Energostatic hypothesis/Bibliography
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Amanda Jayne Swan 16:40, 10 October 2011 (UTC) Amanda Jayne Swan 16:33, 10 October 2011 (UTC) Amanda Jayne Swan 17:01, 10 October 2011 (UTC) Amanda Jayne Swan 19:24, 10 October 2011 (UTC) Amanda Jayne Swan 11:40, 11 October 2011 (UTC) 1. Andersson U, Filipsson K, Abbott CR, Woods A, Smith K, Bloom SR, et al. AMP-activated protein kinase plays a role in the control of food intake. Journal of Biological Chemistry. 2004;279(13):12005-8.
Studies the effects leptin, ghrelin and pharmacological substances have on AMPK, believed to be part of an intracellular signalling cascade that ultimately controls energy balance.
2. Booth DA. POSTABSORPTIVELY INDUCED SUPPRESSION OF APPETITE AND ENERGOSTATIC CONTROL OF FEEDING. Physiology & Behavior. 1972;9(2):199-202.
Proposed that a common metabolic measure of energy, rather than a particular nutrient, controls eating and appetite.
3. Booth DA, Lovett D, Simson PC. SUBCUTANEOUS DIALYSIS IN STUDY OF EFFECTS OF NUTRIENTS ON FEEDING. Physiology & Behavior. 1970;5(10):1201-&.
Investigates the effect of sodium chloride, hydrolysed casein and glucose have on feeding patterns when administered through subcutaneous dialysis. There is an uncompensated decrease in food intake following the glucose load without altering water intake. They concluded that the release of GI hormones is not necessary to induce satiety and propose that signals may in fact arise in the liver.
4. Friedman MI. CONTROL OF ENERGY-INTAKE BY ENERGY-METABOLISM. American Journal of Clinical Nutrition. 1995;62(5):S1096-S100.
How eating behaviour is linked with energy metabolism. Changes in liver metabolism provide signals for satiety and hunger.
5. Havel PJ. Peripheral signals conveying metabolic information to the brain: Short-term and long-term regulation of food intake and energy homeostasis. Experimental Biology and Medicine. 2001;226(11):963-77.
Details the numerous peripheral signals related to feeding and adiposity that work centrally to ultimately control energy balance. It is noted that some of these signals work differently in the short and long term.
6. Langhans W, Egli G, Scharrer E. REGULATION OF FOOD-INTAKE BY HEPATIC OXIDATIVE-METABOLISM. Brain Research Bulletin. 1985;15(4):425-8.
How metabolites and their products affected feeding behaviour and the role of vagally mediated signals from hepatic oxidation in food intake
7. Langhans W. Fatty acid oxidation in the energostatic control of eating-A new idea. Appetite. 2008;51(3):446-51.
Discusses the arguments surrounding the view that inhibition of FAO by MA causes an increase in food intake as a consequence of effects on the liver. Langhans raises the possibility that it is not the liver but enterocytes that are the main regulator of FAO in appetite signalling.
8. Lemagnen J, Devos M. METABOLIC CORRELATES OF MEAL ONSET IN FREE FOOD INTAKE OF RATS. Physiology & Behavior. 1970;5(7):805-&.
Aims to determine whether metabolic events control the eating pattern of mice. In the light period there was a low rate of food intake due to associated lipolysis, the onset of a meal was linked to the amount of glucose for cell oxidation. They concluded that the availability of glucose appears to be a stimulus for eating.
9. Nicolaidis S, Even PC. THE ISCHYMETRIC CONTROL OF FEEDING. International Journal of Obesity. 1990;14:35-52
Suggested that the metabolic rate is metered in the brain to affect eating. Whenever locomotion-free metabolism (MF) was low, hunger was promoted. When MF levels were replenished, hunger was prevented.
10. Obici S, Feng ZH, Arduini A, Conti R, Rossetti L. Inhibition of hypothalamic carnitine palmitoyltransferase-1 decreases food intake and glucose production. Nature Medicine. 2003;9(6):756-61.
Investigates how central metabolism of lipids controls energy balance. They reduced lipid oxidation by either genetic of pharmacological inhibition of CPT1 in the hypothalamus, thus demonstrated reduced food intake and endogenous glucose production in mice. They concluded that the rate of lipid oxidation was a signal to hypothalamic neurons that go on to control energy balance.
11. Niijima A. GLUCOSE-SENSITIVE AFFERENT NERVE-FIBERS IN THE LIVER AND THEIR ROLE IN FOOD-INTAKE AND BLOOD-GLUCOSE REGULATION. Journal of the Autonomic Nervous System. 1983;9(1):207-20
Studies the effect of insulin, glucagon and CCK on the discharge from hepatic vagal afferents, thought to feedback to control appetite. They conclude that these vagal afferents are glucose sensitive playing an important role in not only controlling food intake but also blood glucose levels.
12. Woods SC, Ramsay DS. Homeostasis: Beyond Curt Richter. Appetite. 2007;49(2):388-98.
Discusses the homeostatic mechanism of regulation vs. control with regard to adiposity and food intake. It considers feeding to be the controlled effector response that is not regulated but impacts on body adiposity, as regulated variable.