Nutrition
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Recent pharmacologic studies in our laboratory have suggested that the spinal neuropeptide Y (NPY) Y1 receptor contributes to pain inhibition and to the analgesic effects of NPY. To rule out off-target effects, the present study used Y1-receptor-deficient (-/-) mice to further explore the contribution of Y1 receptors to pain modulation. ⋯ The Y1 receptor contributes to pain inhibition and to the analgesic effects of NPY.
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The regulation of energy balance depends on the precise co-ordination of multiple peripheral and central systems. Much recent research has highlighted the importance of behavioral mechanisms is this control and suggested that the regulation of body weight shares central nervous system pathways in common with other complex behaviors, including learning and drug addiction. ⋯ Additional evidence supports the idea that appetitive mechanisms are engaged that are critical for the regulation of intake during the act of ingestion. We briefly discuss the recent work on the potential role for central nervous system reward centers, how those might be critically linked to the central regulation of food intake, and how they may be dysregulated by the abundance of highly palatable, energy-dense foods.
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Multidisciplinary research from my and my colleagues' laboratory has shown that disruption at various levels of leptin signaling to the interactive hypothalamic network of neuropeptide Y (NPY) and cohorts contributes to the antecedent pathophysiologic sequelae of the disease cluster of the metabolic syndrome. Disruptions in NPY signaling due to high or low abundance of NPY and cognate receptors dysregulate the homeostatic milieu to promote hyperinsulinemia, hyperglycemia, fat accrual, and overt diabetes. Hyperleptinemia induced by consumption of energy-rich diets inhibits leptin transport across the blood-brain barrier and thereby produces leptin insufficiency in the hypothalamus. ⋯ This chain of events culminates in hyperinsulinemia, hyperglycemia, and diabetes. Our recent studies have shown that increasing the supply of leptin centrally by gene therapy reinstates the restraint on hypothalamic NPY signaling and ameliorates diabetes and the attendant disease cluster of the metabolic syndrome. Thus, newer therapies that would enhance leptin transport across the blood-brain barrier in a timely manner or reinstate leptin restraint on NPY signaling through central leptin gene therapy or pharmacologically with leptin mimetics are likely to curtail the pathophysiologic sequelae of diabetes and related ailments of the metabolic syndrome.
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To establish the functional significance of endogenous peptide YY (PYY) and neuropeptide Y (NPY) as mediators of Y(1) and Y(2) absorptive tone in colonic mucosa. ⋯ Endogenous PYY mediates Y(1) absorptive tone that is epithelial in origin, whereas Y(2) tone is a combination of PYY and NPY mediation.
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Case Reports
Rapidly developing weakness mimicking Guillain-Barré syndrome in beriberi neuropathy: two case reports.
We examined the diagnostic difficulty in thiamine deficiency. ⋯ Thiamine deficiency must be actively considered as a possible cause of polyneuropathy, and variability in its clinical features should be taken into consideration.