Gregory J. Morton

Arcuate nucleus-specific leptin receptor gene therapy attenuates the obesity phenotype of Koletsky (fa(k)/fa(k)) rats.

Neuropeptide Y is required for hyperphagic feeding in response to neuroglucopenia.

Increased hypothalamic melanin concentrating hormone gene expression during energy restriction involves a melanocortin-independent, estrogen-sensitive mechanism.

Leptin action in the forebrain regulates the hindbrain response to satiety signals.

Leptin inhibits hypothalamic Npy and Agrp gene expression via a mechanism that requires phosphatidylinositol 3-OH-kinase signaling.

Effects of hypothalamic neurodegeneration on energy balance.

Leptin regulates insulin sensitivity via phosphatidylinositol-3-OH kinase signaling in mediobasal hypothalamic neurons.

Insulin action in the brain contributes to glucose lowering during insulin treatment of diabetes.

Thermoregulatory and metabolic defects in Huntington's disease transgenic mice implicate PGC-1alpha in Huntington's disease neurodegeneration.

Central interleukin-1 (IL1) signaling is required for pharmacological, but not physiological, effects of leptin on energy balance.

Hypothalamic leptin regulation of energy homeostasis and glucose metabolism.

Signal transducer and activator of transcription-3 is required in hypothalamic agouti-related protein/neuropeptide Y neurons for normal energy homeostasis.

Deficiency of TNFalpha converting enzyme (TACE/ADAM17) causes a lean, hypermetabolic phenotype in mice.

Vascular inflammation, insulin resistance, and reduced nitric oxide production precede the onset of peripheral insulin resistance.

Forebrain melanocortin signaling enhances the hindbrain satiety response to CCK-8.

Hypothalamic proinflammatory lipid accumulation, inflammation, and insulin resistance in rats fed a high-fat diet.

The action of leptin in the ventral tegmental area to decrease food intake is dependent on Jak-2 signaling.

Hypothalamic leptin signaling regulates hepatic insulin sensitivity via a neurocircuit involving the vagus nerve.

Mice lacking hepatic lipase are lean and protected against diet-induced obesity and hepatic steatosis.

Fibroblast growth factor 21 action in the brain increases energy expenditure and insulin sensitivity in obese rats.

Central administration of interleukin-4 exacerbates hypothalamic inflammation and weight gain during high-fat feeding.

Identification of body fat mass as a major determinant of metabolic rate in mice.

Leptin deficiency causes insulin resistance induced by uncontrolled diabetes.

A new oxytocin-saporin cytotoxin for lesioning oxytocin-receptive neurons in the rat hindbrain.

Assessment of feeding behavior in laboratory mice.

Standard operating procedures for describing and performing metabolic tests of glucose homeostasis in mice.

Identification of a physiological role for leptin in the regulation of ambulatory activity and wheel running in mice.

Leptin activates a novel CNS mechanism for insulin-independent normalization of severe diabetic hyperglycemia.

A novel rodent model that mimics the metabolic sequelae of obese craniopharyngioma patients.

Leptin and the central nervous system control of glucose metabolism.

Subcutaneous administration of leptin normalizes fasting plasma glucose in obese type 2 diabetic UCD-T2DM rats.

Endothelial NO/cGMP/VASP signaling attenuates Kupffer cell activation and hepatic insulin resistance induced by high-fat feeding.

Peripheral oxytocin suppresses food intake and causes weight loss in diet-induced obese rats.

Obesity is associated with hypothalamic injury in rodents and humans.

Acutely decreased thermoregulatory energy expenditure or decreased activity energy expenditure both acutely reduce food intake in mice.

BDNF action in the brain attenuates diabetic hyperglycemia via insulin-independent inhibition of hepatic glucose production.

In uncontrolled diabetes, thyroid hormone and sympathetic activators induce thermogenesis without increasing glucose uptake in brown adipose tissue.

Leptin, diabetes, and the brain.

Leptin action in the ventromedial hypothalamic nucleus is sufficient, but not necessary, to normalize diabetic hyperglycemia.

Molecular and functional analysis of human β-defensin 3 action at melanocortin receptors.

FGF19 action in the brain induces insulin-independent glucose lowering.

Is there evidence that estrogen therapy promotes weight maintenance via effects on leptin?

Rapid glutamate release in the mediobasal hypothalamus accompanies feeding and is exaggerated by an obesogenic food.

Cooperation between brain and islet in glucose homeostasis and diabetes.

Carbohydrate feeding dissociates the postprandial FGF19 response from circulating bile acid levels in humans.

Neurobiology of food intake in health and disease.

Hindbrain oxytocin receptors contribute to the effects of circulating oxytocin on food intake in male rats.

Genetic determinants of atherosclerosis, obesity, and energy balance in consomic mice.

Role of melanocortin signaling in neuroendocrine and metabolic actions of leptin in male rats with uncontrolled diabetes.

Chronic oxytocin administration inhibits food intake, increases energy expenditure, and produces weight loss in fructose-fed obese rhesus monkeys.

Evidence That in Uncontrolled Diabetes, Hyperglucagonemia Is Required for Ketosis but Not for Increased Hepatic Glucose Production or Hyperglycemia.

Leptin signaling is required for adaptive changes in food intake, but not energy expenditure, in response to different thermal conditions.

In vivo structure-function studies of human hepatic lipase: the catalytic function rescues the lean phenotype of HL-deficient (hl-/-) mice.

Glucose intolerance induced by blockade of central FGF receptors is linked to an acute stress response.

Evidence against hypothalamic-pituitary-adrenal axis suppression in the antidiabetic action of leptin.

Chronic CNS oxytocin signaling preferentially induces fat loss in high-fat diet-fed rats by enhancing satiety responses and increasing lipid utilization.

The role of leptin in diabetes: metabolic effects.

Functional identification of a neurocircuit regulating blood glucose.

Central injection of fibroblast growth factor 1 induces sustained remission of diabetic hyperglycemia in rodents.

Physiological role for leptin in the control of thermal conductance.

Deletion of Protein Kinase C λ in POMC Neurons Predisposes to Diet-Induced Obesity.

Evidence That the Sympathetic Nervous System Elicits Rapid, Coordinated, and Reciprocal Adjustments of Insulin Secretion and Insulin Sensitivity During Cold Exposure.

Sex differences in microglial CX3CR1 signalling determine obesity susceptibility in mice.

Metabolically distinct weight loss by 10,12 CLA and caloric restriction highlight the importance of subcutaneous white adipose tissue for glucose homeostasis in mice.

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How Should We Think About the Role of the Brain in Glucose Homeostasis and Diabetes?

Chronic hindbrain administration of oxytocin is sufficient to elicit weight loss in diet-induced obese rats.

Androgen receptor deficiency in monocytes/macrophages does not alter adiposity or glucose homeostasis in male mice.

In Uncontrolled Diabetes, Hyperglucagonemia and Ketosis Result From Deficient Leptin Action in the Parabrachial Nucleus.

Leptin regulation of core body temperature involves mechanisms independent of the thyroid axis.

Distinct Neuronal Projections From the Hypothalamic Ventromedial Nucleus Mediate Glycemic and Behavioral Effects.

Peripheral Mechanisms Mediating the Sustained Antidiabetic Action of FGF1 in the Brain.

Glucoregulatory responses to hypothalamic preoptic area cooling.

The Hypothalamic Arcuate Nucleus-Median Eminence Is a Target for Sustained Diabetes Remission Induced by Fibroblast Growth Factor 1.

The central fibroblast growth factor receptor/beta klotho system: Comprehensive mapping in Mus musculus and comparisons to nonhuman primate and human samples using an automated in situ hybridization platform.

The role of vasodilator-stimulated phosphoprotein (VASP) in the control of hepatic gluconeogenic gene expression.