Results 61 to 70 of about 31,735 (160)
By assembling cortical‐hypothalamic circuits, we show that cortical input protects hypothalamic neurons from fatty acid‐induced damage, which activates PGC1α to boost mitochondrial function. This reveals a cortico‐hypothalamic axis that defends against metabolic stress.
Mengdan Tao +10 more
wiley +1 more source
Conditional Expression ofPomcin theLepr-Positive Subpopulation of POMC Neurons Is Sufficient for Normal Energy Homeostasis and Metabolism [PDF]
Peptides derived from the proopiomelanocortin (POMC) precursor are critical for the normal regulation of many physiological parameters, and POMC deficiency results in severe obesity and metabolic dysfunction. Conversely, augmentation of central nervous system melanocortin function is a promising therapeutic avenue for obesity and diabetes but is ...
Lam, Daniel D. +5 more
openaire +3 more sources
Summary Background The diagnosis and management of pituitary pars intermedia dysfunction (PPID) in horses includes evaluating abnormal plasma concentrations of adrenocorticotrophic hormone (ACTH). Treatment commonly includes the oral dopamine agonist pergolide mesylate, which suppresses the pathologic overproduction of ACTH.
A. Bracken +5 more
wiley +1 more source
Ire1α in Pomc Neurons Is Required for Thermogenesis and Glycemia [PDF]
Whether neuronal inositol-requiring enzyme 1 (Ire1) is required for the proper regulation of energy balance and glucose homeostasis is unclear. We found that pro-opiomelanocortin (Pomc)–specific deficiency of Ire1α accelerated diet-induced obesity concomitant with a decrease in energy expenditure.
Ting, Yao +19 more
openaire +2 more sources
Summary: Mechanistic studies in rodents evidenced synaptic remodeling in neuronal circuits that control food intake. However, the physiological relevance of this process is not well defined.
Danaé Nuzzaci +19 more
doaj +1 more source
Toll Like Receptor 4: A Potential Link Between Obesity and Metabolic Diseases
ABSTRACT Epidemiological evidence shows that obesity increases the risk of developing metabolic diseases. Nevertheless, the mechanisms behind this connection remain underappreciated. The substantial impact of these disorders on global health has led to extensive research efforts aimed at identifying the pathophysiological links between them.
Ghadeer Alhamar +4 more
wiley +1 more source
Innovations in Obesity Treatment: Beyond Adipose Tissue Dysfunction
Obesity drives chronic inflammation, insulin resistance, type 2 diabetes, and cancer development through adipocyte dysfunction. Addressing this multisystemic disorder requires integrated strategies beyond diet and exercise, such as thermogenesis activation via menthol or capsinoids and appetite control through GLP‐1/GIP agonists and neuromodulation to ...
Jesica Martínez‐Godfrey +7 more
wiley +1 more source
TRPC1/5-CaV3 Complex Mediates Leptin-Induced Excitability in Hypothalamic Neurons
Leptin regulates hypothalamic POMC+ (pro-opiomelanocortin) neurons by inducing TRPC (Transient Receptor Potential Cation) channel-mediate membrane depolarization.
Paula P. Perissinotti +2 more
doaj +1 more source
Setmelanotide in Bardet‐Biedl Syndrome: A Case Report
ABSTRACT Setmelanotide is a melanocortin‐4‐receptor agonist used for the treatment of hyperphagia in the genetic obesity syndrome Bardet‐Biedl. Presented is a case of diffuse hyperpigmentation in a patient treated with setmelanotide, which represents the most common side effect of this medication.
Shelby Smith +2 more
wiley +1 more source
Abstract figure legend Mitochondria are highly dynamic organelles that continuously remodel their architecture through coordinated cycles of fusion and fission. This review examines the four key GTPases that orchestrate mitochondrial dynamics in mammals: MFN1, MFN2, OPA1, and DRP1.
Rémi Chaney +4 more
wiley +1 more source

