Allen S. Levine - US grants
Affiliations: | Food Science and Nutrition | University of Minnesota, Twin Cities, Minneapolis, MN |
Area:
Neuroregulation of food intakeWebsite:
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The funding information displayed below comes from the NIH Research Portfolio Online Reporting Tools and the NSF Award Database.The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
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High-probability grants
According to our matching algorithm, Allen S. Levine is the likely recipient of the following grants.| Years | Recipients | Code | Title / Keywords | Matching score |
|---|---|---|---|---|
| 1986 — 1988 | Levine, Allen S | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Glucose Modulation of Opioid-Induced Feeding @ University of Minnesota Twin Cities The availability and utilization of macronutrients contribute to feeding regulation, as do several chemical systems within the brain. The proposed experiments will examine the relationship between one nutrient, glucose, and a group of neuromodulators, the opioid peptides. An interrelationship between the opioid system and circulating glucose levels is not without precedent. Since the 1950's it has been known that blood glucose concentration can affect the antinociceptive properties of opiates. Our laboratory has described an alteration in responsivity of animals to opioid-induced feeding due to the glycemic state of the organisms. It is the intent of the present grant to answer a variety of questions related to such a glucose-opioid interaction as it relates to the control of ingestive behaviors. In animals made diabetic by the administration of streptozotocin, we will use several agonists with different selectivities to determine which receptor is most affected, as reflected by responsivity to opioid-induction of feeding. We will also study, by ventricular injections and localized infusions into specific brain sites, the neural structures that are most likely involved in glucose modulation of opioid induced feeding. We will evaluate the effect of the glycemic state on the "reverse-tolerance" noted following repeated injection of various opiate agents. The next group of studies will attempt to achieve the same modulation of opioid effects through the use of glucose injections directly into various brain sites. We will conduct in vitro ligand-binding studies with isolated brain membranes using a variety of glucose concentrations in the incubation media. These binding studies will provide information both on the nature of opioid agonist-receptor binding and on the mechanism underlying the expected effects of diabetes on opioid-induced feeding. The results of these experiments should integrate two fields of appetite research: glucose and opioid-regulation. Diseases which involve compulsive eating may represent a type of self-addiction. The addictive characteristic may be due to relationships between nutrients (eg. glucose) and neuroregulators (eg. opioids). Thus, the agents involved and the specific control sites are necessary ingredients to the design of appropriate clinical treatment for such eating disorders. We believe that the results of our studies will be applicable at both the basic and the applied level. |
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| 1990 — 1997 | Levine, Allen S | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
@ University of Minnesota Twin Cities We are interested in the role that opioids play in the regulation of food intake. It has been known for decades that blockade of the opioid receptor decreases short-term food intake and administration of opioid agonists increases short-term feeding. The manner in which these agents alter feeding is not known. One idea championed by a variety of investigators is that opioids increase the value of food by altering palatability. This concept is substantiated by the following findings: 1) Opioid receptor blockade (naloxone, naltrexone and nalmefene) results in a decrease in the perceived pleasantness of sweet and salty foods and drinks; 2) Naloxone more potently decreases palatable food consumption compared with that of rat chow; 3) Morphine increases intake of a preferred food when presented concurrently with a less preferred food; 4) Consumption of palatable foods alters opioid binding and beta-endorphin content in the hypothalamus of rats; and 5) Ingestion of palatable foods results in a naloxone reversible increase in nociceptive thresholds in rats. The idea that opioids increase the value of food through enhancing palatability lead us to speculate that opioids are involved in the maintenance of the meal, rather than initiation of feeding. Eating might lead to the release of endogenous opioids which would then enhance the value of the food and elongate the meal. To test this hypothesis we propose five sets of studies which address the following specific questions: 1) Are opioids involved in the maintenance of all types of feeding behavior, and if so which opioid receptors are important for such effects? 2) Do opioid antagonists stop a rat from "working hard" to initiate feeding; or does opioid blockade inhibit a rat from "hardly working" to maintain food delivery? Also will opioid antagonists block a rat from working "more and more" to maintain feeding? 3) Do opioids have discriminative stimulus effects similar to the discriminative stimulus effects of agents which initiate feeding? 4) Can the sequence of macronutrient selection help us understand whether opioids are involved in latency or maintenance of the meal? 5) Which brain sites are involved in opioid-induced changes in meal architecture; and are feeding initiating and maintaining sites different? Answers to these questions will help understand whether opioids contribute to the initiation or maintenance of feeding. Such information could eventually lead to the development of pharmacologic agents to treat obesity and other eating disorders. |
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| 1995 — 1999 | Levine, Allen S | P30Activity Code Description: To support shared resources and facilities for categorical research by a number of investigators from different disciplines who provide a multidisciplinary approach to a joint research effort or from the same discipline who focus on a common research problem. The core grant is integrated with the center's component projects or program projects, though funded independently from them. This support, by providing more accessible resources, is expected to assure a greater productivity than from the separate projects and program projects. |
@ University of Minnesota Twin Cities |
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| 1998 | Levine, Allen S | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
@ University of Minnesota Twin Cities We are interested in the role that opioids play in the regulation of food intake. It has been known for decades that blockade of the opioid receptor decreases short-term food intake and administration of opioid agonists increases short-term feeding. The manner in which these agents alter feeding is not known. One idea championed by a variety of investigators is that opioids increase the value of food by altering palatability. This concept is substantiated by the following findings: 1) Opioid receptor blockade (naloxone, naltrexone and nalmefene) results in a decrease in the perceived pleasantness of sweet and salty foods and drinks; 2) Naloxone more potently decreases palatable food consumption compared with that of rat chow; 3) Morphine increases intake of a preferred food when presented concurrently with a less preferred food; 4) Consumption of palatable foods alters opioid binding and beta-endorphin content in the hypothalamus of rats; and 5) Ingestion of palatable foods results in a naloxone reversible increase in nociceptive thresholds in rats. The idea that opioids increase the value of food through enhancing palatability lead us to speculate that opioids are involved in the maintenance of the meal, rather than initiation of feeding. Eating might lead to the release of endogenous opioids which would then enhance the value of the food and elongate the meal. To test this hypothesis we propose five sets of studies which address the following specific questions: 1) Are opioids involved in the maintenance of all types of feeding behavior, and if so which opioid receptors are important for such effects? 2) Do opioid antagonists stop a rat from "working hard" to initiate feeding; or does opioid blockade inhibit a rat from "hardly working" to maintain food delivery? Also will opioid antagonists block a rat from working "more and more" to maintain feeding? 3) Do opioids have discriminative stimulus effects similar to the discriminative stimulus effects of agents which initiate feeding? 4) Can the sequence of macronutrient selection help us understand whether opioids are involved in latency or maintenance of the meal? 5) Which brain sites are involved in opioid-induced changes in meal architecture; and are feeding initiating and maintaining sites different? Answers to these questions will help understand whether opioids contribute to the initiation or maintenance of feeding. Such information could eventually lead to the development of pharmacologic agents to treat obesity and other eating disorders. |
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| 1999 — 2003 | Levine, Allen S | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Sucrose and/or Fat Ingestion Effect On Opioids @ University of Minnesota Twin Cities DESCRIPTION: (Adapted From The Applicant's Abstract) Opioids represent one set of regulators thought to be involved in eating induced by the rewarding properties of food. Opioid antagonists are particularly effective at decreasing intake of preferred foods including high sucrose and/or high fat foods. For example, we found that extremely low doses of the opioid antagonist naloxone (0.01 mg/kg) decreased intake of a preferred food, whereas much higher dose (3-10 mg/kg) were needed to decrease eating stimulated by energy needs. We also found that dynorphin gene expression was higher in the arcuate nucleus of animals fed a highly palatable diet (high sucrose/fat diet) compared with those fed a less preferred high starch diet. Such data have led us to hypothesize that ingestion of palatable foods (sweet and/or fat) results in an increase in the release of endogenous opioids at brain sites involved in feeding behavior and/or "reward." We propose four sets of studies to test this hypothesis: Do palatable foods or solutions (containing sucrose, saccharin and/or fat) result in an increase in gene expression of opioid peptides in brain sites known to be involved in feeding behavior or reward? These sites include the nucleus of the solitary tract (NTS), paraventricular nucleus of the hypothalamus (PVN), central nucleus of the amygdala (CNA), ventral tegmental area (VTA) and shell of the nucleus accumbens (s-ACC). Does acute or chronic ingestion of sucrose alter the ability of rats to discriminate morphine? We hypothesize that ingestion of sucrose releases opioids or alters receptor binding/density leading to a change in potency, i.e., a leftward shift in the agonist dose response curve of a rat trained to discriminate morphine. Does chronic ingestion of sucrose result in cellular changes resembling opioid dependence? If sucrose results in the release of opioids one might speculate that rats would display mild opioid withdrawal upon cessation of sucrose availability or following injection of naloxone. We will use cFos immunohistochemistry to observe the pattern associated with chronic sucrose ingestion followed by naloxone injection. Comparison will be made to opioid dependent animals (relatively mild dependence). Must a rat ingest a "critical" amount of a palatable food before opioids are released? We believe that the reason that naloxone does not affect latency to feeding and only seems to effect maintenance of feeding is that opioids are only released after feeding begins. These experiments address how much food must be eaten (volume, time spent eating etc.) before naloxone administration decreases feeding. |
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| 2000 — 2014 | Levine, Allen S | P30Activity Code Description: To support shared resources and facilities for categorical research by a number of investigators from different disciplines who provide a multidisciplinary approach to a joint research effort or from the same discipline who focus on a common research problem. The core grant is integrated with the center's component projects or program projects, though funded independently from them. This support, by providing more accessible resources, is expected to assure a greater productivity than from the separate projects and program projects. |
@ University of Minnesota Twin Cities [unreadable] DESCRIPTION, OVERALL (provided by applicant): [unreadable] The mission of the Minnesota Obesity Center is to find ways to prevent weight gain and secondarily the onset of obesity and complications of obesity. Obesity is clearly a major source of illness and death, and is the most common nutritional ailment in the United States. Despite its prevalence, there is little known about effective measures to prevent obesity, and therefore its attendant complications. Further, it is well known that obese individuals can more easily lose weight than maintain the loss. It now seems clear that the emphasis should be prevention of initial weight gain, and failing that, prevention of regain after weight loss. With the mission of prevention defined, our vision establishes three goals: 1) find the underlying problems that lead to obesity, 2) identify behaviors that lead to obesity and find ways to help change those behaviors, and 3) determine public health and public policy measures that will reduce the frequency and severity of [unreadable] obesity. Our Center is primarily a research center, so we plan encouragement and support of studies directed at these aims. With respect to these goals, the role of our center is to: assist principal investigators in conducting relevant research by providing resources through the core system; stimulate new interest and new collaborations in research into obesity, eating disorders and energy metabolism; support new research efforts in these areas related to obesity; and support education in obesity and eating disorders in our academic and public communities. [unreadable] [unreadable] The Minnesota Obesity Center has a strong and diverse research base consisting of 60 active [unreadable] investigators with 114 funded projects in obesity, energy metabolism and eating disorders. We propose the establishment of five core facilities including: 1) Administration will provide vision, leadership, and oversight of other core activities, 2) Obesity and Energy Metabolism Core will provide the latest tools for developing and evaluating gain-offunction and loss-of-function models and the techniques to assess the consequences at the level of gene and/or protein expression, 3) Disordered Eating Assessment Core will assist ONRC investigators in the assessment of disordered eating and other psychopathology, and the development of interventions for such disordered eating, 4) Epidemiology and Intervention Core is to make high quality services for epidemiological and behavioral intervention studies available to ONRC participants, 5) Metabolic Studies Core laboratory will provide access to established and state-of-the-art methods for studying energy metabolism and nutrient partitioning at the whole body level in humans and animals. In addition, resources for pilot/feasibility projects and an educational program will be established. [unreadable] [unreadable] [unreadable] |
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| 2002 — 2004 | Levine, Allen S | R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Alcohol Modulation of Brain Reward Pathways @ University of Minnesota Twin Cities DESCRIPTION (provided by applicant): This exploratory/developmental proposal (R21) evaluating potential rewarding aspects of ethanol in the central nervous system and therefore the etiology of alcoholism is relevant to the NIAAA mission. Opioid peptides have been implicated in "rewarding" behaviors, including food and alcohol ingestion. The theory that opioids impact alcohol imbibition is fairly well accepted, reflected by the use of the opioid receptor antagonist naltrexone as a treatment for alcohol abuse. In addition to the observation that opioid administration affects alcohol intake it has been found that alcohol intake affects the opioidergic system. The concept that eating leads to release of opioids, which then maintain food intake might also be applied to ingestion of alcohol. Alcohol, like palatable foods, is reinforcing. Gatto et al demonstrated that alcohol preferring rats self-administer 100 mg% ethanol into the ventral tegmental area. We hypothesized that central administration of ethanol bypasses the aversive effects of ingesting ethanol, perhaps due to orosensory cues, and instead results in a positive hedonic state. As expected, central administration of ethanol did not condition a taste aversion as has been observed with peripheral administration of alcohol. Rather, central administered ethanol resulted in conditioned taste preference acceptance when paired with saccharin intake. Also, subcutaneous injection of naloxone 15 minutes before central administration of ethanol blocked the ethanol-induced intake of saccharin. Based on the above data our hypothesis is that the reinforcing effects of ethanol are mediated in part by the opioidergic system in brain sites associated with rewarding behaviors. The specific aims of this project are to establish 1) whether the intake and behavior patterns for ethanol-induced effects are dose dependent; 2) to determine if an opioid antagonist blockade will dose dependently alter the ethanol-induced intake or behavior; 3) to locate specific sites of ethanol action and measure the induced behavior and intake patterns; and 4) to develop a neural map of intake sensitivity to ethanol (cFos-immunohistochemistry, intake/preference studies). Experiments designed to accomplish these aims will provide important information on the relationship between ethanol and opioids along the palatability reward pathways of the central nervous system that lead to ethanol-induced addiction. |
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| 2006 | Levine, Allen S | P30Activity Code Description: To support shared resources and facilities for categorical research by a number of investigators from different disciplines who provide a multidisciplinary approach to a joint research effort or from the same discipline who focus on a common research problem. The core grant is integrated with the center's component projects or program projects, though funded independently from them. This support, by providing more accessible resources, is expected to assure a greater productivity than from the separate projects and program projects. |
Administrative Core and Enrichment Program @ University of Minnesota Twin Cities |
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| 2007 — 2010 | Levine, Allen S | P30Activity Code Description: To support shared resources and facilities for categorical research by a number of investigators from different disciplines who provide a multidisciplinary approach to a joint research effort or from the same discipline who focus on a common research problem. The core grant is integrated with the center's component projects or program projects, though funded independently from them. This support, by providing more accessible resources, is expected to assure a greater productivity than from the separate projects and program projects. |
Disorderd Eating Assessment Core @ University of Minnesota Twin Cities Affect; Behavior; Behavior Therapy, Cognitive; Behavior assessment; Behavioral Therapy; Clinical; Clinical Trials; Clinical Trials, Unspecified; Clinical assessments; Cognitive Therapy; Collection; Consultations; Cost Effective Analyses; Cost Effectiveness Analysis; Data; Data Set; Dataset; Development; Diagnosis; Disease; Disorder; Eating; Eating Behavior; Eating Disorders; Emergent Technologies; Emerging Technologies; Food Intake; Goals; Individual; Investigators; Manuals; Methods; Obesity; Population; Psychopathology; Psychotherapy, Cognitive; Research; Research Personnel; Researchers; Sampling; Scanning; Services; Structure; Technology; Therapeutic Intervention; Therapy, Cognition; Training; abnormal psychology; adiposity; base; behavioral assessment; clinical investigation; cognitive behavior intervention; cognitive behavior modification; cognitive behavioral intervention; cognitive behavioral modification; cognitive behavioral therapy; comparison group; corpulence; corpulency; corpulentia; cost; cost effectiveness; cost efficient analysis; disease/disorder; experience; intervention development; intervention therapy; obese; obese people; obese person; obese population; obesity treatment; quality assurance; therapy development; treatment development |
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| 2007 — 2010 | Levine, Allen S | P30Activity Code Description: To support shared resources and facilities for categorical research by a number of investigators from different disciplines who provide a multidisciplinary approach to a joint research effort or from the same discipline who focus on a common research problem. The core grant is integrated with the center's component projects or program projects, though funded independently from them. This support, by providing more accessible resources, is expected to assure a greater productivity than from the separate projects and program projects. |
Epidemiology Intervention Core @ University of Minnesota Behavior Therapy; Clinic; Collaborations; Communities; community setting; Consultations; cost; Data; Data Base Management; Data Collection; Databases; design; Development; diet and exercise; Dietary Assessment; Epidemiology; experience; follow-up; Goals; Health; health care delivery; Health Services Accessibility; instrument; Intervention; Intervention Studies; Managed Care; Medical; member; Methodology; Methods; Minnesota; Nutrient; Nutrition Assessment; Obesity; Outpatients; Participant; Population; Relative (related person); Research Personnel; Research Project Grants; Services; Students; Surveys; therapy development; Training |
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| 2007 — 2010 | Levine, Allen S | P30Activity Code Description: To support shared resources and facilities for categorical research by a number of investigators from different disciplines who provide a multidisciplinary approach to a joint research effort or from the same discipline who focus on a common research problem. The core grant is integrated with the center's component projects or program projects, though funded independently from them. This support, by providing more accessible resources, is expected to assure a greater productivity than from the separate projects and program projects. |
Obesity and Energy Metabolism Core @ University of Minnesota Twin Cities 3T3-L1 Cells; Adipocytes; Adipose Cell; Adipose tissue; Affect; Animal Model; Animal Models and Related Studies; Antimorphic mutation; Biochemical; Cell Function; Cell Line; Cell Lines, Strains; Cell Process; Cell physiology; CellLine; Cellular Function; Cellular Physiology; Cellular Process; Chondrogenesis; D-Glucose; Development; Dextrose; Dominant Negative; Dominant-Negative Mutant; Dominant-Negative Mutation; EC 2.7; Energy Expenditure; Energy Metabolism; Enzymes; Evaluation; Fat Cells; Fatty Tissue; Flies; Fructose; Gene Expression; Genes; Genetic; Genomics; Glucose; Hepatic; Human; Human, General; Insulin Resistance; Intermediary Metabolism; Investigators; Kinases; Laboratories; Lead; Levulose; Light; Lipocytes; Liver; METBL; Mammals, Mice; Mammals, Rodents; Man (Taxonomy); Man, Modern; Mass Spectrum; Mass Spectrum Analysis; Mature Lipocyte; Mature fat cell; Measures; Metabolic Control; Metabolic Processes; Metabolism; Methods; Methods and Techniques; Methods, Other; Mice; Microarray Analysis; Microarray-Based Analysis; Modeling; Molecular; Molecular Genetic; Molecular Genetics; Murine; Mus; Muscle, Skeletal; Muscle, Voluntary; Numbers; Nutritional; Obesity; Outcome; PCR; Pb element; Phosphotransferases; Photometry/Spectrum Analysis, Mass; Photoradiation; Physiology; Polymerase Chain Reaction; Process Measure; Production; Proteomics; Purpose; RNA, Small Interfering; Research; Research Personnel; Researchers; Rodent; Rodentia; Rodentias; Role; Services; Skeletal Muscle Tissue; Skeletal muscle structure; Small Interfering RNA; Spectrometry, Mass; Spectroscopy, Mass; Spectrum Analyses, Mass; Spectrum Analysis, Mass; Subcellular Process; Techniques; Technology; Time; Today; Training; Transphosphorylases; Triacylglycerol; Triglycerides; Virus; Viruses, General; Weight Gain; Weight Increase; adipogenesis; adipose; adiposity; blood glucose regulation; body system, hepatic; body weight gain; body weight increase; corpulence; corpulency; corpulentia; cost; cultured cell line; energy balance; fatty acid-transport protein; fly; gain of function; glucose RA; glucose control; glucose homeostasis; glucose production; glucose rate of appearance; glucose regulation; heavy metal Pb; heavy metal lead; insulin resistant; lipid biosynthesis; lipogenesis; loss of function; microarray technology; model organism; obese; obese people; obese person; obese population; organ system, hepatic; protein expression; siRNA; social role; tool; transcription factor; white adipose tissue; wt gain; yellow adipose tissue |
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| 2007 — 2011 | Levine, Allen S | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Effect of Sweet Tastants On Opioid-Melanocortin Interactions @ University of Minnesota Twin Cities [unreadable] DESCRIPTION (provided by applicant): The readily available energy and pleasant taste of sugars make them potent contributors to the obesity epidemic. We have studied the neurobiology of reward-related feeding and propose to examine interactions between opioids, neuropeptides involved in sweet taste consumption, and oxytocin and melanocortins, which are associated with meal termination. The circuitry of these interactions includes the hypothalamic arcuate nucleus (ARC) and paraventricular (PVN) nuclei, and the central nucleus of the amygdala (CeA). Our hypothesis is that over-consumption of sweet foods/fluids occurs, in part, due to opioid-controlled inhibition of circuitry responsible for the termination of feeding, including oxytocin and alpha-MSH containing pathways. To test this hypothesis we propose: 1) To determine whether the hyperphagia associated with ingestion of sweet diets involves inhibition of oxytocin and alpha-MSH neurons in the PVN and ARC respectively; and 2) To determine whether PVN and CeA opioid receptors participate in sweet diet-induced hyperphagia by inhibiting termination of consumption (alpha-MSH to oxytocin) in response to acute versus chronic intake of rewarding diets rich in sugars. We will study the activation of neurons involved in the terminal portion of the meal (alpha-MSH to oxytocin) in response to acute versus chronic intake of diets rich in sugars. We speculate that orexigenic doses of an opioid receptor agonist will decrease activation of hypophagia- mediating alpha-MSH and oxytocin neurons. Similarly, acute exposure to a sweet palatable ingestant (which results in a modest level of intake compared to that observed during prolonged experience with an ingestant) leads to more robust activity within this pathway. These studies will help identify potential targets, both anatomical and neurochemical, which are involved in regulating ingestion of sweet fluids and/or diets and has important implications for obesity. [unreadable] [unreadable] [unreadable] |
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| 2007 — 2015 | Levine, Allen S | P30Activity Code Description: To support shared resources and facilities for categorical research by a number of investigators from different disciplines who provide a multidisciplinary approach to a joint research effort or from the same discipline who focus on a common research problem. The core grant is integrated with the center's component projects or program projects, though funded independently from them. This support, by providing more accessible resources, is expected to assure a greater productivity than from the separate projects and program projects. |
@ University of Minnesota Twin Cities |
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