA-seq data were generated from two biological replicates in most cases.</p> <p>- Read direction: R1 (Forward), R2 (Reverse).</p>
Revisiting peak serum cortisol response to insulin-induced hypoglycemia in children and adolescents
<p>Purpose: To evaluate factors that could potentially affect the hypothalamic-pituitary adrenal (HPA) axis response to insulin-induced hypoglycemia in children without history or symptoms of adrenal insufficiency and to propose a cut-off value to define a normal response in this population. Methods: Exploratory single-centre study involving 78 children that prospectively underwent insulin tolerance test (ITT) for suspected growth hormone (GH) deficiency. Methods: Glucose, cortisol, GH, adrenocorticotropic hormone (ACTH), epinephrine and norepinephrine levels were measured at baseline and after insulin-induced hypoglycemia. Serum cortisol was measured using Access automated immunoassay. Results: Mean (range) basal morning serum cortisol of 8 (2.2-19.5) µg/dL/ 222 (61-542) nmol/L increased after hypoglycemia to 20.5 (14.6-29.5) µg/dL / 570 nmol/L (405 -819) nmol/L. Peak serum cortisol levels of 14.6 µg/dL (405nmol/L) and 15.4 µg/dL (428 nmol/L) corresponded to the 2.5<sup>th</sup> and 5<sup>th</sup> percentiles, respectively. Peak serum cortisol correlated with peak plasma epinephrine (r = 0.367; <em>P</em> = 0.0014) but did not correlate with age, BMI-SD or peak serum GH. Children with intact and abnormal GH responses presented similar mean peak serum cortisol levels (20.0 vs. 20.6 µg/dL / 555 vs. 572 nmol/L; <em>P</em> = 0.21). Conclusion: Our data indicate that the current cut-off to define normal HPA axis response in children after insulin-induced hypoglycemia warrants reevaluation in order to avoid overdiagnosis of adrenal insufficiency. Our results suggest that peak serum cortisol levels ³ 15.4 µg/dL (428 nmol/L) in children undergoing ITT might represent a normal cortisol response to stress, regardless of age, BMI or GH secretory capacity.</p>
Supplementary Materials for Digenic Variants in the FGF21 Signaling Pathway Associated with Severe Insulin Resistance and Pseudoacromegaly
<p>Supplementary Materials for Digenic Variants in the FGF21 Signaling Pathway Associated with Severe Insulin Resistance and Pseudoacromegaly. This includes additional photographs of the proband and family, bone age x-ray, smell identification testing, ERK phosphorylation in HeLa Cells, Candidate genes from research exome, and full plasmid sequences used in the study.</p>
Insulin
<a href="https://spectroscopyhub.com/measurements/e525865a-abe3-4625-a906-4be56e399277">Insulin</a>
Supplementary Tables (Mapping the Associations of the Plasma Lipidome With Insulin Resistance and Response to an Oral Glucose Tolerance Test)
<p><span><b>Context: </b>Insulin resistance (IR) remained a global health challenge. Lipidomics offers a unique opportunity to identify biomarkers; a key step towards understanding mechanisms of IR associated with abnormal lipid metabolism.</span></p> <p class="CxSpMiddle"><span><b>Objective:</b> To determine whether plasma lipid species are associated with indices of insulin resistance and to evaluate the plasma lipidome response to an OGTT. </span></p> <p><span><b>Design and Setting: </b>Community based cross-sectional </span></p> <p><span><b>Participants and sample: </b>Plasma samples (collected at 0 and 120 min during an OGTT) from non-obese, young adults aged between 18-34 years (n = 246) were analysed using liquid chromatography tandem mass spectrometry.</span></p> <p><span><b>Main outcome measures: </b>Using linear models (controlling for age, sex, BMI, total cholesterol, HDL-cholesterol and triglycerides), the associations between indices of insulin resistance and individual lipid species or changes in lipid levels during an OGTT were tested.</span></p> <p><span><b>Results: </b>Some (213) and (199) lipid species associate with HOMA-IR and insulin AUC respectively. Alkylphosphatidylcholine (10), alkenylphosphatidylcholine (23) and alkylphosphatidylethanolamine (6) species were associated with insulin AUC in men only. Species of phosphatidylcholine (7) and sphingomyelin (5) were associated in women only. In response to an oral glucose tolerance test, a perturbation in the plasma lipidome, particularly in acylcarnitine species was observed; and the changes in many lipid species were associated with insulin AUC. </span></p> <p><span><b>Conclusions: </b>The plasma lipidome and changes in lipid levels during an OGTT were associated with indices of insulin resistance. These findings underlie the involvement of molecular lipid species in the pathogenesis of insulin resistance and possibly crosstalk between insulin resistance and sex-specific regulation of lipid metabolism. </span></p>
Data from: Insulin signaling's role in mediating tissue-specific nutritional plasticity and robustness in the horn-polyphenic beetle Onthophagus taurus
Organisms cope with nutritional variation via developmental plasticity, adjusting trait size to nutrient availability for some traits while enabling others to develop in a nutritionally robust manner. Yet, the developmental mechanisms that regulate organ-specific growth across nutritional gradients remain poorly understood. We assessed the functions of members of the insulin/insulin-like signaling pathway (IIS) in the regulation of nutrition sensitivity and robustness in males of the horn-polyphenic beetle Onthophagus taurus, as well as potential regulatory interactions between IIS and two other growth-regulating pathways: Doublesex and Hedgehog signaling. Using RNA interference (RNAi) we experimentally knocked down both insulin receptors (InR1, InR2) and Foxo, a growth inhibitor. We then performed morphometric measurements on horns, a highly nutrition-sensitive trait, and genitalia, a largely nutrition-insensitive trait. Finally, we used qRT-PCR to assess expression levels of Doublesex and the Hedgehog-signaling gene smoothened following IIS-RNAi. Our results suggest that nutrition responsiveness of both traits is regulated by different IIS components, which transduce nutritional conditions to both Doublesex and Hedgehog pathways, albeit via different IIS pathway members. Combined with previous studies our findings suggest that separate origins of trait exaggeration among insect lineages were enabled through the independent cooption of IIS, yet via reliance on different components therein.
Dataset of Insulin sensitizers for improving endocrine metabolism in overweight women with PCOS: a network meta-analysis
<p><span><b>Objective: </b>To evaluate the efficacy of insulin sensitizers on menstrual frequency, sex hormone and metabolic parameters in overweight women with PCOS. </span></p> <p><span><b>Methods:</b> We searched multiple databases from inception to September 2019 for RCTs. Network meta-analysis was conducted using multivariate random effects method. </span></p> <p><span><b>Results:</b> 14 trials reporting on 619 women were included. Compared with metformin, metformin + TZDs was more superior in menstrual recovery (WMD 3.68, 95% CrI 1.65 to 8.20), metformin + GLP-1 receptor agonists was more effective in decreasing AND (WMD -2.53, 95% CrI -3.96 to -1.09), both metformin + GLP-1 receptor agonists (WMD 9.22, 95% CrI 5.46 to 12.98) and metformin + TZDs (WMD 4.30, 95% CrI 0.78 to 7.82) were more effective in increasing SHBG, while TZDs was less effective in decreasing BMI (WMD 1.69, 95% CrI 0.72 to 2.66). Compared with GLP-1 receptor agonists, metformin + GLP-1 receptor agonists was associated with higher SHBG (WMD 7.80, 95% CrI 4.75 to 10.85), lower FT (WMD -1.77, 95% CrI -3.25 to -0.29), lower AND (WMD -2.70, 95% CrI -3.91 to -1.50) and lower FG (WMD -0.41, 95% CrI -0.73 to -0.08).</span></p> <p><span><b>Conclusion: </b>For overweight women with PCOS, both metformin combined with GLP-1 receptor agonists and metformin combined with TZDs appear superior to monotherapy in improving hyperandrogenemia. Metformin combined with TZDs could be particularly effective in promoting the recovery of menstruation. Metformin combined with GLP-1 receptor agonists has additional advantage in improving fasting glucose when compared with GLP-1 receptor agonists alone. TZDs is inferior to metformin in decreasing BMI.</span></p>
Data from: The Drosophila HNF4 nuclear receptor promotes glucose-stimulated insulin secretion and mitochondrial function in adults
Although mutations in HNF4A were identified as the cause of Maturity Onset Diabetes of the Young 1 (MODY1) two decades ago, the mechanisms by which this nuclear receptor regulates glucose homeostasis remain unclear. Here we report that loss of Drosophila HNF4 recapitulates hallmark symptoms of MODY1, including adult-onset hyperglycemia, glucose intolerance and impaired glucose-stimulated insulin secretion (GSIS). These defects are linked to a role for dHNF4 in promoting mitochondrial function as well as the expression of Hex-C, a homolog of the MODY2 gene Glucokinase. dHNF4 is required in the fat body and insulin-producing cells to maintain glucose homeostasis by supporting a developmental switch toward oxidative phosphorylation and GSIS at the transition to adulthood. These findings establish an animal model for MODY1 and define a developmental reprogramming of metabolism to support the energetic needs of the mature animal.
Data from: Perinatal lead (Pb) exposure results in sex-specific effects on food intake, fat, weight, and insulin response across the murine life-course
Developmental lead (Pb) exposure has been associated with lower body weight in human infants and late onset obesity in mice. We determined the association of perinatal Pb exposure in mice with changes in obesity-related phenotypes into adulthood. Mice underwent exposure via maternal drinking water supplemented with 0 (control), 2.1 (low), 16 (medium), or 32 (high) ppm Pb-acetate two weeks prior to mating through lactation. Offspring were phenotyped at ages 3, 6, and 9 months for energy expenditure, spontaneous activity, food intake, body weight, body composition, and at age 10 months for glucose tolerance. Data analyses were stratified by sex and adjusted for litter effects. Exposed females and males exhibited increased energy expenditure as compared to controls (p<0.0001 for both). In females, horizontal activity differed significantly from controls (p = 0.02) over the life-course. Overall, food intake increased in exposed females and males (p<0.0008 and p<0.0001, respectively) with significant linear trends at 9 months in females (p = 0.01) and 6 months in males (p<0.01). Body weight was significantly increased in males at the medium and high exposures (p = 0.001 and p = 0.006). Total body fat differed among exposed females and males (p<0.0001 and p<0.0001, respectively). Insulin response was significantly increased in medium exposure males (p<0.05). Perinatal Pb exposure at blood lead levels between 4.1 µg/dL and 32 µg/dL is associated with increased food intake, body weight, total body fat, energy expenditure, activity, and insulin response in mice. Physiological effects of developmental Pb exposure persist and vary according to sex and age.
Data from: Effects of chronic consumption of sugar-enriched diets on brain metabolism and insulin sensitivity in adult Yucatan Minipigs
Excessive sugar intake might increase the risk to develop eating disorders via an altered reward circuitry, but it remains unknown whether different sugar sources induce different neural effects and whether these effects are dependent from body weight. Therefore, we compared the effects of three high-fat and isocaloric diets varying only in their carbohydrate sources on brain activity of reward-related regions, and assessed whether brain activity is dependent on insulin sensitivity. Twenty-four minipigs underwent 18FDG PET brain imaging following 7-month intake of high-fat diets of which 20% in dry matter weight (36.3% of metabolisable energy) was provided by starch, glucose or fructose (n = 8 per diet). Animals were then subjected to a euglycemic hyperinsulinemic clamp to determine peripheral insulin sensitivity. After a 7-month diet treatment, all groups had substantial increases in body weight (from 36.02±0.85 to 63.33±0.81 kg; P<0.0001), regardless of the diet. All groups presented similar insulin sensitivity index (ISI = 1.39±0.10 mL·min-1·μUI·kg). Compared to starch, chronic exposure to fructose and glucose induced bilateral brain activations, i.e. increased basal cerebral glucose metabolism, in several reward-related brain regions including the anterior and dorsolateral prefrontal cortex, the orbitofrontal cortex, the anterior cingulate cortex, the caudate and putamen. The lack of differences in insulin sensitivity index and body weight suggests that the observed differences in basal brain glucose metabolism are not related to differences in peripheral insulin sensitivity and weight gain. The differences in basal brain metabolism in reward-related brain areas suggest the onset of cerebral functional alterations induced by chronic consumption of dietary sugars. Further studies should explore the underlying mechanisms, such as the availability of intestinal and brain sugar transporter, or the appearance of addictive-like behavioral correlates of these brain functional characteristics.
Data from: Maternal obesity increases insulin resistance, low-grade inflammation and osteochondrosis lesions in foals and yearlings until 18 months of age
Obesity is a growing concern in horses. The effects of maternal obesity on maternal metabolism and low-grade inflammation during pregnancy, as well as offspring growth, metabolism, low-grade inflammation, testicular maturation and osteochondrotic lesions until 18 months of age were investigated. Twenty-four mares were used and separated into two groups at insemination according to body condition score (BCS): Normal (N, n=10, BCS ≤4) and Obese (O, n=14, BCS ≥4.25). BCS and plasma glucose, insulin, triglyceride, urea, non-esterified fatty acid, serum amyloid A (SAA), leptin and adiponectin concentrations were monitored throughout gestation. At 300 days of gestation, a Frequently Sampled Intravenous Glucose Tolerance Test (FSIGT) was performed. After parturition, foals' weight and size were monitored until 18 months of age with plasma SAA, leptin, adiponectin, triiodothyronine (T3), thyroxine (T4) and cortisol concentrations measured at regular intervals. At 6, 12 and 18 months of age, FSIGT and osteoarticular examinations were performed. Males were gelded at one year and expression of genes involved in testicular maturation analysed by RT-qPCR. Throughout the experiment, maternal BCS was higher in O versus N mares. During gestation, plasma urea and adiponectin were decreased and SAA and leptin increased in O versus N mares. O mares were also more insulin resistant than N mares with a higher glucose effectiveness. Postnatally, there was no difference in offspring growth between groups. Nevertheless, SAA plasma concentrations were increased in O versus N foals until 6 months, with O foals being consistently more insulin resistant with a higher glucose effectiveness. At 12 months of age, O foals were significantly more affected by osteochondrosis than N foals. All other parameters were not different between groups. In conclusion, maternal obesity altered metabolism and increased low-grade inflammation in both dams and foals. The risk of developing osteochondrosis at 12 months of age was also higher in foals born to obese dams.
Data from: Cephalic phase of insulin secretion in response to a meal is unrelated to family history of Type 2 diabetes
The pre-absorptive cephalic phase of insulin secretion is elicited during the first ten min of a meal and before glucose levels rise. Its importance for insulin release during the post-absorptive phase has been well documented in animals but its presence or importance in man has become increasingly controversial. We here examined the presence of an early cephalic phase of insulin release in 31 well matched individuals without (n=15) or with (n=16) a known family history of type 2 diabetes (first-degree relatives; FDR). We also examined the potential differences in individuals with or without impaired fasting (IFG) and impaired glucose tolerance (IGT). We here demonstrate that a cephalic phase of insulin secretion was present in all individuals examined and without any differences between control persons and FDR or IFG/IGT. However, the overall importance of the cephalic phase is conjectural since it was unrelated to the subsequent post-absorptive insulin release or glucose tolerance. One of the best predictors of the incremental cephalic phase of insulin release was fasting insulin level and, thus, a relation to degree of insulin sensitivity is likely. In conclusion, an early pre-absorptive and cephalic phase of insulin release is robustly present in man. However, we could not document any relation to family history of Type 2 diabetes nor to the post-absorptive phase and, thus, confirm its importance for subsequent degree of insulin release or glucose tolerance.
Data from: Hyperandrogenism and insulin resistance induce gravid uterine defects in association with mitochondrial dysfunction and aberrant ROS production
Women with polycystic ovary syndrome (PCOS) are at increased risk of miscarriage, which often accompanies the hyperandrogenism and insulin resistance seen in these patients. However, neither the combinatorial interaction between these two PCOS-related etiological factors nor the mechanisms of their actions in the uterus during pregnancy are well understood. We hypothesised that hyperandrogensim and insulin resistance exert a causative role in miscarriage by inducing defects in uterine function that are accompanied by mitochondrial-mediated oxidative stress, inflammation and perturbed gene expression. Here we tested this hypothesis by studying the metabolic, endocrine and uterine abnormalities in pregnant rats after exposure to daily injection of 5α-dihydrotestosterone (DHT, 1.66 mg/kg body weight/day) and/or insulin (6.0 IU/day) from gestational day 7.5 to 13.5. We showed that while DHT-exposed and insulin-exposed pregnant rats presented impaired insulin sensitivity, DHT+insulin-exposed pregnant rats exhibited hyperandrogenism and peripheral insulin resistance, which mirrors pregnant PCOS patients. Compared to controls, hyperandrogenism and insulin resistance in the dam was associated with alterations in uterine morphology and aberrant expression of genes responsible for decidualization (Prl8a2, Fxyd2, and Mt1g), placentation (Fcgr3 and Tpbpa), angiogenesis (Flt1, Angpt1, Angpt2, Ho1, Ccl2, Ccl5, Cxcl9, and Cxcl10) and insulin signaling (Akt, Gsk3 and Gluts). Moreover, we observed changes in uterine mitochondrial function and homeostasis (i.e. mitochondrial DNA copy number and the expression of genes responsible for mitochondrial fusion, fission, biogenesis, and mitophagy) and suppression of both oxidative and antioxidative defenses (i.e. reactive oxygen species, Nrf2 signaling, and interactive networks of antioxidative stress responses) in response to the hyperandrogenism and insulin resistance. These findings demonstrate that hyperandrogenism and insulin resistance induce mitochondria-mediated damage and a resulting imbalance between oxidative and antioxidative stress responses in the gravid uterus.
Data from: Hypoglycemia Following intravenous insulin plus glucose for hyperkalemia in patients with impaired renal function
Background: Hypoglycemia is a serious complication following the administration of insulin for hyperkalemia. We determined the incidence of hypoglycemia and severe hypoglycemia (blood glucose <70 or ≤40 mg/dl, respectively) in a cohort of AKI and non-dialysis dependent CKD patients who received an intravenous infusion of insulin plus glucose to treat hyperkalemia. Methods: We retrospectively reviewed charts of all AKI and non-dialysis dependent CKD patients who received 10 U of insulin plus 50 g glucose to treat hyperkalemia from December 1, 2013 to May 31, 2015 at our Department. Results: One hundred sixty four episodes of hyperkalemia were treated with insulin plus glucose and were eligible for analysis. Serum potassium levels dropped by 1.18 ± 1.01 mmol/l. Eleven treatments (6.1%) resulted in hypoglycemia and two (1.2%) in severe hypoglycemia. A lower pretreatment blood glucose tended to associate with a higher subsequent risk of hypoglycemia. Age, sex, renal function, an established diagnosis of diabetes or previous treatment were not associated with the development of this complication. We did not register any significant adverse events. Conclusion: Our intravenous regimen combining an infusion of insulin plus glucose effectively reduced serum potassium levels compared to previous studies and associated a low risk of symptomatic hypoglycemia and other complications.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
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