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219 results for “Leptin”
Role of Leptin in the Neuroendocrine and Immune Response to Fasting
ClinicalTrials.gov study NCT00140231. IPD Sharing: UNDECIDED. Countries: 1. Publications: 6.
Combination of Insulin Sensitizer and Leptin as Treatment for the HAART -Induced Metabolic Syndrome
ClinicalTrials.gov study NCT00362440. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Effects of Human Leptin Replacement
ClinicalTrials.gov study NCT00657605. IPD Sharing: NO. Countries: 1. Publications: 13.
Short-term Effects of Leptin in People With Lipodystrophy
ClinicalTrials.gov study NCT01778556. IPD Sharing: Not stated. Countries: 1. Publications: 12.
Data from: KCNB1-Leptin receptor complexes couple electric and endocrine function in the melanocortin neurons of the hypothalamus
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Data from: To eat or not to eat: ontogeny of hypothalamic feeding controls and a role for leptin in modulating life history transition in amphibian tadpoles
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Adipose-derived leptin and complement factor D mediate osteoarthritis severity and pain
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Contrasting association of Leptin receptor polymorphisms and haplotypes with polycystic ovary syndrome in Bahraini and Tunisian women: a case–control study
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The impact of Rhodiola Rosea on biomarkers of diabetes, inflammation, and microbiota in a leptin receptor-knockout mouse model
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Data from: Leptin increases sympathetic nerve activity via induction of its own receptor in the paraventricular nucleus
Whether leptin acts in the paraventricular nucleus (PVN) to increase sympathetic nerve activity (SNA) is unclear, since PVN leptin receptors (LepR) are sparse. We show in rats that PVN leptin slowly increases SNA to muscle and brown adipose tissue, because it induces the expression of its own receptor and synergizes with local glutamatergic neurons. PVN LepR are not expressed in astroglia and rarely in microglia; instead, glutamatergic neurons express LepR, some of which project to a key presympathetic hub, the rostral ventrolateral medulla (RVLM). In PVN slices from mice expressing GCaMP6, leptin excites glutamatergic neurons. LepR are expressed mainly in thyrotropin-releasing hormone (TRH) neurons, some of which project to the RVLM. Injections of TRH into the RVLM and dorsomedial hypothalamus increase SNA, highlighting these nuclei as likely targets. We suggest that this neuropathway becomes important in obesity, in which elevated leptin maintains the hypothalamic pituitary thyroid axis, despite leptin resistance.
Data from: Plasma mammalian leptin analogue predicts reproductive phenology, but not reproductive output in a capital-income breeding seaduck
To invest in energetically demanding life history stages, individuals require a substantial amount of resources. Physiological traits, particularly those related to energetics, can be useful for examining variation in life history decisions and trade-offs because they result from individual responses to environmental variation. Leptin is a protein hormone found in mammals that is proportional to the amount of endogenous fat stores within an individual. Recently, researchers have confirmed that a mammalian leptin analogue (MLA), based on the mammalian sequence of leptin, is present with associated receptors and proteins in avian species, with an inhibitory effect on foraging and body mass gain at high circulating levels. While MLA has been both quantified and manipulated in avian species, little is currently known regarding whether plasma MLA in wild-living species and individuals is associated with key reproductive decisions. We quantified plasma MLA in wild, Arctic-nesting female common eiders (Somateria mollissima) at arrival on the breeding grounds and followed them to determine subsequent breeding propensity, and reproductive phenology, investment, and success. Common eiders are capital-income breeding birds that require the accumulation of substantial fat stores to initiate laying and successfully complete incubation. We found that females with lower plasma MLA initiated breeding earlier and in a shorter period of time. However, we found no links between plasma MLA levels and breeding propensity, clutch size or reproductive success. Although little is still known about plasma MLA, based on the current study and due to its role in influencing foraging behaviours and condition gain, it appears to be closely linked to reproductive timing and is therefore likely to underlie trade-offs surrounding life history decisions.
AgRP neuron cis-regulatory analysis across hunger states reveals that IRF3 mediates leptin's acute effects
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AristaBotha/Buffalo_Tb_leptin: Buffalo body temperature and leptin
<p>Buffalo body temperature and leptin data with fecal chlorophyll and expected body mass added.</p>
Metabolomic Analysis of the Effects of Leptin Replacement Therapy in Patients with Lipodystrophy
<p>Context and Objective </p><p>Leptin treatment has dramatic clinical effects on glucose and lipid metabolism in leptin-deficient patients with lipodystrophy. Further elucidation of metabolic effects of exogenous leptin therapy will shed light on understanding leptin physiology in humans. Our objective was to utilize metabolomic profiling to examine the changes associated with administration of short-term metreleptin therapy in patients with lipodystrophy.</p> Study Design <p>We conducted a pre-post treatment study in 19 patients (75% female) with varying forms of lipodystrophy (congenital generalized lipodystrophy, n=10; acquired generalized lipodystrophy, n=1; familial partial lipodystrophy, n=8) who received daily subcutaneous metreleptin injections for a period of 16 - 23 weeks. A 3-hour oral glucose tolerance test and body composition measurements were conducted before and after the treatment period, and fasting blood samples were used for metabolomic profiling. The study outcome aimed at measuring changes in physiologically relevant metabolites pre- and post- leptin therapy.</p> Results <p>Metabolomic analysis revealed changes in pathways involving branched-chain amino acid metabolism, fatty acid oxidation, protein degradation, urea cycle, tryptophan metabolism, nucleotide catabolism, vitamin E, and steroid metabolism. Fold-changes in pre- to post-treatment metabolite levels indicated increased breakdown of fatty acids, branched chain amino acids proteins, and nucleic acids.</p> Conclusions <p>Leptin replacement therapy has significant effects on important metabolic pathways implicated in patients with lipodystrophy. Continued metabolomic studies may provide further insight into the mechanisms of action of leptin replacement therapy and provide novel biomarkers of lipodystrophy.</p> <p></p>
Hypoxia preconditioned mesenchymal stem cells prevent cardiac fibroblast activation and collagen production via leptin
<p><strong>Aims</strong>: Activation of cardiac fibroblasts into myofibroblasts constitutes a key step in cardiac remodeling after myocardial infarction (MI), due to interstitial fibrosis. Mesenchymal stem cells (MSCs) have been shown to improve post-MI remodeling an effect that is enhanced by hypoxia preconditioning (HPC). Leptin has been shown to promote cardiac fibrosis. The expression of leptin is significantly increased in MSCs after HPC, but it is unknown whether leptin contributes to MSC therapy or the fibrosis process. The objective of this study was to determine whether leptin secreted from MSCs modulates cardiac fibrosis.</p> <p><strong>Methods</strong>: Cardiac fibroblast (CF) activation was induced by hypoxia (0.5% O<sub>2</sub>). The effects of MSCs on fibroblast activation were analyzed by co-culturing MSCs with CFs and detecting the expression of a-SMA, SM22a, and collagen IaI in CFs by western blot, immunofluorescence and Sirius red staining. In vivo MSCs antifibrotic effects on left ventricular remodeling were investigated using an acute MI model involving permanent ligation of the left anterior descending coronary artery.</p> <p><strong>Results</strong>: Co-cultured MSCs decreased fibroblast activation and HPC enhanced the effects. Leptin deficit MSCs from Ob/Ob mice did not decrease fibroblast activation. Consistent with this, H-MSCs significantly inhibited cardiac fibrosis after MI and mediated decreased expression of TGF-b/Smad2 and MRTF-A in CFs. These effects were again absent in leptin-deficient MSCs.</p> <p><strong>Conclusion</strong>: Our data demonstrate that activation of cardiac fibroblast was inhibited by MSCs in a manner that was leptin-dependent. The mechanism may involve blocking TGF-b/Smad2 and MRTF-A signal pathway.</p>
Comparison of Perilipin, Leptin, Adipolipin, Adiponectin, Resistin, Visfatin, Estrone Levels Pre-post Omentectomy
ClinicalTrials.gov study NCT03258307. IPD Sharing: NO. Countries: 1. Publications: 1.
Omega-3 on Lipid Profile and Serum Leptin Level n Neonates With Intrauterine Growth Restriction
ClinicalTrials.gov study NCT05242107. IPD Sharing: YES. Countries: 1. Publications: 1.
Leptin to Treat Lipodystrophy
ClinicalTrials.gov study NCT00005905. IPD Sharing: Not stated. Countries: 1. Publications: 6.
Effect of Vitamin D3 and Omega-3FA on Leptin and HbA1C With Vitamin D Deficiency
ClinicalTrials.gov study NCT03735303. IPD Sharing: YES. Countries: 1. Publications: 1.
Leptin and Cytokines in Diabetic Pregnancy - Physiologic or Pathogenic Role
ClinicalTrials.gov study NCT00334841. IPD Sharing: Not stated. Countries: 1. Publications: 1.
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