Regulation of Appetite and Obesity

The paper identifies a circuit between the insular cortex and central amygdala that promotes overconsumption by suppressing satiety signals through nitric oxide synthase-1 neurons.

The paper shows that central and peripheral GLP-1 systems independently suppress eating, and PPGNTS neuron activation addsitively enhances this effect with GLP-1 agonists.

This study identifies GFRAL-expressing neurons in the hindbrain that suppress food intake through aversive pathways by responding to non-meal-related signals.

This study shows that autophagy in Sf1 neurons of the VMH is essential for metabolic responses to fasting and mitochondrial function.

This study identifies LHAVgat+ GABAergic neurons in mice that encode and potentiate sucrose palatability by modulating licking responses and consumption behavior.

This study identifies distinct roles of TrkB-expressing neurons in the dorsomedial hypothalamus for regulating thermogenesis and feeding through specific neural projections.

The paper shows that AgRP-neuron activation is required for cold-induced hyperphagia in mice.

This study shows that inhibiting mitochondrial fission and iNOS in the dorsal vagal complex reduces body weight and food intake in rats fed a high-fat diet.

This study shows that leptin reduces excitatory input from PPG neurons to PVH GLP-1 receptor neurons, diminishing visceral sensory impact on these neurons.

This study shows that central oxytocin reduces food-seeking behavior and VTA dopamine responses to food cues in male rats, but not postingestive reward value encoding.

This study identifies RIP-Cre25Mgn neurons expressing leptin receptors as critical for leptin's anti-dyslipidemia and glucose-lowering effects in insulin-deficient mice.

This study shows that ghrelin signaling through vagal afferent neurons affects feeding, metabolism, and memory by targeting GHSR on these neurons.

This study introduces gain-of-function MC4R mutations into mice and finds they lead to leaner, shorter phenotypes and improved glucose homeostasis but do not protect against diet-induced obesity and diabetes.

The paper identifies a neural circuit in the nucleus of the solitary tract (NTS) that suppresses feeding by inhibiting AgRP neurons through leucine sensing and leptin-receptor-expressing neurons.

This study shows that MCH signaling in the nucleus accumbens shell promotes feeding in male rats but not females, with estradiol reducing this effect in females.

The paper identifies six distinct neuron clusters in the VMH using single-cell RNA sequencing and shows sex-specific differences in gene expression and function related to energy expenditure.

This study identifies TrkB-expressing paraventricular hypothalamic neurons as key regulators of appetite through multiple neurocircuits, showing their role in suppressing food intake.

The paper identifies a neural circuit mechanism where insula-CeA pathway activation suppresses feeding and develops a model to explain how CeA neurons process inputs to regulate feeding behavior.

This study uses optogenetics to map functional differences in subregions of the rat lateral hypothalamus, finding that tuberal LH promotes food intake but shifts toward self-stimulation with repeated stimulation.

The paper examines age-related differences in brain responses to glucose intake using resting state fMRI, finding frequency-dependent changes in BOLD signal amplitude in specific brain regions.

This study shows that astrocytes in the brainstem dorsal vagal complex regulate food intake by inhibiting appetite through a circuit without causing aversion.

This study finds that nucleus accumbens volume is positively related to BMI in younger individuals but negatively related in older adults, using meta-analysis and UK Biobank data.

This study identifies a bidirectional interaction between hypothalamic nuclei in larval zebrafish that regulates hunger and satiety through opposing activity patterns.

The paper maps genomic and epigenomic features of leptin-responsive hypothalamic neurons and identifies regulatory elements overlapping obesity-associated SNPs.

This study investigates tanycytic leptin receptor expression and function in mice, finding no detectable LepR in tanycytes and no effect of their deletion on hypothalamic leptin signaling.

This study shows ghrelin increases reward prediction error activity and functional connectivity during food odor conditioning in humans, enhancing cue incentive salience and potentially contributing to obesity risk.

The paper identifies β-MSH and desacetyl-MSH as major POMC-derived peptides in human hypothalamic neurons, suggesting their underappreciated role in obesity.

This paper develops a context-induced feeding task to study non-homeostatic feeding in mice and identifies brain regions involved in appetitive conditioning.