Showing papers by "Harvey J. Grill published in 2019"
University of Tübingen1, Novo Nordisk2, Imperial College London3, Duke University4, Lunenfeld-Tanenbaum Research Institute5, Ulster University6, University of Cambridge7, University of Pennsylvania8, Harvard University9, University of Copenhagen10, ETH Zurich11, Ruhr University Bochum12, University of Cincinnati Academic Health Center13, Janssen Pharmaceutica14, University of Michigan15, University of Cincinnati16, Indiana University17, Technische Universität München18
TL;DR: The numerous beneficial effects of GLP-1 render this hormone an interesting candidate for the development of pharmacotherapies to treat obesity, diabetes, and neurodegenerative disorders.
Abstract: Background The glucagon-like peptide-1 (GLP-1) is a multifaceted hormone with broad pharmacological potential. Among the numerous metabolic effects of GLP-1 are the glucose-dependent stimulation of insulin secretion, decrease of gastric emptying, inhibition of food intake, increase of natriuresis and diuresis, and modulation of rodent β-cell proliferation. GLP-1 also has cardio- and neuroprotective effects, decreases inflammation and apoptosis, and has implications for learning and memory, reward behavior, and palatability. Biochemically modified for enhanced potency and sustained action, GLP-1 receptor agonists are successfully in clinical use for the treatment of type-2 diabetes, and several GLP-1-based pharmacotherapies are in clinical evaluation for the treatment of obesity. Scope of review In this review, we provide a detailed overview on the multifaceted nature of GLP-1 and its pharmacology and discuss its therapeutic implications on various diseases. Major conclusions Since its discovery, GLP-1 has emerged as a pleiotropic hormone with a myriad of metabolic functions that go well beyond its classical identification as an incretin hormone. The numerous beneficial effects of GLP-1 render this hormone an interesting candidate for the development of pharmacotherapies to treat obesity, diabetes, and neurodegenerative disorders
679 citations
TL;DR: It is shown that brain-produced IL-6 is decreased in obese mice and rats in a neuroanatomically and sex-specific manner and pinpoints (patho)physiological contexts interacting with lPBN IL- 6 indicate that lPbn-producedIL-6 regulates feeding and metabolism and pin points ( Patho)Physiological contexts interact with the cytokine.
38 citations
TL;DR: It is shown that centrally-delivered leptin reduced food intake and conditioned a place preference in food-restricted as well as ad libitum fed rats, suggesting that leptin signaling is intrinsically preferred, and support the view that signals of energy surfeit are associated with positive affect.
3 citations
TL;DR: This study investigated whetherindividual differences in behavioral responses to palatable food and to the satiation signal cholecystokinin in outbred chow‐maintained Sprague‐Dawley rats enabled prediction of individual differences in weight gained after subsequent high‐fat/high‐sugar diet (HFHSD) maintenance.
Abstract: OBJECTIVE This study investigated whether individual differences in behavioral responses to palatable food and to the satiation signal cholecystokinin (CCK) in outbred chow-maintained Sprague-Dawley rats enabled prediction of individual differences in weight gained after subsequent high-fat/high-sugar diet (HFHSD) maintenance. METHODS Meal size, meal number, and early dark cycle intake during initial HFHSD exposure were measured, as were early dark cycle sucrose solution and chow intake, chow meal size and meal number, the intake-suppressive effects of 0.5-µg/kg CCK injection, and CCK-induced c-Fos activation in the nucleus tractus solitarius. Subsequently, rats were maintained on an HFHSD for 5 weeks, and weight gain was determined. RESULTS Rats that took larger and less frequent meals on the first day of HFHSD exposure, whose early dark cycle intake (HFHSD and sucrose) was larger during initial HFHSD exposure, gained more weight after HFHSD maintenance. Rats with lesser sucrose intake suppression in response to CCK gained more weight after HFHSD maintenance and displayed reduced CCK-induced c-Fos activation in the nucleus tractus solitarius. CONCLUSIONS Together, these data identify individual differences in behavioral responses to palatable food and to CCK as novel predictors of diet-induced obesity.
3 citations