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Psy137Homeostasis Hunger

In the early stages of the disease the first phase

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In the early stages of the disease, the first-phase insulin response is lost and the second-phase insulin response is raised for a given glucose load compared with non-diabetic controls. Thus, glucose tolerance is maintained by increased insulin levels that compensate for peripheral insulin resistance. Eventually, pancreatic β-cells lose the ability to compensate by increasing insulin release, and the resulting reduced insulin levels often occur in parallel with increased glucagon levels. Thus, changes in both glucose production and tissue glucose uptake in T2DM lead to a chronic maintenance of raised basal and postprandial (after eating) glucose levels. Bernadette E. Grayson, Randy J. Seeley & Darleen A. Sandoval Nature Reviews Neuroscience 14, 24-37 (January 2013)
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Why do we eat? Social and environmental factors Need energy Taste of food Dietary selection –prefer a varied diet Physiological signals for hunger Glucoprivation (drop in blood glucose levels) stimulates eatin glucostatic hypothesis (glucose homoestasis) Lipoprivation (drop in fat signals) stimulates hunger Both brain and liver contain detectors
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Brain Areas Brain stem Experiment with decerebrated rats Cannot approach or eat food (experimenter fed) Can distinguish tastes Sweet & salt vs. bitter Can respond to satiety signals Ex. Drink more after deprivation
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Brain Areas Lateral hypothalamus (LH) Thought to be a feeding center Lesion LH Ventromedial hypothalamus (VMH) Thought to be a satiety center Lesion VMH VMH is thought to regulate the LH Not quite this simple VMH lesioned rat
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How do VMH lesions lead to obesity?
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Lateral Hypothalamus Elicits Feeding 2 population of neurons Melanin-concentrating hormone (MCH) Orexin Stimulate appetite Reduce metabolic rate Experiments show that ICV injections of MCH or orexin induces eating Neuropeptide Y (NPY) Neurons in the arcuate nucleus that project to the MCH & orexin neurons in the LH Pathway Glucoreceptors & liporeceptors NST parabrachial area NPY neurons in arcuate MCH & orexin neurons in LH stimulates appetite & reduces metabolic rate Leptin inhibits NPY neurons in the arcuate
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Arcuate Nucleus Neurons Arcuate nucleus integrates blood glucose levels and body fat levels. Two types of arcuate nucleus neurons are responsive to both insulin and leptin : Neuropeptide Y (NPY) and Agouti-Related Peptide (AgRP) expressing neurons. αMelanocyte stimulating hormone (αMSH) and cocaine and amphetamine-regulated transcipt (CART) expressing neurons. These neurons have opposing effects on feeding behavior and metabolism via interconnections with other hypothalamic structures.
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Hormonal Control of ARC Insulin and Leptin have opposite effects on specific ARC neurons: NPY/AgRP neurons are inhibited by leptin and insulin.
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