- Regulation of Appetite and Obesity
- Adipose Tissue and Metabolism
- Biochemical Analysis and Sensing Techniques
- Circadian rhythm and melatonin
- Sleep and Wakefulness Research
- Estrogen and related hormone effects
- Neuropeptides and Animal Physiology
- Adipokines, Inflammation, and Metabolic Diseases
- Receptor Mechanisms and Signaling
- Stress Responses and Cortisol
- Hypothalamic control of reproductive hormones
- Dietary Effects on Health
- Neuroendocrine regulation and behavior
- Diet and metabolism studies
- Pancreatic function and diabetes
- Eating Disorders and Behaviors
- Neurotransmitter Receptor Influence on Behavior
- Neurobiology and Insect Physiology Research
- Neuroscience of respiration and sleep
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Metabolism, Diabetes, and Cancer
- Hormonal Regulation and Hypertension
- Pancreatic and Hepatic Oncology Research
- Neuroscience and Neuropharmacology Research
- Vitamin D Research Studies
Baylor College of Medicine
2016-2025
Children's Nutrition Research Center at Baylor College of Medicine
2016-2025
Tianjin Medical University General Hospital
2024
Pennington Biomedical Research Center
2023
Louisiana State University
2023
Creative Commons
2023
Chinese People's Liberation Army
2014-2023
Texas Diabetes & Endocrinology
2023
Chinese PLA General Hospital
2023
Shanxi Medical University
2022
Drugs activating 5-hydroxytryptamine 2C receptors (5-HT2CRs) potently suppress appetite, but the underlying mechanisms for these effects are not fully understood. To tackle this issue, we generated mice with global 5-HT2CR deficiency (2C null) and 5-HT2CRs re-expression only in pro-opiomelanocortin (POMC) neurons (2C/POMC mice). We show that null predictably developed hyperphagia, hyperactivity, obesity showed attenuated responses to anorexigenic 5-HT drugs. Remarkably, all deficiencies were...
Premenopausal women exhibit enhanced insulin sensitivity and reduced incidence of type 2 diabetes (T2D) compared with age-matched men, but this advantage disappears after menopause disrupted glucose homeostasis, in part owing to a reduction circulating 17β-estradiol (E2). Fasting hyperglycemia is hallmark T2D derived largely from dysregulation hepatic production (HGP), which Foxo1 plays central role the regulation gluconeogenesis. Here, we investigated action E2 on homeostasis male...
Significance Activation of the cGAMP-cGAS-STING pathway has recently been shown to mediate virus- or bacteria-induced activation innate immune response. Here we report that this also plays an important role in obesity-induced inflammation and metabolic dysfunction, beyond its well-characterized roles surveillance. We have identified adipose disulfide-bond A oxidoreductase-like protein as a key regulator mitochondrial integrity function, which protects mice from insulin resistance by...
Our data demonstrate that estrogens, estrogen receptor-α (ERα), and receptor-β (ERβ) regulate adipose tissue distribution, inflammation, fibrosis, glucose homeostasis, by determining αERKO mice have increased inflammation fibrosis prior to obesity onset. Selective deletion of ERα in adult using a novel viral vector technology recapitulated the findings total body null mice. Generation mouse model, lacking specifically from adipocytes (AdipoERα), demonstrated markers especially males....
Energy and glucose homeostasis are regulated by central serotonin 2C receptors. These receptors attractive pharmacological targets for the treatment of obesity; however, identity receptor-expressing neurons that mediate effects receptor agonists on energy unknown. Here, we show mice lacking (Htr2c) specifically in pro-opiomelanocortin (POMC) had normal body weight but developed glucoregulatory defects including hyperinsulinemia, hyperglucagonemia, hyperglycemia, insulin resistance. Moreover,...
The transcription factor steroidogenic 1 (SF-1) is exclusively expressed in the brain ventral medial hypothalamic nucleus (VMH) and required for development of this nucleus. However, physiological importance transcriptional programs regulated by SF-1 VMH not well defined. To delineate functional significance itself brain, we generated pre- postnatal VMH-specific KO mice. Both models were susceptible to high fat diet-induced obesity displayed impaired thermogenesis after acute exposure diet....
Circadian disruption has deleterious effects on metabolism. Global deletion of Bmal1, a core clock gene, results in β-cell dysfunction and diabetes. However, it is unknown if this due to loss cell-autonomous function Bmal1 β cells. To address this, we generated mice with by deleting cells (β-Bmal1(-/-)). β-Bmal1(-/-) develop diabetes glucose-stimulated insulin secretion (GSIS). This GSIS the accumulation reactive oxygen species (ROS) consequent mitochondrial uncoupling, as fully rescued...
Binge eating afflicts approximately 5% of US adults, though effective treatments are limited. Here, we showed that estrogen replacement substantially suppresses binge-like behavior in ovariectomized female mice. Estrogen-dependent inhibition was blocked mice specifically lacking receptor-α (ERα) serotonin (5-HT) neurons the dorsal raphe nuclei (DRN). Administration a recently developed glucagon-like peptide-1-estrogen (GLP-1-estrogen) conjugate designed to deliver GLP1 receptor-enhanced...
BackgroundNeural networks that regulate binge eating remain to be identified, and effective treatments for are limited.MethodsWe combined neuroanatomic, pharmacologic, electrophysiological, Cre-lox, chemogenetic approaches investigate the functions of 5-hydroxytryptamine (5-HT) 2C receptor (5-HT2CR) expressed by dopamine (DA) neurons in regulation binge-like behavior mice.ResultsWe showed 5-HT stimulates DA neural activity through a 5-HT2CR-mediated mechanism, activation this midbrain...
Estrogen receptor–α (ERα) activity in the brain prevents obesity both males and females. However, ERα-expressing neural populations that regulate body weight remain to be fully elucidated. Here we showed single-minded–1 (SIM1) neurons medial amygdala (MeA) express abundant levels of ERα. Specific deletion gene encoding ERα (Esr1) from SIM1 neurons, which are mostly within MeA, caused hypoactivity male female mice fed with regular chow, increased susceptibility diet-induced (DIO) but not...
Abstract The high comorbidity between obesity and mental disorders, such as depression anxiety, often exacerbates metabolic neurological symptoms significantly. However, neural mechanisms that underlie reciprocal control of feeding states are largely elusive. Here we report melanocortin 4 receptor (MC4R) neurons located in the dorsal bed nucleus stria terminus (dBNST) engage regulation mentally associated weight gain by receiving GABAergic projections from hypothalamic AgRP onto...
Abstract Feeding is known to be profoundly affected by stress-related emotional states and eating disorders are comorbid with psychiatric symptoms altered responses. The neural basis underlying feeding regulation changes poorly understood. Here, we identify a novel projection from the paraventricular hypothalamus (PVH) ventral lateral septum (LSv) that shows scalable on behavioral related emotion. Weak photostimulation of glutamatergic PVH→LSv terminals elicits self-grooming strong causes...
Nutrient excess, a major driver of obesity, diminishes hypothalamic responses to exogenously administered leptin, critical hormone energy balance. Here, we aimed identify physiological signal that arises from excess caloric intake and negatively controls leptin action. We found deficiency the gastric inhibitory polypeptide receptor (Gipr) for gut-derived incretin GIP protected against diet-induced neural resistance. Furthermore, centrally antibody neutralizes GIPR had remarkable antiobesity...
Abstract Homeotherms maintain a stable internal body temperature despite changing environments. During energy deficiency, some species can cease to defend their and enter hypothermic hypometabolic state known as torpor. Recent advances have revealed the medial preoptic area (MPA) key site for regulation of torpor in mice. The MPA is estrogen-sensitive estrogens also potent effects on both metabolism. Here, we demonstrate that neurons coordinate hypothermia hypometabolism Selectively...