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Journal of Neuroscience, ISSN 0270-6474, 11/2008, Volume 28, Issue 46, pp. 12107 - 12119
Recent studies in adult and weanling rats show that dietary fat, in close association with circulating lipids, can stimulate expression of hypothalamic... 
Lipids | Maternal high-fat diet | Hypothalamus | Food intake | Orexigenic peptides | Neurogenesis | orexigenic peptides | lipids | EMBRYONIC-DEVELOPMENT | LEPTIN RECEPTOR ISOFORMS | CELL GENERATION | DOPAMINERGIC-NEURONS | DIABETIC MOTHER RATS | NEUROSCIENCES | NEUROPEPTIDE-Y | CIRCULATING TRIGLYCERIDES | PARAVENTRICULAR NUCLEUS | MESSENGER-RNA | maternal high-fat diet | neurogenesis | hypothalamus | food intake | Dietary Fats - metabolism | Cell Proliferation | Fetal Nutrition Disorders - metabolism | Male | Intracellular Signaling Peptides and Proteins - metabolism | Melanins - metabolism | Galanin - metabolism | Pituitary Hormones - metabolism | Female | Obesity - etiology | Neurons - metabolism | Animals, Newborn | Dietary Fats - adverse effects | Hyperphagia - etiology | Orexins | Rats | Neuropeptides - metabolism | Obesity - physiopathology | Prenatal Exposure Delayed Effects - physiopathology | Hyperphagia - metabolism | Hypothalamus - physiopathology | Opioid Peptides - metabolism | Rats, Sprague-Dawley | Prenatal Exposure Delayed Effects - metabolism | Obesity - metabolism | Pregnancy | Animals | Hypothalamus - metabolism | Hypothalamic Hormones - metabolism | Neurogenesis - physiology | Hyperphagia - physiopathology | Appetite Regulation - physiology | Body Weight - physiology | Fetal Nutrition Disorders - physiopathology
Journal Article
Nature, ISSN 0028-0836, 04/2018, Volume 556, Issue 7702, pp. 505 - 509
Leptin, a hormone produced in white adipose tissue, acts in the brain to communicate fuel status, suppress appetite following a meal, promote energy... 
POMC NEURONS | SYSTEM | OBESITY | METABOLISM | MULTIDISCIPLINARY SCIENCES | INSULIN-SECRETION | MOUSE | MICE | AGRP NEURONS | ARCUATE NUCLEUS | SUPPRESSION | Satiety Response | Body Weight | Receptors, Leptin - genetics | Leptin - metabolism | Diabetes Mellitus, Experimental - genetics | Homeostasis | Male | Neural Pathways - physiology | Obesity - genetics | Potassium Channels - metabolism | Female | Neurons - metabolism | GABAergic Neurons - metabolism | Diabetes Mellitus, Experimental - metabolism | Eating | Agouti-Related Protein - metabolism | Gene Editing | Obesity - metabolism | Hyperglycemia - metabolism | Receptors, Leptin - deficiency | Animals | Energy Metabolism | Hyperphagia - physiopathology | Presynaptic Terminals - metabolism | Mice | Receptors, Leptin - metabolism | Blood Glucose - metabolism | Glucose metabolism | Energy metabolism | Neural circuitry | Bioenergetics | Leptin | Physiological aspects | Genetic aspects | Gene expression | Observations | Potentiation | Brain | Adipose tissue | Circuits | Streptozocin | Proopiomelanocortin | Genomes | Glucose | Hypothalamus | Receptors | Hyperglycemia | γ-Aminobutyric acid | Replicating | Clonal deletion | Energy | Rodents | Deletion | Inhibition | Hyperphagia | Appetite | CRISPR | Obesity | Phenotypes | Neurons | Therapeutic applications | Diabetes mellitus | Energy expenditure | Potassium channels | Ablation | Insulin | Molecular chains | Energy balance | Weight control | Neural networks | Diabetes | Potassium | Neurotransmission | Metabolic disorders | KATP | blood glucose | fuel metabolism | GABA | AgRP | leptin | and diabetes | obesity
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 9/2014, Volume 111, Issue 36, pp. 13193 - 13198
Journal Article
International journal of obesity, ISSN 0307-0565
Journal
PLoS ONE, ISSN 1932-6203, 05/2016, Volume 11, Issue 5, p. e0155108
Background The regulation of microRNAs (miRNAs) at different stages of the progression of type 2 diabetes mellitus (T2DM) and their role in glucose homeostasis... 
OFFSPRING HYPERPHAGIA | MITOCHONDRIAL BIOGENESIS | PHOSPHORYLATION | INSULIN-RESISTANCE | MULTIDISCIPLINARY SCIENCES | GLYCOGEN-SYNTHASE KINASE-3 | DISEASE | RATS | LEADS | ADIPOSITY | DIET-INDUCED OBESITY | Prediabetic State - metabolism | Prediabetic State - genetics | Diabetes Mellitus, Type 2 - genetics | Humans | Diet, High-Fat - adverse effects | Male | MicroRNAs - metabolism | Muscle, Skeletal - metabolism | Diabetes Mellitus, Type 2 - metabolism | Proto-Oncogene Proteins c-akt - genetics | Myoblasts - metabolism | Glycogen - metabolism | Female | Prediabetic State - pathology | Prediabetic State - etiology | Proto-Oncogene Proteins c-akt - metabolism | Disease Models, Animal | Cell Line | Signal Transduction | Mice, Inbred C57BL | Gene Expression Regulation | Insulin Resistance | Oxidative Phosphorylation | Rats | Mitochondria - metabolism | Glycogen Synthase Kinase 3 - metabolism | Myoblasts - pathology | Rats, Sprague-Dawley | Insulin - metabolism | Animals | Glycogen Synthase Kinase 3 - genetics | Glucose - metabolism | MicroRNAs - genetics | Diabetes Mellitus, Type 2 - pathology | Muscle, Skeletal - pathology | Type 2 diabetes | Glucose metabolism | Complications and side effects | MicroRNA | Genetic aspects | Research | Comparative analysis | Diabetes therapy | Heart | Plasma | Phosphorylation | Sucrose | Homeostasis | AKT protein | Biosynthesis | Glucose | High fat diet | Proteins | Mitochondria | Control | Rodents | Oxidation | Diabetes mellitus (non-insulin dependent) | Medical research | Obesity | Glycogen | Diabetes mellitus | MiRNA | Muscles | Metabolism | Gene expression | Insulin | Patients | Skeletal muscle | Pregnancy | Musculoskeletal system | Progeny | Offspring | Oxidative phosphorylation | Ribonucleic acids | Biopsy | MicroRNAs | Glycolysis | Insulin resistance | Diabetes | Lactic acid | Laboratory animals
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 05/2016, Volume 291, Issue 21, pp. 11124 - 11132
Journal Article
Cell Metabolism, ISSN 1550-4131, 05/2016, Volume 23, Issue 5, pp. 821 - 836
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 01/2017, Volume 127, Issue 1, pp. 293 - 305
Prader-Willi syndrome (PWS) is caused by a loss of paternally expressed genes in an imprinted region of chromosome 15q. Among the canonical PWS phenotypes are... 
MEDICINE, RESEARCH & EXPERIMENTAL | PLASMA GHRELIN | BODY-WEIGHT | HORMONE-RELEASING-HORMONE | HYPERPHAGIA | FOOD-INTAKE | PROPROTEIN CONVERTASE-1 | ONSET OBESITY | KNOCKOUT MICE | CIRCULATING GHRELIN LEVELS | CHILDREN | Diabetes Mellitus - pathology | Neurons - pathology | Proinsulin - metabolism | Diabetes Mellitus - genetics | Humans | Male | Obesity - genetics | RNA, Small Nucleolar - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Hypogonadism - metabolism | Prader-Willi Syndrome - genetics | Female | Neurons - metabolism | Induced Pluripotent Stem Cells - metabolism | Hypogonadism - pathology | Induced Pluripotent Stem Cells - pathology | Basic Helix-Loop-Helix Transcription Factors - genetics | Protein Precursors - genetics | Diabetes Mellitus - metabolism | Proinsulin - genetics | Prader-Willi Syndrome - metabolism | Growth Hormone-Releasing Hormone - genetics | Hyperphagia - metabolism | Proprotein Convertase 1 - deficiency | RNA, Small Nucleolar - genetics | Mice, Knockout | Obesity - metabolism | Obesity - pathology | Protein Precursors - metabolism | Hyperphagia - genetics | Hyperphagia - pathology | Hypogonadism - genetics | Growth Hormone-Releasing Hormone - metabolism | Animals | Prader-Willi Syndrome - pathology | Prader-Willi syndrome | Gene expression | Neurons | Analysis | Risk factors | Proteins | Enzymes | Plasma | Obesity | Rodents | Fibroblasts | Patients | Binding sites
Journal Article
Cell Metabolism, ISSN 1550-4131, 07/2017, Volume 26, Issue 1, pp. 185 - 197.e3
Journal Article
Nature Communications, ISSN 2041-1723, 04/2015, Volume 6, Issue 1, p. 6794
Journal Article